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    2365 results match your criteria Complement Receptor Deficiency

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    Bacteroidetes Neurotoxins and Inflammatory Neurodegeneration.
    Mol Neurobiol 2018 Apr 10. 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

    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

    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

    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

    Response gene to complement 32 suppresses adipose tissue thermogenic genes through inhibiting β3-adrenergic receptor/mTORC1 signaling.
    FASEB J 2018 Mar 26:fj201701508R. 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

    Complement 5a stimulates macrophage polarization and contributes to tumor metastases of colon cancer.
    Exp Cell Res 2018 May 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

    Complement component 3a receptor deficiency attenuates chronic stress-induced monocyte infiltration and depressive-like behavior.
    Brain Behav Immun 2018 Mar 5. 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

    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

    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

    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

    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

    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

    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

    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

    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

    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

    Complement 5a Receptor deficiency does not influence adverse cardiac remodeling after pressure-overload in mice.
    Sci Rep 2017 Dec 6;7(1):17045. Epub 2017 Dec 6.
    Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.
    Hypertension is one of the most common risk factors for the development heart failure in the general population. Inflammation plays a central role in this adverse remodeling and eventually to the development of heart failure. Circulating levels of Complement factor 5a (C5a) are increased in hypertensive patients and the C5a receptor is associated with the presence of cardiac fibrosis and inflammation in an experimental hypertension model. Read More

    Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig-a gene Mutation: Support from an in vitro assay based on L5178Y/Tk cells and the CD90.2 antigen.
    Environ Mol Mutagen 2018 Jan 8;59(1):18-29. Epub 2017 Nov 8.
    Litron Laboratories, Rochester, New York.
    Lack of cell surface glycosylphosphatidylinositol (GPI)-anchored protein(s) has been used as a reporter of Pig-a gene mutation in several model systems. As an extension of this work, our laboratory initiated development of an in vitro mutation assay based on the flow cytometric assessment of CD90.2 expression on the cell surface of the mouse lymphoma cell line L5178Y/Tk . Read More

    Circadian clock cryptochrome proteins regulate autoimmunity.
    Proc Natl Acad Sci U S A 2017 Nov 6;114(47):12548-12553. Epub 2017 Nov 6.
    Department of Hematology and Oncology, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
    The circadian system regulates numerous physiological processes including immune responses. Here, we show that mice deficient of the circadian clock genes and [ double knockout (DKO)] develop an autoimmune phenotype including high serum IgG concentrations, serum antinuclear antibodies, and precipitation of IgG, IgM, and complement 3 in glomeruli and massive infiltration of leukocytes into the lungs and kidneys. Flow cytometry of lymphoid organs revealed decreased pre-B cell numbers and a higher percentage of mature recirculating B cells in the bone marrow, as well as increased numbers of B2 B cells in the peritoneal cavity of DKO mice. Read More

    Autoantibodies against complement components in systemic lupus erythematosus - role in the pathogenesis and clinical manifestations.
    Lupus 2017 Dec 18;26(14):1550-1555. Epub 2017 May 18.
    2 Department of Chemistry, Biochemistry, Physiology and Pathophysiology, Sofia University "St. Kliment Ohridski", Bulgaria.
    Many complement structures and a number of additional factors, i.e. autoantibodies, receptors, hormones and cytokines, are implicated in the complex pathogenesis of systemic lupus erythematosus. Read More

    Electronegative Low-Density Lipoprotein L5 Induces Adipose Tissue Inflammation Associated With Metabolic Syndrome.
    J Clin Endocrinol Metab 2017 Dec;102(12):4615-4625
    Lipid Science and Aging Research Center, Kaohsiung Medical University, Taiwan.
    Context: Electronegative low-density lipoprotein (LDL) L5 is a naturally occurring, atherogenic entity found at elevated levels in the plasma of patients with metabolic syndrome (MetS) in the absence of elevated plasma LDL levels.

    Objective: To investigate the role of L5 in the mechanism of adipose tissue inflammation associated with MetS.

