2,431 results match your criteria Complement Receptor Deficiency


Adiponectin deficiency has no effect in murine autoimmune myocarditis.

Cytokine 2019 Apr 1;116:139-149. Epub 2019 Feb 1.

Department of Cardiology, University of Heidelberg, Heidelberg, Germany. Electronic address:

Background: Adiponectin is a hormone that together with its receptors modulates a number of metabolic processes including gluconeogenesis and lipid catabolism. It belongs to the C1QTNF (complement C1q tumor necrosis factor-related protein) family, which has a variety of members with high amino acid sequence homology and overlapping functions. Concentration of adiponectin in blood is inversely correlated with body fat percentage and cardiac risk factors like blood pressure and CRP (C-reactive protein) level. Read More

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http://dx.doi.org/10.1016/j.cyto.2018.12.022DOI Listing
April 2019
1 Read

Data on inflammatory cytokines and pathways involved in clearance of from the lungs during cigarette smoking and vitamin D deficiency.

Data Brief 2019 Feb 18;22:703-708. Epub 2018 Dec 18.

Laboratory of Respiratory Diseases, Department of Chronic Diseases, Metabolism and Ageing (CHROMETA), KU Leuven, Leuven, Belgium.

This article contains data related to the inflammatory cytokine and investigated pathways involved in bacterial clearance reported in "Airway infection with Nontypeable is more rapidly eradicated in vitamin D deficient mice" (Serré et al., 2018) [1]. Vitamin D deficient or sufficient mice were oropharyngeally instilled with 10 NTHi and sacrificed at 4, 8, 24 and 72 h post-infection. Read More

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http://dx.doi.org/10.1016/j.dib.2018.12.048DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329200PMC
February 2019
2 Reads

Activation of mGluR1 Mediates C1q-Dependent Microglial Phagocytosis of Glutamatergic Synapses in Alzheimer's Rodent Models.

Mol Neurobiol 2019 Jan 16. Epub 2019 Jan 16.

Anesthesiology Institute, Cleveland Clinic, 9500 Euclid Ave., Cleveland, OH, 44195, USA.

Microglia and complements appear to be involved in the synaptic and cognitive deficits in Alzheimer's disease (AD), though the mechanisms remain elusive. In this study, utilizing two types of rodent model of AD, we reported increased complement C1q-mediated microglial phagocytosis of hippocampal glutamatergic synapses, which led to synaptic and cognitive deficits. We also found increased activity of the metabotropic glutamate receptor 1 (mGluR1) in hippocampal CA1 in the modeled rodents. Read More

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http://dx.doi.org/10.1007/s12035-019-1467-8DOI Listing
January 2019
4 Reads

Melkersson-Rosenthal syndrome: a case report of a rare disease with overlapping features.

Allergy Asthma Clin Immunol 2019 5;15. Epub 2019 Jan 5.

2Department of Neuroscience, Division of Dentistry, University of Padua, Via Giustiniani 2, 35128 Padua, Italy.

Background: Melkersson-Rosenthal syndrome (MRS) is a rare, neuro-mucocutaneous disease which presents as orofacial swelling, facial palsy and fissured tongue. These symptoms may occur simultaneously or, more frequently, with a oligosymptomatic or monosymptomatic pattern. Swelling, that is the most common initial finding, may mimic hereditary or acquired angioedema, a disorder caused by histamine or bradykinin-mediated plasma-leakage affecting subcutaneous and/or submucosal tissue. Read More

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https://aacijournal.biomedcentral.com/articles/10.1186/s1322
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http://dx.doi.org/10.1186/s13223-018-0316-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6320604PMC
January 2019
5 Reads

Complement C3a and C5a receptors promote GVHD by suppressing mitophagy in recipient dendritic cells.

JCI Insight 2018 Dec 20;3(24). Epub 2018 Dec 20.

Department of Microbiology and Immunology and.

Graft-versus-host disease (GVHD) is a major complication of allogeneic hematopoietic cell transplantation (HCT). DCs play critical roles in GVHD induction. Modulating autophagy represents a promising therapeutic strategy for the treatment of immunological diseases. Read More

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http://dx.doi.org/10.1172/jci.insight.121697DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6338312PMC
December 2018
2 Reads

Absence of recipient C3aR1 signaling limits expansion and differentiation of alloreactive CD8 T cell immunity and prolongs murine cardiac allograft survival.

Am J Transplant 2018 Dec 19. Epub 2018 Dec 19.

Translational Transplant Research Center, Icahn School of Medicine at Mount Sinai, New York, New York.

Activation, differentiation, and expansion of alloreactive CD8 T cells, the dominant effectors that mediate murine heart allograft rejection, requires allorecognition, costimulation, and cytokine-initiated signals. While previous work showed that alloreactive CD4 T cell immunity entails immune cell-produced and locally activated complement, whether and how C3a receptor 1 (C3aR1) signaling impacts transplant outcomes and the mechanisms linking C3aR1 to alloreactive CD8 T cell activation/expansion remain unclear. Herein we show that recipient C3aR1 deficiency or pharmacological C3aR1 blockade synergizes with tacrolimus to significantly prolong allograft survival versus tacrolimus-treated controls (median survival time 21 vs. Read More

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http://dx.doi.org/10.1111/ajt.15222DOI Listing
December 2018
2 Reads

Tregopathies: Monogenic diseases resulting in regulatory T-cell deficiency.

