2,449 results match your criteria Complement Receptor Deficiency


The complement receptor C5aR2 promotes protein kinase R expression and contributes to NLRP3 inflammasome activation and HMGB1 release from macrophages.

J Biol Chem 2019 Apr 10. Epub 2019 Apr 10.

Department of Hematology and Key Laboratory of non-resolving inflammation and tumor, The Third Xiangya Hospital, Central South University, China.

The NLR family pyrin domain-containing 3 (NLRP3) inflammasome is a multimeric protein complex that mediates the maturation of the cytokines interleukin (IL)-1β and IL-18, as well as the release of the proinflammatory protein high mobility group box 1 (HMGB1) and contributes to several inflammatory diseases, including sepsis, gout and type 2 diabetes. In this context, the well-studied active complement fragment C5a and its receptor C5aR1 or C5aR2 orchestrate the inflammatory responses in many diseases. Although a C5a-C5aR interaction in NLRP3-associated diseases has been suggested, little is known about the details of C5a-C5aR crosstalk with the NLRP3 inflammasome in macrophages. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1074/jbc.RA118.006508DOI Listing

HDAC1 and HDAC2 independently regulate common and specific intrinsic responses in murine enteroids.

Sci Rep 2019 Mar 29;9(1):5363. Epub 2019 Mar 29.

Département d'anatomie et biologie cellulaire, Faculté de médecine et des sciences de la santé, Pavillon de recherche appliquée sur le cancer, Université de Sherbrooke, Sherbrooke, Québec, J1E 4K8, Canada.

Both HDAC1 and HDAC2 are class I deacetylases acting as erasers of lysine-acetyl marks on histones and non-histone proteins. Several histone deacetylase inhibitors, either endogenous to the cell, such as the ketogenic β-hydroxybutyrate metabolite, or exogenous, such as butyrate, a microbial-derived metabolite, regulate HDAC activity. Different combinations of intestinal epithelial cell (IEC)-specific Hdac1 and/or Hdac2 deletion differentially alter mucosal homeostasis in mice. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41598-019-41842-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6441098PMC
March 2019
1 Read

Differential contribution of C5aR and C5b-9 pathways to renal thrombic microangiopathy and macrovascular thrombosis in mice carrying an atypical hemolytic syndrome-related factor H mutation.

Kidney Int 2019 Feb 27. Epub 2019 Feb 27.

Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Electronic address:

Atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) caused by dysregulated complement activation. Clinically, aHUS is effectively treated by an anti-C5 monoclonal antibody (mAb) but whether the disease is mediated by the C5a receptor (C5aR) or C5b-9 pathway, or both, is unknown. Here we address this in a factor H mutant mouse (FH) which developed complement-mediated TMA as well as macrovascular thrombosis caused by an aHUS-related factor H point mutation (mouse W1206R, corresponding to human W1183R). Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.kint.2019.01.009DOI Listing
February 2019
1 Read

Deficiency of urokinase-type plasminogen activator and its receptor affects social behavior and increases seizure susceptibility.

Epilepsy Res 2019 03 25;151:67-74. Epub 2019 Feb 25.

Epilepsy Research Laboratory, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, FI-70211 Kuopio, Finland. Electronic address:

Extracellular proteolysis initiated by the binding of urokinase-type plasminogen activator (uPA) to its receptor (uPAR) regulates the development of inhibitory neuronal circuits in the cerebral cortex and tissue remodeling after epileptogenic brain injury. To study the function of different components of the uPA-uPAR system on behavior and epileptogenesis, and to complement our previous studies on naïve and injured mice deficient in the uPA-encoding gene Plau or the uPAR-encoding gene Plaur, we analyzed the behavioral phenotype, seizure susceptibility, and perineuronal nets surrounding parvalbumin-positive inhibitory interneurons in Plau and Plaur (double knockout dKO) mice. In a climbing test, dKO mice showed reduced interest towards the environment as compared with Wt mice (p < 0. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.eplepsyres.2019.02.009DOI Listing
March 2019
3 Reads

Deletion of a flippase subunit Tmem30a in hematopoietic cells impairs mouse fetal liver erythropoiesis.

Haematologica 2019 Feb 28. Epub 2019 Feb 28.

Key Laboratory of Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou, China;

Transmembrane protein 30A (Tmem30a) is the β-subunit of P4-ATPases which function as flippase that transports aminophospholipids such as phosphatidylserine from the outer to the inner leaflets of the plasma membrane to maintain asymmetric distribution of phospholipids. It has been documented that deficiency of Tmem30a led to exposure of phosphatidylserine. However, the role of Tmem30a in vivo remains largely unknown. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.3324/haematol.2018.203992DOI Listing
February 2019
1 Read

CD11b Regulates Fungal Outgrowth but Not Neutrophil Recruitment in a Mouse Model of Invasive Pulmonary Aspergillosis.

Front Immunol 2019 4;10:123. Epub 2019 Feb 4.

Department of Dermatology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.