    Patients/setting: Plasma LDL isolated from patients with MetS (n = 29) and controls (n = 29) with similar plasma LDL levels was separated into five subfractions, L1 to L5, with increasing electronegativity. Read More

    Spred2-deficiecy Protects Mice from Polymicrobial Septic Peritonitis by Enhancing Inflammation and Bacterial Clearance.
    Sci Rep 2017 Oct 9;7(1):12833. Epub 2017 Oct 9.
    Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700-8558, Japan.
    Sepsis is an infection-induced systemic inflammatory syndrome and a major cause of death for critically ill patients. Here, we examined whether the absence of Sprouty-related EVH1-domain-containing protein 2 (Spred2), a negative regulator of the Ras/Raf/ERK/MAPK pathway, influences host defense against polymicrobial sepsis (PMS) induced by cecal ligation and puncture (CLP). Compared to wild-type mice, Spred2 mice exhibited higher survival rates with increased level of leukocyte infiltration and local chemokine production and reduced plasma and peritoneal bacterial loads after CLP. Read More

    An ABC of the Warning Signs of Hereditary Angioedema.
    Int Arch Allergy Immunol 2017 27;174(1):1-6. Epub 2017 Sep 27.
    Faculdade de Medicina ABC, Santo Andre, Brazil.
    Hereditary angioedema (HAE) with C1 inhibitor deficiency is a genetic disorder that clinically manifests with attacks of angioedema in the subcutaneous and submucosal tissues, mainly in the extremities, abdomen, and upper airway. During attacks, vascular permeability is increased due to increased bradykinin (BK). This means that special therapies are needed for attacks that do not respond to traditional antiallergic therapies involving antihistamines, corticosteroids, and epinephrine. Read More

    Vitamin K-Dependent Protein S: Beyond the Protein C Pathway.
    Semin Thromb Hemost 2018 Mar 13;44(2):176-184. Epub 2017 Sep 13.
    Department of Translational Medicine, Lund University, Malmö, Sweden.
    Protein S is a vitamin K-dependent plasma glycoprotein circulating in plasma at a concentration of around 350 nM. Approximately 60% of protein S in human plasma is bound to the complement regulatory protein C4b-binding protein (C4BP) in a high-affinity, high-molecular-weight complex. Protein S in plasma has multiple anticoagulant properties and heterozygous protein S deficiency is associated with increased risk of venous thrombosis. Read More

    Complement C5a receptors C5L2 and C5aR in renal fibrosis.
    Am J Physiol Renal Physiol 2018 01 13;314(1):F35-F46. Epub 2017 Sep 13.
    Division of Gastroenterology, Saarland University Medical Center , Homburg , Germany.
    Complement factor C5a has two known receptors, C5aR, which mediates proinflammatory effects, and C5L2, a potential C5a decoy receptor. We previously identified C5a/C5aR signaling as a potent profibrotic pathway in the kidney. Here we tested for the first time the role of C5L2 in renal fibrosis. Read More

    CD18 deficiency improves liver injury in the MCD model of steatohepatitis.
    PLoS One 2017 5;12(9):e0183912. Epub 2017 Sep 5.
    Department of Medicine, University of California, San Francisco, San Francisco, California, United States of America.
    Neutrophils and macrophages are important constituents of the hepatic inflammatory infiltrate in non-alcoholic steatohepatitis. These innate immune cells express CD18, an adhesion molecule that facilitates leukocyte activation. In the context of fatty liver, activation of infiltrated leukocytes is believed to enhance hepatocellular injury. Read More

    Mac-1 deficiency induces respiratory failure by affecting type I alveolar epithelial cells.
    Genet Mol Res 2017 Aug 31;16(3). Epub 2017 Aug 31.
    Department of Nursing, People's Hospital of Laizhou City, Laizhou, , China.
    As a β2 integrin family member, Mac-1 plays an important role in the inflammatory response. Inflammation and lung injury are closely associated, but the involvement of Mac-1 in the occurrence and development of such pathologies remains poorly understood. We aimed to investigate the relationship between Mac-1 deficiency and respiratory failure in Mac-1 knockout {Mac-1} mice, using C57BL/6J mice as a control. Read More