J Allergy Clin Immunol 2018 Dec;142(6):1679-1695

Department of Pediatrics, Division of Stem Cell Transplantation and Regenerative Medicine, Stanford School of Medicine, Stanford, Calif; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, Calif. Electronic address:

Monogenic diseases of the immune system, also known as inborn errors of immunity, are caused by single-gene mutations resulting in immune deficiency and dysregulation. More than 350 diseases have been described to date, and the number is rapidly expanding, with increasing availability of next-generation sequencing facilitating the diagnosis. The spectrum of immune dysregulation is wide, encompassing deficiencies in humoral, cellular, innate, and adaptive immunity; phagocytosis; and the complement system, which lead to autoinflammation and autoimmunity. Read More

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http://dx.doi.org/10.1016/j.jaci.2018.10.026DOI Listing
December 2018
4 Reads

Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion.

Nat Commun 2018 10 26;9(1):4470. Epub 2018 Oct 26.

Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC, H2W 1R7, Canada.

Myoblast fusion is tightly regulated during development and regeneration of muscle fibers. BAI3 is a receptor that orchestrates myoblast fusion via Elmo/Dock1 signaling, but the mechanisms regulating its activity remain elusive. Here we report that mice lacking BAI3 display small muscle fibers and inefficient muscle regeneration after cardiotoxin-induced injury. Read More

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http://www.nature.com/articles/s41467-018-06897-5
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http://dx.doi.org/10.1038/s41467-018-06897-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6203814PMC
October 2018
7 Reads

Mannose-Binding Lectin Drives Platelet Inflammatory Phenotype and Vascular Damage After Cerebral Ischemia in Mice via IL (Interleukin)-1α.

Arterioscler Thromb Vasc Biol 2018 Nov;38(11):2678-2690

From the Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy (F.O., S.F., D.D.B., R.Z., M.-G.D.S.).

Objective- Circulating complement factors are activated by tissue damage and contribute to acute brain injury. The deposition of MBL (mannose-binding lectin), one of the initiators of the lectin complement pathway, on the cerebral endothelium activated by ischemia is a major pathogenic event leading to brain injury. The molecular mechanisms through which MBL influences outcome after ischemia are not understood yet. Read More

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https://www.ahajournals.org/doi/10.1161/ATVBAHA.118.311058
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http://dx.doi.org/10.1161/ATVBAHA.118.311058DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6221395PMC
November 2018
8 Reads

Complement receptor CD46 co-stimulates optimal human CD8 T cell effector function via fatty acid metabolism.

Nat Commun 2018 10 10;9(1):4186. Epub 2018 Oct 10.

School of Immunology and Microbial Sciences, King's College London, London, UK.

The induction of human CD4 Th1 cells requires autocrine stimulation of the complement receptor CD46 in direct crosstalk with a CD4 T cell-intrinsic NLRP3 inflammasome. However, it is unclear whether human cytotoxic CD8 T cell (CTL) responses also rely on an intrinsic complement-inflammasome axis. Here we show, using CTLs from patients with CD46 deficiency or with constitutively-active NLRP3, that CD46 delivers co-stimulatory signals for optimal CTL activity by augmenting nutrient-influx and fatty acid synthesis. Read More

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http://www.nature.com/articles/s41467-018-06706-z
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http://dx.doi.org/10.1038/s41467-018-06706-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6180132PMC
October 2018
7 Reads

Cubilin, the intrinsic factor-vitamin B12 receptor in development and disease.

Curr Med Chem 2018 Oct 8. Epub 2018 Oct 8.

INSERM UMRS_1138, Centre de Recherche des Cordeliers, Paris-Diderot University. France.

Gp280/Intrinsic factor-vitamin B12 receptor/Cubilin (CUBN) is a large endocytic receptor serving multiple functions in vitamin B12 homeostasis, renal reabsorption of protein or toxic substances including albumin, vitamin D-binding protein or cadmium.Cubilin is a peripheral membrane protein consisting of 8 epidermal growth factor (EGF)-like repeats and 27 CUB (defined as Complement C1r/C1s, Uegf, BMP1) domains. This structurally unique protein interacts with at least two molecular partners, amnionless (AMN) and Lrp2/Megalin. Read More

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http://www.eurekaselect.com/166041/article
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http://dx.doi.org/10.2174/0929867325666181008143945DOI Listing
October 2018
12 Reads

Integrative approach to sporadic Alzheimer's disease: deficiency of TYROBP in a tauopathy mouse model reduces C1q and normalizes clinical phenotype while increasing spread and state of phosphorylation of tau.

Mol Psychiatry 2018 Oct 3. Epub 2018 Oct 3.

Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.

TYROBP/DAP12 forms complexes with ectodomains of immune receptors (TREM2, SIRPβ1, CR3) associated with Alzheimer's disease (AD) and is a network hub and driver in the complement subnetwork identified by multi-scale gene network studies of postmortem human AD brain. Using transgenic or viral approaches, we characterized in mice the effects of TYROBP deficiency on the phenotypic and pathological evolution of tauopathy. Biomarkers usually associated with worsening clinical phenotype (i. Read More

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http://dx.doi.org/10.1038/s41380-018-0258-3DOI Listing
October 2018
6 Reads

Limited Innovations After More Than 65 Years of Immunoglobulin Replacement Therapy: Potential of IgA- and IgM-Enriched Formulations to Prevent Bacterial Respiratory Tract Infections.