ß2 integrin receptors consist of an alpha subunit (CD11a-CD11d) and CD18 as the common beta subunit, and are differentially expressed by leukocytes. ß2 integrins are required for cell-cell interaction, transendothelial migration, uptake of opsonized pathogens, and cell signaling processes. Functional loss of CD18-termed leukocyte-adhesion deficiency type 1 (LAD1)-results in an immunocompromised state characterized by frequent occurrence of severe infections. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.3389/fimmu.2019.00123DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6369709PMC
February 2019
2 Reads

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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.cyto.2018.12.022DOI Listing
April 2019
2 Reads

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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.dib.2018.12.048DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329200PMC
February 2019
3 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12035-019-1467-8DOI Listing
January 2019
9 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

View Article

Download full-text PDF

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

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

JCI Insight 2018 12 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1172/jci.insight.121697DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6338312PMC
December 2018
3 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1111/ajt.15222DOI Listing
December 2018
3 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

View Article

Download full-text PDF

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

Complement C3a receptor modulates embryonic neural progenitor cell proliferation and cognitive performance.

Mol Immunol 2018 09 27;101:176-181. Epub 2018 Jun 27.

School of Biomedical Sciences, Faculty of Medicine, The University of Queensland, Brisbane, Australia. Electronic address:

The complement system of innate immunity is emerging as a novel player in neurodevelopmental processes. The receptor for C3a, C3aR, shares a close evolutionary and functional relationship with C5a receptors. Whilst the C5a receptor, C5aR1, has been demonstrated to promote embryonic neural stem cell proliferation, little is known about the role of C3aR in this process. Read More

View Article

Download full-text PDF

Source
https://linkinghub.elsevier.com/retrieve/pii/S01615890183050
Publisher Site
http://dx.doi.org/10.1016/j.molimm.2018.06.271DOI Listing
September 2018
11 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

View Article

Download full-text PDF

Source
http://www.nature.com/articles/s41467-018-06897-5
Publisher Site
http://dx.doi.org/10.1038/s41467-018-06897-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6203814PMC
October 2018
9 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

View Article

Download full-text PDF

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

CD18 is redundant for the response to multiple vaccines: A case study.

Pediatr Allergy Immunol 2019 02 13;30(1):136-139. Epub 2018 Nov 13.

Hans Christian Andersen Children's Hospital, Odense University Hospital, Odense, Denmark.

View Article

Download full-text PDF

Source
http://doi.wiley.com/10.1111/pai.12989
Publisher Site
http://dx.doi.org/10.1111/pai.12989DOI Listing
February 2019
11 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

View Article

Download full-text PDF

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

Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis.

MBio 2018 10 9;9(5). Epub 2018 Oct 9.

Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA

Acute respiratory distress syndrome (ARDS) is immune-driven pathologies that are observed in severe cases of severe acute respiratory syndrome coronavirus (SARS-CoV) infection. SARS-CoV emerged in 2002 to 2003 and led to a global outbreak of SARS. As with the outcome of human infection, intranasal infection of C57BL/6J mice with mouse-adapted SARS-CoV results in high-titer virus replication within the lung, induction of inflammatory cytokines and chemokines, and immune cell infiltration within the lung. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1128/mBio.01753-18DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6178621PMC
October 2018
6 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

View Article

Download full-text PDF

Source
http://www.eurekaselect.com/166041/article
Publisher Site
http://dx.doi.org/10.2174/0929867325666181008143945DOI Listing
October 2018
20 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41380-018-0258-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6447470PMC
October 2018
9 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.3389/fimmu.2018.01925DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6115500PMC
August 2018
5 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

View Article

Download full-text PDF

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

[Novel mutations of ITGB2 induced leukocyte adhesion defect type 1].

Zhonghua Er Ke Za Zhi 2018 Aug;56(8):617-622

Department of Pediatric Cardiology, Nephrology and Rheumatology, Affiliated Hospital of Qingdao University, Qingdao 266003, China.

To investigate the pathogenic mechanism of two novel ITGB2 mutations in leukocyte adhesion defect type 1 (LAD1). The clinical history and blood sample of an 11 years old patient admitted to Affiliated Hospital of Qingdao University in August 2014 were collected. Expression of CD18 (encoded by ITGB2) was analyzed by flow cytometry. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.3760/cma.j.issn.0578-1310.2018.08.012DOI Listing
August 2018
1 Read

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

View Article

Download full-text PDF

Source
https://linkinghub.elsevier.com/retrieve/pii/S00029440173118
Publisher Site
http://dx.doi.org/10.1016/j.ajpath.2018.04.013DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099337PMC
August 2018
45 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11064-018-2574-zDOI Listing
August 2018
4 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.3390/ijms19061804DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032375PMC
June 2018
3 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41385-018-0048-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6162114PMC
September 2018
25 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.29271/jcpsp.2018.06.S87DOI Listing
June 2018
4 Reads

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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1155/2018/8947230DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5964551PMC
October 2018
3 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

View Article

Download full-text PDF

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

The ITIM Domain-Containing NK Receptor Ly49Q Impacts Pulmonary Infection by Mediating Neutrophil Functions.