    IgG is elevated in obese white adipose tissue but does not induce glucose intolerance via Fcγ-receptor or complement.
    Int J Obes (Lond) 2018 Feb 30;42(2):260-269. Epub 2017 Aug 30.
    Einthoven Laboratory for Experimental Vascular Medicine, Leiden, The Netherlands.
    Background/objectives: In obesity, B cells accumulate in white adipose tissue (WAT) and produce IgG, which may contribute to the development of glucose intolerance. IgG signals by binding to Fcγ receptors (FcγR) and by activating the complement system. The aim of our study was to investigate whether activation of FcγR and/or complement C3 mediates the development of high-fat diet-induced glucose intolerance. Read More

    IL-17A deficiency mitigates bleomycin-induced complement activation during lung fibrosis.
    FASEB J 2017 12 17;31(12):5543-5556. Epub 2017 Aug 17.
    Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, USA;
    Interleukin 17A (IL-17A) and complement (C') activation have each been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We have reported that IL-17A induces epithelial injury TGF-β in murine bronchiolitis obliterans; that TGF-β and the C' cascade present signaling interactions in mediating epithelial injury; and that the blockade of C' receptors mitigates lung fibrosis. In the present study, we investigated the role of IL-17A in regulating C' in lung fibrosis. Read More

    Feline leukocyte adhesion (CD18) deficiency caused by a deletion in the integrin β (ITGB2) gene.
    Vet Clin Pathol 2017 Sep 27;46(3):391-400. Epub 2017 Jul 27.
    Section of Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
    Background: Leukocyte adhesion deficiency (LAD) or CD18 deficiency is an autosomal recessive immunodeficiency which has been described in people, cattle, dogs, and knockout mice.

    Objectives: The study goals were to characterize the clinicopathologic, immunologic, and molecular genetic features of feline LAD (FLAD) in a neutered male adult Domestic Longhair cat with severe leukocytosis and recurrent infections.

    Methods: Flow cytometry evaluated surface expression of CD18 on neutrophils. Read More

    The atypical receptor CCRL2 is required for CXCR2-dependent neutrophil recruitment and tissue damage.
    Blood 2017 09 25;130(10):1223-1234. Epub 2017 Jul 25.
    Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
    CCRL2 is a 7-transmembrane domain receptor that shares structural and functional similarities with the family of atypical chemokine receptors (ACKRs). CCRL2 is upregulated by inflammatory signals and, unlike other ACKRs, it is not a chemoattractant-scavenging receptor, does not activate β-arrestins, and is widely expressed by many leukocyte subsets. Therefore, the biological role of CCRL2 in immunity is still unclear. Read More

    Disruption of the ATP/adenosine balance in CD39 mice is associated with handling-induced seizures.
    Immunology 2017 12 25;152(4):589-601. Epub 2017 Aug 25.
    Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
    Seizures are due to excessive, synchronous neuronal firing in the brain and are characteristic of epilepsy, the fourth most prevalent neurological disease. We report handling-induced and spontaneous seizures in mice deficient for CD39, a cell-surface ATPase highly expressed on microglial cells. CD39 mice with handling-induced seizures had normal input-output curves and paired-pulse ratio measured from hippocampal slices and lacked microgliosis, astrogliosis or overt cell loss in the hippocampus and cortex. Read More

    Anti-Neu5Gc and anti-non-Neu5Gc antibodies in healthy humans.
    PLoS One 2017 17;12(7):e0180768. Epub 2017 Jul 17.
    Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, PA, United States of America.
    Our group previously investigated the levels of anti-Gal and anti-nonGal IgM and IgG in a cohort of 75 healthy humans of various backgrounds, and found some significant differences related to factors such as age, gender, ABO blood group, diet, vaccination history, and geographic location during childhood. We have now expanded our cohort (n = 84) to investigate the levels of anti-Neu5Gc and anti-nonGal/nonNeu5Gc antibodies in healthy humans. Anti-nonGal and anti-nonGal/nonNeu5Gc human IgM and IgG binding to pRBCs and pAECs from GTKO/CD46 and GTKO/CD46/Neu5GcKO pigs were measured by flow cytometry. Read More