Front Immunol 2018 23;9:1925. Epub 2018 Aug 23.

Section Pediatric Infectious Diseases, Laboratory of Medical Immunology, Radboud Institute for Molecular Life Sciences, Nijmegen, Netherlands.

Patients with primary immunoglobulin deficiency have lower immunoglobulin levels or decreased immunoglobulin function, which makes these patients more susceptible to bacterial infection. Most prevalent are the selective IgA deficiencies (~1:3,000), followed by common variable immune deficiency (~1:25,000). Agammaglobulinemia is less common (~1:400,000) and is characterized by very low or no immunoglobulin production resulting in a more severe disease phenotype. Read More

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http://dx.doi.org/10.3389/fimmu.2018.01925DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115500PMC
August 2018
4 Reads

The Effects of Cholesterol-Derived Oncometabolites on Nuclear Receptor Function in Cancer.

Cancer Res 2018 Sep 17;78(17):4803-4808. Epub 2018 Aug 17.

Cholesterol Metabolism and Therapeutic Innovations, Cancer Research Center of Toulouse (CRCT), UMR 1037, Université de Toulouse, CNRS, Inserm, Toulouse, France.

Epidemiologic studies are controversial concerning the roles played by cholesterol in cancer risk and development, possibly as it is not cholesterol per se that is pathologic in cancers. Indeed, recent data reveal that the cholesterol metabolism in cancer cells can generate endogenous oncopromoter metabolites at higher levels compared with normal tissues and/or can be deregulated in the production of endogenous oncosuppressor metabolites in an opposite way. These metabolites are oxysterols, which are cholesterol oxygenation products generated by enzymatic and/or autoxidation processes. Read More

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http://dx.doi.org/10.1158/0008-5472.CAN-18-1487DOI Listing
September 2018
4 Reads

Innate Immune Cells Are Regulated by Axl in Hypertensive Kidney.

Am J Pathol 2018 Aug;188(8):1794-1806

Department of Medicine and Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York; Department of Biomedical Genetics, University of Rochester School of Medicine and Dentistry, Rochester, New York. Electronic address:

The balance between adaptive and innate immunity in kidney damage in salt-dependent hypertension is unclear. We investigated early renal dysfunction and the influence of Axl, a receptor tyrosine kinase, on innate immune response in hypertensive kidney in mice with lymphocyte deficiency (Rag1). The data suggest that increased presence of CD11b myeloid cells in the medulla might explain intensified salt and water retention as well as initial hypertensive response in Rag1 mice. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00029440173118
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http://dx.doi.org/10.1016/j.ajpath.2018.04.013DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099337PMC
August 2018
32 Reads

Complement Component C3 Promotes Cerebral Ischemia/Reperfusion Injury Mediated by TLR2/NFκB Activation in Diabetic Mice.

Neurochem Res 2018 Aug 13;43(8):1599-1607. Epub 2018 Jun 13.

Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.

Complement component C3 (C3), a key factor in the complement system, is heavily involved in various inflammation-associated diseases. However, it remains obscure for its role in the pathogenesis of cerebral ischemia/reperfusion (I/R) injury in diabetes. A transient middle cerebral artery occlusion (tMCAO) model was used for cerebral I/R injury in streptozotocin-induced diabetic mice. Read More

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http://dx.doi.org/10.1007/s11064-018-2574-zDOI Listing
August 2018
3 Reads

The Type 3 Deiodinase: Epigenetic Control of Brain Thyroid Hormone Action and Neurological Function.

Int J Mol Sci 2018 Jun 19;19(6). Epub 2018 Jun 19.

Center for Molecular Medicine, Maine Medical Center Research Institute, Maine Medical Center, Scarborough, ME 04074, USA.

Thyroid hormones (THs) influence multiple processes in the developing and adult central nervous system, and their local availability needs to be maintained at levels that are tailored to the requirements of their biological targets. The local complement of TH transporters, deiodinase enzymes, and receptors is critical to ensure specific levels of TH action in neural cells. The type 3 iodothyronine deiodinase (DIO3) inactivates THs and is highly present in the developing and adult brain, where it limits their availability and action. Read More

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http://dx.doi.org/10.3390/ijms19061804DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032375PMC
June 2018
2 Reads

C3a receptor antagonism as a novel therapeutic target for chronic rhinosinusitis.

Mucosal Immunol 2018 09 15;11(5):1375-1385. Epub 2018 Jun 15.

Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammatory disease with an unknown etiology. Recent studies have implicated the complement system as a potential modulator of disease immunopathology. We performed proteomic pathway enrichment analysis of differentially increased proteins, and found an enrichment of complement cascade pathways in the nasal mucus of individuals with CRSwNP as compared to control subjects. Read More

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http://dx.doi.org/10.1038/s41385-018-0048-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6162114PMC
September 2018
15 Reads
7.374 Impact Factor

Leukocyte Adhesion Deficiency Type 1 with Low Expression of CD 11b.

J Coll Physicians Surg Pak 2018 Jun;28(6):S87-S88

Department of Immunology, Armed Forces Institute of Pathology (AFIP), Rawalpindi.