J Immunol 2018 06 30;200(12):4085-4093. Epub 2018 Apr 30.

Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Muenster, University of Muenster, Muenster 48149, Germany;

Pulmonary infection is a frequent pathology associated with excessive neutrophil infiltration. Ly49Q, an ITIM domain-bearing receptor expressed on different leukocytes, has been recently reported to impact neutrophil migration and polarization. Utilizing a murine model of induced pulmonary infection in combination with additional in vivo and in vitro assays, we show that Ly49Q is critically involved in different steps of the leukocyte adhesion cascade. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.4049/jimmunol.1701084DOI Listing
June 2018
6 Reads

Sialidase Deficiency in Increases IL-12 Secretion in Stimulated Macrophages Through Regulation of CR3, IncRNA GAS5 and miR-21.

Front Cell Infect Microbiol 2018 5;8:100. Epub 2018 Apr 5.

Department of Periodontics, School of Stomatology, China Medical University, Shenyang, China.

() is a major periodontal pathogen that can induce an immune response leading to a destructive inflammatory process. During the inflammatory process, interleukin-12 (IL-12) is secreted, correlating with bacterial clearance by macrophages. Bacterial sialidase has recently been shown to influence the synthesis and modification of the macromolecules on its surface, and is associated with the interaction between bacteria and host cells. Read More

View Article

Download full-text PDF

Source
http://journal.frontiersin.org/article/10.3389/fcimb.2018.00
Publisher Site
http://dx.doi.org/10.3389/fcimb.2018.00100DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5895773PMC
April 2019
6 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

View Article

Download full-text PDF

Source
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

View Article

Download full-text PDF

Source
http://link.springer.com/10.1007/s12035-018-1015-y
Publisher Site
http://dx.doi.org/10.1007/s12035-018-1015-yDOI Listing
December 2018
9 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1155/2018/3017571DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5829314PMC
January 2018
36 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.3389/fimmu.2018.00535DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5865061PMC
March 2018
12 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11255-018-1844-7DOI Listing
August 2018
12 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

View Article

Download full-text PDF

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

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

FASEB J 2018 09 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1096/fj.201701508RDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6103168PMC
September 2018
9 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

View Article

Download full-text PDF

Source
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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.yexcr.2018.03.009DOI Listing
May 2018
14 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbi.2018.03.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5967612PMC
May 2018
5 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

View Article

Download full-text PDF

Source
http://dx.doi.org/10.4110/in.2018.18.e11DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5833118PMC
February 2018
8 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

View Article

Download full-text PDF

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

αβ Is Antiatherogenic in Female but Not Male Mice.

J Immunol 2018 04 19;200(7):2426-2438. Epub 2018 Feb 19.

Department of Molecular Cardiology, Cleveland Clinic, Cleveland, OH 44195;

Atherosclerosis is a complex inflammatory process characterized by monocyte recruitment into the arterial wall, their differentiation into macrophages, and lipid accumulation. Because integrin αβ (CD11b/CD18) mediates multiple diverse functions of leukocytes, we examined its role in atherogenesis. and mice were fed a control or high fat diet for 3 or 16 wk to induce atherogenesis. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.4049/jimmunol.1700313DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5973813PMC
April 2018
9 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

View Article

Download full-text PDF

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

T Cell Expression of C5a Receptor 2 Augments Murine Regulatory T Cell (T) Generation and T-Dependent Cardiac Allograft Survival.

J Immunol 2018 03 7;200(6):2186-2198. Epub 2018 Feb 7.

Nephrology Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029;

C5aR2 (C5L2/gp77) is a seven-transmembrane spanning receptor that binds to C5a but lacks motifs essential for G protein coupling and associated signal transduction. C5aR2 is expressed on immune cells, modulates various inflammatory diseases in mice, and has been shown to facilitate murine and human regulatory T cell (T) generation in vitro. Whether and how C5aR2 impacts in vivo T generation and pathogenic T cell-dependent disease models have not been established. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.4049/jimmunol.1701638DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5894525PMC
March 2018
3 Reads

Microglial activation and vascular responses that are associated with early thalamic neurodegeneration resulting from thiamine deficiency.

Neurotoxicology 2018 03 7;65:98-110. Epub 2018 Feb 7.

Office of Testing & Research, CDER/FDA, White Oak, MD, 20993, United States.

Thiamine/vitamin B1 deficiency can lead to behavioral changes and neurotoxicity in humans. This may due in part to vascular damage, neuroinflammation and neuronal degeneration in the diencephalon, which is seen in animal models of pyrithiamine-enhanced thiamine deficiency. However, the time course of the progression of these changes in the animal models has been poorly characterized. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.neuro.2018.02.005DOI Listing
March 2018
4 Reads
3.380 Impact Factor