    Increased aggression and lack of maternal behavior in Dio3-deficient mice are associated with abnormalities in oxytocin and vasopressin systems.
    Genes Brain Behav 2018 01 4;17(1):23-35. Epub 2017 Aug 4.
    Maine Medical Center Research Institute, Center for Molecular Medicine, Scarborough, ME, USA.
    Thyroid hormones regulate many aspects of brain development and function, and alterations in the levels of thyroid hormone action lead to abnormal anxiety- and depression-like behaviors. A complement of factors in the brain function independently of circulating levels of hormone to strictly controlled local thyroid hormone signaling. A critical factor is the type 3 deiodinase (DIO3), which is located in neurons and protects the brain from excessive thyroid hormone. Read More

    Circulating dsDNA, endothelial injury, and complement activation in thrombotic microangiopathy and GVHD.
    Blood 2017 09 13;130(10):1259-1266. Epub 2017 Jul 13.
    Division of Bone Marrow Transplantation and Immune Deficiency and.
    Transplant-associated thrombotic microangiopathy (TA-TMA) is a common and poorly recognized complication of hematopoietic stem cell transplantation (HSCT) associated with excessive complement activation, likely triggered by endothelial injury. An important missing piece is the link between endothelial injury and complement activation. We hypothesized that neutrophil extracellular traps (NETs) mechanistically link endothelial damage with complement activation and subsequent TA-TMA. Read More

    Interferon Regulatory Factor 5 Controls Necrotic Core Formation in Atherosclerotic Lesions by Impairing Efferocytosis.
    Circulation 2017 Sep 11;136(12):1140-1154. Epub 2017 Jul 11.
    From Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, United Kingdom (A.N.S., A.E., J.E.C., C.K., M.S., I.P., P.G., T.K., D.S., M.E.G., S.N.S., I.A.U., C.M.); Department of Bioengineering, Imperial College London, United Kingdom (A.N.S., R.K.); Experimental Cardiovascular Research Unit, Clinical Research Centre, Clinical Sciences Malmö, Lund University, Sweden (A.E., I.G.); Department of Cardiology, Skåne University Hospital, Lund/Malmö, Sweden (A.E., I.G.); and School of Engineering and Materials Science, Queen Mary University of London, United Kingdom (R.K.).
    Background: Myeloid cells are central to atherosclerotic lesion development and vulnerable plaque formation. Impaired ability of arterial phagocytes to uptake apoptotic cells (efferocytosis) promotes lesion growth and establishment of a necrotic core. The transcription factor interferon regulatory factor (IRF)-5 is an important modulator of myeloid function and programming. Read More

    Interferon-β regulates dendritic cell activation and migration in experimental autoimmune encephalomyelitis.
    Immunology 2017 11 21;152(3):439-450. Epub 2017 Jul 21.
    Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
    CD11c dendritic cells (DCs) exert a critical role as antigen-presenting cells in regulating pathogenic T cells in multiple sclerosis (MS). To determine whether the therapeutic benefit of interferon-β (IFN-β) treatment for MS is in part influenced by IFN regulation of DC function, we examined the immunophenotype of DCs derived from IFN-β and IFN-β mice using a myelin oligodendrocyte glycoprotein (MOG) peptide-induced mouse model of MS, experimental autoimmune encephalomyelitis (EAE). Our earlier work identified that IFN-β mice exhibit earlier onset and more rapid progression of neurological impairment compared with IFN-β mice. Read More

    MECHANISMS OF COIX SEED COMPOSITIONS IN THE TREATMENT OF SPLEEN DEFICIENCY AND WET DAMPNESS ZHENG.
    Afr J Tradit Complement Altern Med 2017 5;14(4):239-246. Epub 2017 Jun 5.
    College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.
    Background: Coix seed has the functions of fortifying the spleen and inhibiting the dampness. However, it remains unclear which Coix seed compositions is responsible for these functions. Previous investigations have revealed that the main compositions of Coix seed are proteins, polysaccharides, oils and starches. Read More

    Measurement of Aortic Cell Fluid-Phase Pinocytosis in vivo by Flow Cytometry.
    J Vasc Res 2017 16;54(4):195-199. Epub 2017 Jun 16.
    Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, USA.
    Objective: Fluid-phase pinocytosis is a receptor-independent mechanism of endocytosis that occurs in all mammalian cells and may be a mechanism for the uptake of LDL by macrophages. As there are currently no methods for the measurement of fluid-phase pinocytosis by individual aortic cells in vivo, we sought to identify a suitable method.