Leukocyte adhesion deficiency type 1 (LAD-1) is a rare autosomal recessive disorder caused by mutations in the gene that codes for CD18, the beta chain of beta-2 integrins, located on the long arm of chromosome 21. This defect results in failure of leukocyte migration to the site of infection due to the absence of surface integrins. Leukocyte adhesion deficiency should be suspected in any patient with recurrent infections, impaired wound healing, history of delayed umbilical cord separation, periodontitis, leukocytosis, recurrent soft tissue and oral infections. Read More

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http://dx.doi.org/10.29271/jcpsp.2018.06.S87DOI Listing
June 2018
1 Read

CD11c-Specific Deletion Reveals CREB as a Critical Regulator of DC Function during the Germinal Center Response.

J Immunol Res 2018 7;2018:8947230. Epub 2018 May 7.

Department of Pediatrics, Medical Faculty, RWTH Aachen, Aachen, Germany.

Dendritic cells (DCs) are crucial for the balance between immune response and tolerance, but the molecular mechanism regulating development, differentiation, and homeostasis are poorly understood. The transcriptional activator CREB is involved in regulating different cells of the innate and adaptive immune system and is a transcriptional regulator of development, survival, activation, or proliferation in macrophages, dendritic cells, B cells, and T cells. To directly examine the role of CREB in the regulation of DCs, the gene was targeted for deletion with a transgene. Read More

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http://dx.doi.org/10.1155/2018/8947230DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5964551PMC
October 2018
2 Reads

Epidemiology of hypocomplementaemic urticarial vasculitis (anti-C1q vasculitis).

Rheumatology (Oxford) 2018 08;57(8):1400-1407

Department of Clinical Sciences Lund, Rheumatology, Lund University, Skåne University Hospital, Lund, Sweden.

Objectives: The aim was to describe the clinical characteristics and epidemiology of hypocomplementaemic urticarial vasculitis (HUV; anti-C1q vasculitis) in two geographically defined areas of Sweden.

Methods: In the health-care districts surrounding Skåne University Hospital (mean population 950 560) and Linköping University Hospital (mean population 428 503), all incident cases of HUV residing within the study areas at the onset of disease were identified during the years 2000-15. The diagnosis of HUV was confirmed by review of medical records. Read More

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http://dx.doi.org/10.1093/rheumatology/key110DOI Listing
August 2018
4 Reads

[Acquired C1 esterase inhibitor deficiency via bradykinin-mediated angioedema: Four cases].

Ann Dermatol Venereol 2018 Oct 17;145(10):598-602. Epub 2018 Apr 17.

Dermatologie, CHRU Minjoz, 3, boulevard Alexandre-Fleming, 25030 Besançon, France.

Background: Acquired C1-esterase inhibitor (C1-INH) deficiency angioedema (C1-INH-AAE) is a form of bradykinin-mediated angioedema. This rare disorder is due to acquired consumption of C1-INH, hyperactivation of the classic pathway of human complement, and potentially fatal recurrent angioedema symptoms. Clinical symptoms of C1-INH-AAE are very similar to those of hereditary angioedema (HAE) but usually appear after the fourth decade of life and induce abdominal pain less frequently. Read More

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http://dx.doi.org/10.1016/j.annder.2018.02.012DOI Listing
October 2018
8 Reads

Bacteroidetes Neurotoxins and Inflammatory Neurodegeneration.

Mol Neurobiol 2018 Dec 10;55(12):9100-9107. Epub 2018 Apr 10.

LSU Neuroscience Center, Louisiana State University Health Sciences Center, 2020 Gravier Street, Suite 904, New Orleans, LA, 70112, USA.

The gram-negative facultative anaerobe Bacteroides fragilis (B. fragilis) constitutes an appreciable proportion of the human gastrointestinal (GI)-tract microbiome. As is typical of most gram-negative bacilli, B. Read More

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http://link.springer.com/10.1007/s12035-018-1015-y
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http://dx.doi.org/10.1007/s12035-018-1015-yDOI Listing
December 2018
8 Reads

and Ameliorate Lipopolysaccharide-Induced Acute Lung Injury in Rats by Regulating the Toll-Like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway.

Evid Based Complement Alternat Med 2018 29;2018:3017571. Epub 2018 Jan 29.

Department of Traditional Chinese Medicine, Chinese PLA General Hospital, Beijing 100853, China.

and (AM/SM) are well used in Traditional Chinese Medicines (TCM) for nourishing Qi and activating blood circulation method. From TCM theory, the pathogenesis of acute lung injury (ALI) was determined as Qi deficiency and blood stagnation. In this study, we are aiming to investigate the protective and therapeutic effects of AM/SM on a rat model of lipopolysaccharide- (LPS-) induced ALI in rats and to elucidate potential molecular mechanisms. Read More

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http://dx.doi.org/10.1155/2018/3017571DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5829314PMC
January 2018
29 Reads

Specific Inhibition of Complement Activation Significantly Ameliorates Autoimmune Blistering Disease in Mice.

Front Immunol 2018 16;9:535. Epub 2018 Mar 16.

Institute of Genetics, Department of Biology, University of Erlangen-Nuremberg, Erlangen, Germany.

Epidermolysis bullosa acquisita (EBA) is an antibody-mediated blistering skin disease associated with tissue-bound and circulating autoantibodies to type VII collagen (COL7). Transfer of antibodies against COL7 into mice results in a subepidermal blistering phenotype, strictly depending on the complement component C5. Further, activation predominantly by the alternative pathway is required to induce experimental EBA, as blistering was delayed and significantly ameliorated only in factor B mice. Read More

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http://dx.doi.org/10.3389/fimmu.2018.00535DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5865061PMC
March 2018
9 Reads

Mesenchymal stem cells alleviate acute kidney injury by down-regulating C5a/C5aR pathway activation.

Int Urol Nephrol 2018 Aug 28;50(8):1545-1553. Epub 2018 Mar 28.

Department of Nephrology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.

Background: Acute kidney injury (AKI) leads to serious renal damage, and early inhibition of inflammation is necessary for its treatment. C5a/C5aR signaling activation promotes inflammatory response in tissue injury. Anti-inflammatory activity of mesenchymal stem cells (MSCs) makes it possible to alleviate AKI by controlling the C5a/C5aR signaling activation. Read More

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http://dx.doi.org/10.1007/s11255-018-1844-7DOI Listing
August 2018
11 Reads

Innate immune system activation in zebrafish and cellular models of Diamond Blackfan Anemia.

Sci Rep 2018 Mar 26;8(1):5165. Epub 2018 Mar 26.

Department of Molecular, Cell & Developmental Biology, University of California, Los Angeles, CA, USA.

Deficiency of ribosomal proteins (RPs) leads to Diamond Blackfan Anemia (DBA) associated with anemia, congenital defects, and cancer. While p53 activation is responsible for many features of DBA, the role of immune system is less defined. The Innate immune system can be activated by endogenous nucleic acids from non-processed pre-rRNAs, DNA damage, and apoptosis that occurs in DBA. Read More

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http://dx.doi.org/10.1038/s41598-018-23561-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5980095PMC
March 2018
5 Reads

Response gene to complement 32 suppresses adipose tissue thermogenic genes through inhibiting β3-adrenergic receptor/mTORC1 signaling.

FASEB J 2018 Sep 26;32(9):4836-4847. Epub 2018 Mar 26.

Department of Physiology and Pharmacology, University of Georgia, Athens, Georgia, USA.

Our previous studies have shown that response gene to complement (RGC)-32 deficiency (Rgc32) protects mice from diet-induced obesity and increases thermogenic gene expression in adipose tissues. However, the underlying mechanisms by which RGC-32 regulates thermogenic gene expression remain to be determined. In the present study, RGC-32 expression in white adipose tissue (WAT) was suppressed during cold exposure-induced WAT browning. Read More

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http://dx.doi.org/10.1096/fj.201701508RDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6103168PMC
September 2018
6 Reads

Granulocyte and monocyte CD11b expression during plasma separation is dependent on complement factor 5 (C5) - an ex vivo study with blood from a C5-deficient individual.

APMIS 2018 Apr;126(4):342-352

Institute of Clinical Medicine and K. G. Jebsen TREC, University of Tromsø, Tromsø, Norway.

The aim of the study was to investigate the role of complement factor 5 (C5) in reactions elicited by plasma separation using blood from a C5-deficient (C5D) individual, comparing it to C5-deficient blood reconstituted with C5 (C5DR) and blood from healthy donors. Blood was circulated through an ex vivo plasma separation model. Leukocyte CD11b expression and leukocyte-platelet conjugates were measured by flow cytometry during a 30-min period. Read More

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http://dx.doi.org/10.1111/apm.12821DOI Listing
April 2018
4 Reads

Complement 5a stimulates macrophage polarization and contributes to tumor metastases of colon cancer.

Exp Cell Res 2018 05 15;366(2):127-138. Epub 2018 Mar 15.

Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing 100029, China; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing collaborative innovative research center for cardiovascular diseases, Beijing 100029, China. Electronic address:

Inflammatory cells such as macrophages can play a pro-tumorigenic role in the tumor stroma. Tumor-associated macrophages (TAMs) generally display an M2 phenotype with tumor-promoting activity; however, the mechanisms regulating the TAM phenotype remain unclear. Complement 5a (C5a) is a cytokine-like polypeptide that is generated during complement system activation and is known to promote tumor growth. Read More

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http://dx.doi.org/10.1016/j.yexcr.2018.03.009DOI Listing
May 2018
12 Reads

Complement component 3a receptor deficiency attenuates chronic stress-induced monocyte infiltration and depressive-like behavior.

Brain Behav Immun 2018 05 5;70:246-256. Epub 2018 Mar 5.

Department of Psychiatry and Health Behavior, Medical College of Georgia, Augusta University, Augusta, GA 30912, United States. Electronic address:

Major depressive disorder (MDD) is one of the most common and debilitating neuropsychiatric illnesses. Accumulating evidence suggests a potential role of the immune system in the pathophysiology of MDD. The complement system represents one of the major effector mechanisms of the innate immune system, and plays a critical role in inflammation. Read More

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http://dx.doi.org/10.1016/j.bbi.2018.03.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5967612PMC
May 2018
4 Reads

Beyond the Role of CD55 as a Complement Component.

Immune Netw 2018 Feb 20;18(1):e11. Epub 2018 Feb 20.

Severance Biomedical Science Institute and BK21 PLUS Project to Medical Sciences, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06230, Korea.