    Methods: ApoE-/- mice were retro-orbitally injected with AngioSPARK fluorescent nanoparticles specifically designed to not interact with cells. Read More

    Glycolipids: Essential regulator of neuro-inflammation, metabolism and gliomagenesis.
    Biochim Biophys Acta 2017 10 7;1861(10):2479-2484. Epub 2017 Jun 7.
    Department of Biomedical Sciences, Chubu University College of Life and Health, 1200 Matsumoto, Kasugai, Aichi 487-8501, Japan; Department of Biochemistry II, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya 466-0065, Japan.
    Gene knockout mice of glycosyltransferases have clearly showed roles of their products in the bodies, while there are examples where phenotype of knockout was much less severe than expected probably due to functional redundancy. The most striking novel finding obtained from ganglioside-deficient mice was that progressive inflammatory reaction took place, leading to neurodegeneration. In particular, dysfunction of complement-regulatory proteins due to deteriorated architecture of lipid rafts seemed to be essential mechanisms for the inflammation. Read More

    Complement C5a induces mesenchymal stem cell apoptosis during the progression of chronic diabetic complications.
    Diabetologia 2017 Sep 3;60(9):1822-1833. Epub 2017 Jun 3.
    First Department, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital and Research Institute of Surgery, Third Military Medical University, No. 10 Changjiang Branch Road, Daping Street, Yuzhong District, Chongqing, 400042, People's Republic of China.
    Aims/hypothesis: Regeneration and repair mediated by mesenchymal stem cells (MSCs) are key self-protection mechanisms against diabetic complications, a reflection of diabetes-related cell/tissue damage and dysfunction. MSC abnormalities have been reported during the progression of diabetic complications, but little is known about whether a deficiency in these cells plays a role in the pathogenesis of this disease. In addition to MSC resident sites, peripheral circulation is a major source of MSCs that participate in the regeneration and repair of damaged tissue. Read More

    gene disruption is associated with increased hematopoietic stem cells: implication in chronic hypoxia-induced pulmonary hypertension.
    Am J Physiol Heart Circ Physiol 2017 Aug 26;313(2):H293-H303. Epub 2017 May 26.
    Department of Pharmacology, and Translation Cardiovascular Institute, School of Medicine, New York Medical College, Valhalla, New York;
    We have recently demonstrated that disruption of the murine cytochrome -450 2c44 gene ( exacerbates chronic hypoxia-induced pulmonary artery remodeling and hypertension in mice. Subsequently, we serendipitously found that gene disruption also increases hematopoietic stem cell (HSC) numbers in bone marrow and blood. Therefore, the objective of the present study was to investigate whether CYP2C44-derived eicosanoids regulate HSC proliferation/cell growth and whether increased HSCs contribute to chronic hypoxia-induced remodeling of pulmonary arteries in knockout mice. Read More

    Necrotizing Ulcer After BCG Vaccination in a Girl With Leukocyte-adhesion Deficiency Type 1.
    J Pediatr Hematol Oncol 2018 Jan;40(1):63-66
    Department of Pediatrics, Dokkyo Medical University School of Medicine.
    Leukocyte-adhesion deficiency-1 is a recessively inherited disorder associated with recurrent bacterial infections, severe periodontitis, peripheral leukocytosis, and impaired wound healing. We diagnosed moderate-type leukocyte-adhesion deficiency-1 in a 7-year-old girl who developed a necrotizing ulcer after Bacillus Calmette-Guerin vaccination. The patient showed moderate expression of CD18 in neutrophils with a homozygous splice mutation with c. Read More