The complement is a part of the immune system that plays several roles in removing pathogens. Despite the importance of the complement system, the exact role of each component has been overlooked because the complement system was thought to be a nonspecific humoral immune mechanism that worked against pathogens. Decay-accelerating factor (DAF or CD55) is a known inhibitor of the complement system and has recently attracted substantial attention due to its role in various diseases, such as cancer, protein-losing enteropathy, and malaria. Read More

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http://dx.doi.org/10.4110/in.2018.18.e11DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5833118PMC
February 2018
7 Reads

MT4-MMP deficiency increases patrolling monocyte recruitment to early lesions and accelerates atherosclerosis.

Nat Commun 2018 03 2;9(1):910. Epub 2018 Mar 2.

Matrix Metalloproteinases in Angiogenesis and Inflammation Group, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro 3, 28029, Madrid, Spain.

Matrix metalloproteinases are involved in vascular remodeling. Little is known about their immune regulatory role in atherosclerosis. Here we show that mice deficient for MT4-MMP have increased adherence of macrophages to inflamed peritonea, and larger lipid deposits and macrophage burden in atherosclerotic plaques. Read More

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http://dx.doi.org/10.1038/s41467-018-03351-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5834547PMC
March 2018
31 Reads

Deficiency of Complement C3a and C5a Receptors Prevents Angiotensin II-Induced Hypertension via Regulatory T Cells.

Circ Res 2018 Mar 5;122(7):970-983. Epub 2018 Feb 5.

From the State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension at Ruijin Hospital and Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, China (X.-H.C., C.-C.R., Q.G., Y.M., J.-Z.X., D.-R.C., D.-L.Z., P.-J.G.); and Laboratory of Vascular Biology (X.-H.C., C.-C.R., Z.-B.Z., J.-R.L., P.-J.G.) and Key Laboratory of Stem Cell Biology (X.-H.C., C.-C.R., Z.-B.Z., J.-R.L., P.-J.G.), Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

Rationale: Inflammation and immunity play crucial roles in the development of hypertension. Complement activation-mediated innate immune response is involved in the regulation of hypertension and target-organ damage. However, whether complement-mediated T-cell functions could regulate blood pressure elevation in hypertension is still unclear. Read More

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http://dx.doi.org/10.1161/CIRCRESAHA.117.312153DOI Listing
March 2018
12 Reads

In vitro evaluation of the biological activities of IgG in seven Chinese intravenous immunoglobulin preparations.

J Pharm Biomed Anal 2018 Mar 16;151:317-323. Epub 2018 Jan 16.

Institute of Blood Transfusion, Chinese Academy of Medical Sciences, 26 Huacai Road, Longtan Industry Park, Chenghua District, Chengdu, 610052, China. Electronic address:

The IgG activities of antigen recognition, Fc-mediated complement activation and cellular Fcγ-receptors (FcγRs) binding are critical for intravenous immunoglobulin (IVIg) immunotherapy in a variety of immune deficiency diseases. Further, these activities could be influenced by different plasma sources and the IVIg manufacturing processes of different manufacturers. This study evaluated and compared the biological activities of IgG in 7 IVIg preparations produced by different Chinese manufacturers. Read More

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http://dx.doi.org/10.1016/j.jpba.2018.01.021DOI Listing
March 2018
32 Reads

TNIP1 reduction sensitizes keratinocytes to post-receptor signalling following exposure to TLR agonists.

Cell Signal 2018 May 5;45:81-92. Epub 2018 Feb 5.

Department of Pharmaceutical Sciences, University of Connecticut, Storrs, CT 06269-3092, USA; Stem Cell Institute, University of Connecticut, Storrs, CT 06269-3092, USA. Electronic address:

Cell level inflammatory signalling is a combination of initiation at cell membrane receptors and modulation by cytoplasmic regulatory proteins. For keratinocytes, the predominant cell type in the epidermis, this would include toll-like receptors (TLR) and cytoplasmic proteins that propagate or dampen post-receptor signalling. We previously reported that increased levels of tumor necrosis factor α induced protein 3-interacting protein 1 (TNIP1) in HaCaT keratinocytes leads to decreased expression of stress response and inflammation-associated genes. Read More

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http://dx.doi.org/10.1016/j.cellsig.2018.02.004DOI Listing
May 2018
6 Reads

Splenic macrophages are required for protective innate immunity against West Nile virus.

PLoS One 2018 6;13(2):e0191690. Epub 2018 Feb 6.

Department of Immunology, University of Washington, Seattle, WA, United States of America.

Although the spleen is a major site for West Nile virus (WNV) replication and spread, relatively little is known about which innate cells in the spleen replicate WNV, control viral dissemination, and/or prime innate and adaptive immune responses. Here we tested if splenic macrophages (MΦs) were necessary for control of WNV infection. We selectively depleted splenic MΦs, but not draining lymph node MΦs, by injecting mice intravenously with clodronate liposomes several days prior to infecting them with WNV. Read More

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191690PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5800658PMC
March 2018
3 Reads

Integrin CD11b negatively regulates Mincle-induced signaling via the Lyn-SIRPα-SHP1 complex.

Exp Mol Med 2018 02 5;50(2):e439. Epub 2018 Feb 5.

Department of Integrated Omics for Biomedical Science, Graduate School, Yonsei University, Seoul, Republic of Korea.

During mycobacteria infection, anti-inflammatory responses allow the host to avoid tissue damage caused by overactivation of the immune system; however, little is known about the negative modulators that specifically control mycobacteria-induced immune responses. Here we demonstrate that integrin CD11b is a critical negative regulator of mycobacteria cord factor-induced macrophage-inducible C-type lectin (Mincle) signaling. CD11b deficiency resulted in hyperinflammation following mycobacterial infection. Read More

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http://dx.doi.org/10.1038/emm.2017.256DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5992981PMC
February 2018
5 Reads

Plasminogen Activator Inhibitor-1 Promotes Neutrophil Infiltration and Tissue Injury on Ischemia-Reperfusion.

Arterioscler Thromb Vasc Biol 2018 04 25;38(4):829-842. Epub 2018 Jan 25.

From the Walter Brendel Centre of Experimental Medicine (M.P., G.Z., M.H., B.U., J.S., L.M., M.F., D.F., M.L., A.K., F.K., C.A.R.), Department of Otorhinolaryngology (G.Z., M.H., B.U., C.A.R.), Head and Neck Surgery (M.P.), Pharmaceutical Biology, Department of Pharmacy, Center for Drug Research (S.Z.), Department of Surgery (D.F., M.L., A.K.), and Department of Radiation Oncology (K.L.), Ludwig-Maximilians-Universität München, Munich, Germany; Department of Psychiatry and Psychotherapy, University Clinic, Friedrich-Alexander-University of Erlangen-Nuremberg, Germany (M.P); Institute of Pharmaceutical Biology, Goethe University Frankfurt, Germany (R.F.); and Institute of Basic Medical Sciences, University of Oslo, Norway (S.K.).

Objective: Ischemia-reperfusion (I/R) injury significantly contributes to organ dysfunction and failure after myocardial infarction, stroke, and transplantation. In addition to its established role in the fibrinolytic system, plasminogen activator inhibitor-1 has recently been implicated in the pathogenesis of I/R injury. The underlying mechanisms remain largely obscure. Read More

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https://www.ahajournals.org/doi/10.1161/ATVBAHA.117.309760
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http://dx.doi.org/10.1161/ATVBAHA.117.309760DOI Listing
April 2018
15 Reads

The Complement C3aC3aR Axis Promotes Development of Thoracic Aortic Dissection via Regulation of MMP2 Expression.

J Immunol 2018 03 24;200(5):1829-1838. Epub 2018 Jan 24.

Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education, Beijing Collaborative Innovative Research Center for Cardiovascular Diseases, Beijing 100029, China;

Thoracic aortic dissection (TAD), once ruptured, is devastating to patients, and no effective pharmaceutical therapy is available. Anaphylatoxins released by complement activation are involved in a variety of diseases. However, the role of the complement system in TAD is unknown. Read More

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http://dx.doi.org/10.4049/jimmunol.1601386DOI Listing
March 2018
17 Reads

Complement C5a Receptor 1 Exacerbates the Pathophysiology of Sepsis and Is a Potential Target for Disease Treatment.

MBio 2018 01 23;9(1). Epub 2018 Jan 23.

Institute for Hygiene and Microbiology, University of Würzburg, Würzburg, Germany

Sepsis caused by (meningococcus) is a rapidly progressing, life-threatening disease. Because its initial symptoms are rather unspecific, medical attention is often sought too late, i.e. Read More

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http://mbio.asm.org/lookup/doi/10.1128/mBio.01755-17
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http://dx.doi.org/10.1128/mBio.01755-17DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5784250PMC
January 2018
13 Reads

Absence of myeloid Klf4 reduces prostate cancer growth with pro-atherosclerotic activation of tumor myeloid cells and infiltration of CD8 T cells.

PLoS One 2018 11;13(1):e0191188. Epub 2018 Jan 11.

Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.

The microenvironment of prostate cancer often includes abundant tumor-associated macrophages (TAMs), with their acquisition of an M2 phenotype correlating with local aggressiveness and metastasis. Tumor-derived M-CSF contributes to TAM M2 polarization, and M-CSF receptor inhibition slows prostate cancer growth in model systems. As additional cytokines can direct TAM M2 polarization, targeting downstream transcription factors could avoid resistance. Read More

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191188PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5764416PMC
February 2018
8 Reads

C5aR activation in the absence of C5a: A new disease mechanism of autoimmune hemolytic anemia in mice.

Eur J Immunol 2018 04 15;48(4):696-704. Epub 2018 Jan 15.

Molecular Immunology Research Unit, Division of Clinical Immunology and Rheumatology, Hannover Medical School, Hannover, Germany.

IgG Fc receptors (FcγRs) and the C5a anaphylatoxin receptor (C5aR) were identified as key regulators of type II autoimmune injury in mice. However, and with respect to C5aR, the relative importance of C5a for IgG autoantibody-induced cellular destruction remained unclear. Using an experimental model of autoimmune hemolytic anemia (AIHA), we here report marked differences in the development of AIHA between mice lacking C5aR and C5-deficient (Hc ) strain, indicating a limited role of C5 in this type of C5aR-regulated disease. Read More

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http://dx.doi.org/10.1002/eji.201747238DOI Listing
April 2018
8 Reads
1 Citation
4.030 Impact Factor

Age-associated B cells expanded in autoimmune mice are memory cells sharing H-CDR3-selected repertoires.