    The Upregulation of Integrin αβ (CD11d/CD18) on Inflammatory Macrophages Promotes Macrophage Retention in Vascular Lesions and Development of Atherosclerosis.
    J Immunol 2017 06 12;198(12):4855-4867. Epub 2017 May 12.
    Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37604;
    Macrophage accumulation is a critical step during development of chronic inflammation, initiating progression of many devastating diseases. Leukocyte-specific integrin αβ (CD11d/CD18) is dramatically upregulated on macrophages at inflammatory sites. Previously we found that CD11d overexpression on cell surfaces inhibits in vitro cell migration due to excessive adhesion. Read More

    Recurrent respiratory tract infections (RRTI) in the elderly: A late onset mild immunodeficiency?
    Clin Immunol 2017 07 6;180:111-119. Epub 2017 May 6.
    Department of Infectious Diseases, Leiden University Medical Center, Leiden, The Netherlands.
    Elderly with late-onset recurrent respiratory tract infections (RRTI) often have specific anti-polysaccharide antibody deficiency (SPAD). We hypothesized that late-onset RRTI is caused by mild immunodeficiencies, such as SPAD, that remain hidden through adult life. We analyzed seventeen elderly RRTI patients and matched controls. Read More

    Dietary supplementation with long-chain monounsaturated fatty acid isomers decreases atherosclerosis and alters lipoprotein proteomes in LDLr mice.
    Atherosclerosis 2017 Jul 25;262:31-38. Epub 2017 Apr 25.
    Lipoprotein Metabolism Section, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD 20892-1666, USA. Electronic address:
    Background And Aims: Concentrated fish oils, containing a mixture of long-chain monounsaturated fatty acids (LCMUFA) with aliphatic chains longer than 18 C atoms (i.e., C20:1 and C22:1), have been shown to attenuate atherosclerosis development in mouse models. Read More

    Peripheral complement interactions with amyloid β peptide: Erythrocyte clearance mechanisms.
    Alzheimers Dement 2017 Dec 2;13(12):1397-1409. Epub 2017 May 2.
    Center for Neuroscience, SRI International, Menlo Park, CA, USA. Electronic address:
    Introduction: Although amyloid β peptide (Aβ) is cleared from the brain to cerebrospinal fluid and the peripheral circulation, mechanisms for its removal from blood remain unresolved. Primates have uniquely evolved a highly effective peripheral clearance mechanism for pathogens, immune adherence, in which erythrocyte complement receptor 1 (CR1) plays a major role.

    Methods: Multidisciplinary methods were used to demonstrate immune adherence capture of Aβ by erythrocytes and its deficiency in Alzheimer's disease (AD). Read More

    Mutation characterization and heterodimer analysis of patients with leukocyte adhesion deficiency: Including one novel mutation.
    Immunol Lett 2017 07 23;187:7-13. Epub 2017 Apr 23.
    Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Cellular and Molecular Research Center, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Kurdistan, Iran.
    Background And Aim: Leukocyte adhesion deficiency type 1 (LAD-I) is a rare, autosomal recessive disorder of neutrophil migration, characterized by severe, recurrent bacterial infections, inadequate pus formation and impaired wound healing. The ITGB2 gene encodes the β2 integrin subunit (CD18) of the leukocyte adhesion cell molecules, and mutations in this gene cause LAD-I. The aim of the current study was to investigate the mutations in patients diagnosed with LAD-I and functional studies of the impact of two previously reported and a novel mutation on the expression of the CD18/CD11a heterodimer. Read More

    Dysregulated CD46 shedding interferes with Th1-contraction in systemic lupus erythematosus.
    Eur J Immunol 2017 07 22;47(7):1200-1210. Epub 2017 May 22.
    Division of Genetics and Molecular Medicine, Department of Medical and Molecular Genetics, King's College London, Guy's Hospital, London, UK.
    IFN-γ-producing T helper 1 (Th1) cell responses mediate protection against infections but uncontrolled Th1 activity also contributes to a broad range of autoimmune diseases. Autocrine complement activation has recently emerged as key in the induction and contraction of human Th1 immunity: activation of the complement regulator CD46 and the C3aR expressed by CD4 T cells via autocrine generated ligands C3b and C3a, respectively, are critical to IFN-γ production. Further, CD46-mediated signals also induce co-expression of immunosuppressive IL-10 in Th1 cells and transition into a (self)-regulating and contracting phase. Read More

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