Eur J Immunol 2018 03 15;48(3):509-521. Epub 2018 Jan 15.

Department of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.

Age-associated B cells (ABCs) represent a distinct cell population expressing low levels of CD21 (CD21 ). The Ig repertoire expressed by ABCs in aged mice is diverse and exhibits signs of somatic hypermutation (SHM). A CD21 B-cell population is expanded in autoimmune diseases, e. Read More

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http://dx.doi.org/10.1002/eji.201747127DOI Listing
March 2018
5 Reads
4.034 Impact Factor

Immune Responses of HLA Highly Sensitized and Nonsensitized Patients to Genetically Engineered Pig Cells.

Transplantation 2018 05;102(5):e195-e204

Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA.

Background: We investigated in vitro whether HLA highly sensitized patients with end-stage renal disease will be disadvantaged immunologically after a genetically engineered pig kidney transplant.

Methods: Blood was drawn from patients with a calculated panel-reactive antibody (cPRA) 99% to 100% (Gp1, n = 10) or cPRA 0% (Gp2, n = 12), and from healthy volunteers (Gp3, n = 10). Serum IgM and IgG binding was measured (i) to galactose-α1-3 galactose and N-glycolylneuraminic acid glycans by enzyme-linked immunosorbent assay, and (ii) to pig red blood cell, pig aortic endothelial cells, and pig peripheral blood mononuclear cell from α1,3-galactosyltransferase gene-knockout (GTKO)/CD46 and GTKO/CD46/cytidine monophosphate-N-acetylneuraminic acid hydroxylase-knockout (CMAHKO) pigs by flow cytometry. Read More

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http://dx.doi.org/10.1097/TP.0000000000002060DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5924598PMC
May 2018
17 Reads
3 Citations
3.830 Impact Factor

Effects of Salvia miltiorrhiza extract with supplemental liquefied calcium on osteoporosis in calcium-deficient ovariectomized mice.

BMC Complement Altern Med 2017 Dec 20;17(1):545. Epub 2017 Dec 20.

Department of Oriental Medicine and Biotechnology, College of Life Science, Kyung Hee University, Yongin-si, 17104, Republic of Korea.

Background: Extracts from Salvia miltiorrhiza Bunge have been used in traditional Asian medicine to treat coronary heart disease, chronic renal failure, atherosclerosis, myocardial infraction, angina pectoris, myocardial ischemia, dysmenorrheal, neurasthenic insomnia, liver fibrosis and cirrhosis. The aim of the study was to investigate the anti-RANK signal effect of the combination of S.miltiorrhiza Bunge (SME) and liquefied calcium (LCa) supplement with ovariectomized (OVX-SML) mice, a osteoporosis animal model. Read More

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http://dx.doi.org/10.1186/s12906-017-2047-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738837PMC
December 2017
20 Reads

Protective effects of geniposide and ginsenoside Rg1 combination treatment on rats following cerebral ischemia are mediated via microglial microRNA‑155‑5p inhibition.

Mol Med Rep 2018 Feb 7;17(2):3186-3193. Epub 2017 Dec 7.

Experimental Research Center, China Academy of Chinese Medical Sciences, Beijing 100700, P.R. China.

Geniposide, an active component of Gardenia, has been reported to protect against cerebral ischemia in animals. Ginsenoside Rg1, a component of Panax notoginseng, is usually administered in combination with Gardenia for the treatment of acute ischemic stroke; however, there are unknown effects of ginsenoside Rg1 that require further investigation. In the present study, the effects of geniposide and ginsensoide Rg1 combination treatment on focal cerebral ischemic stroke were investigated. Read More

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http://dx.doi.org/10.3892/mmr.2017.8221DOI Listing
February 2018
9 Reads

Complement C3a signaling facilitates skeletal muscle regeneration by regulating monocyte function and trafficking.

Nat Commun 2017 12 12;8(1):2078. Epub 2017 Dec 12.

Beijing AnZhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, 100029, China.

Regeneration of skeletal muscle following injury is accompanied by transient inflammation. Here we show that complement is activated in skeletal muscle injury and plays a key role during regeneration. Genetic ablation of complement C3 or its inactivation with Cobra Venom Factor (CVF) result in impaired muscle regeneration following cardiotoxin-induced injury in mice. Read More

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http://dx.doi.org/10.1038/s41467-017-01526-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5727192PMC
December 2017
21 Reads

VISTA deficiency attenuates antibody-induced arthritis and alters macrophage gene expression in response to simulated immune complexes.

Arthritis Res Ther 2017 Dec 8;19(1):270. Epub 2017 Dec 8.

Department of Veterans Affairs, Research Service, White River Junction, VT, 05009, USA.

Background: In addition to activated T cells, the immune checkpoint inhibitor "V domain-containing Ig suppressor of T-cell activation" (VISTA) is expressed by myeloid cell types, including macrophages and neutrophils. The importance of VISTA expression by myeloid cells to antibody-induced arthritis and its potential for relevance in human disease was evaluated.

Methods: VISTA was immunolocalized in normal and arthritic human synovial tissue sections and synovial tissue lysates were subjected to western blot analysis. Read More

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http://dx.doi.org/10.1186/s13075-017-1474-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721690PMC
December 2017
27 Reads