Publications
216 results found
Kiriakidis S, Hoer SS, Burrows N, et al., 2017, Complement C1q is hydroxylated by collagen prolyl 4 hydroxylase and is sensitive to off-target inhibition by prolyl hydroxylase domain inhibitors that stabilize hypoxia-inducible factor, Kidney International, Vol: 92, Pages: 900-908, ISSN: 0085-2538
Complement C1q is part of the C1 macromolecular complex that mediates the classical complement activation pathway: a major arm of innate immune defense. C1q is composed of A, B, and C chains that require post-translational prolyl 4-hydroxylation of their N-terminal collagen-like domain to enable the formation of the functional triple helical multimers. The prolyl 4-hydroxylase(s) that hydroxylate C1q have not previously been identified. Recognized prolyl 4-hydroxylases include collagen prolyl-4-hydroxylases (CP4H) and the more recently described prolyl hydroxylase domain (PHD) enzymes that act as oxygen sensors regulating hypoxia-inducible factor (HIF). We show that several small-molecule prolyl hydroxylase inhibitors that activate HIF also potently suppress C1q secretion by human macrophages. However, reducing oxygenation to a level that activates HIF does not compromise C1q hydroxylation. In vitro studies showed that a C1q A chain peptide is not a substrate for PHD2 but is a substrate for CP4H1. Circulating levels of C1q did not differ between wild-type mice or mice with genetic deficits in PHD enzymes, but were reduced by prolyl hydroxylase inhibitors. Thus, C1q is hydroxylated by CP4H, but not the structurally related PHD hydroxylases. Hence, reduction of C1q levels may be an important off-target side effect of small molecule PHD inhibitors developed as treatments for renal anemia.
Stratigou V, Doyle, Carlucci F, et al., 2017, Altered expression of signalling lymphocyte activation molecule (SLAM) receptors in T cells from lupus nephritis patients - a potential biomarker of disease activity., Rheumatology, Vol: 56, Pages: 1206-1216, ISSN: 1462-0332
Objectives. The aim was to investigate whether the signalling lymphocyte activation molecule (SLAM) signalling pathways contribute to LN and whether SLAM receptors could be valuable biomarkers of disease activity.Methods. Peripheral blood mononuclear cells from 30National Research Ethics Service SLE patients with biopsy-proven LN were analysed by flow cytometry. Clinical measures of disease activity were assessed. The expression of the SLAM family receptors on T-cell subpopulations [CD4, CD8 and double negative (DN) T cells] was measured and compared between lupus patients with active renal disease and those in remission.Results. The frequency of CD8 T cells expressing SLAMF3, SLAMF5 and SLAMF7 was significantly lower in LN patients who were in remission. In contrast, these subsets were similar in patients with active renal disease and in healthy individuals. Patients with active nephritis had an increased percentage of circulating monocytes, consistent with a potential role played by these cells in glomerular inflammation. Changes in the frequency of DN T cells positive for SLAMF2, SLAMF4 and SLAMF7 were observed in lupus patients irrespective of the disease activity. We detected alterations in the cellular expression of the SLAM family receptors, but these changes were less obvious and did not reveal any specific pattern. The percentage of DN T cells expressing SLAMF6 could predict the clinical response to B-cell depletion in patients with LN.Conclusion. Our study demonstrates altered expression of the SLAM family receptors in SLE T lymphocytes. This is consistent with the importance of the SLAM-associated pathways in lupus pathogenesis.
Giacomassi C, Buang N, Ling GS, et al., 2016, Complement C3 exacerbates imiquimod-induced skin inflammation and psoriasiform dermatitis, Journal of Investigative Dermatology, Vol: 137, Pages: 760-763, ISSN: 1523-1747
The complement system is pivotal in protection against pathogens, but also plays important roles in bridging innate and adaptive immune responses (Scott and Botto, 2015) and in modulating local and systemic inflammation (Markiewski and Lambris, 2007). Activation of complement occurs through three different pathways (classical, alternative and lectin), converges at C3 cleavage and culminates in the formation of the membrane attack complex. The anaphylotoxic fragments, C3a and C5a, generated during the proteolytic cascade, recruit immune cells that can promote the removal of debris and pathogens, but can also cause tissue damage (Markiewski and Lambris, 2007).
Mühlfeld C, Madsen J, Mackay RM, et al., 2016, Effect of irradiation/bone marrow transplantation on alveolar epithelial type II cells is aggravated in surfactant protein D deficient mice., Histochemistry and Cell Biology, Vol: 147, Pages: 49-61, ISSN: 0948-6143
Irradiation followed by bone marrow transplantation (BM-Tx) is a frequent therapeutic intervention causing pathology to the lung. Although alveolar epithelial type II (AE2) cells are essential for lung function and are damaged by irradiation, the long-term consequences of irradiation and BM-Tx are not well characterized. In addition, it is unknown whether surfactant protein D (SP-D) influences the response of AE2 cells to the injurious events. Therefore, wildtype (WT) and SP-D(-/-) mice were subjected to a myeloablative whole body irradiation dose of 8 Gy and subsequent BM-Tx and compared with age- and sex-matched untreated controls. AE2 cell changes were investigated quantitatively by design-based stereology. Compared with WT, untreated SP-D(-/-) mice showed a higher number of larger sized AE2 cells and a greater amount of surfactant-storing lamellar bodies. Irradiation and BM-Tx induced hyperplasia and hypertrophy in WT and SP-D(-/-) mice as well as the formation of giant lamellar bodies. The experimentally induced alterations were more severe in the SP-D(-/-) than in the WT mice, particularly with respect to the surfactant-storing lamellar bodies which were sometimes extremely enlarged in SP-D(-/-) mice. In conclusion, irradiation and BM-Tx have profound long-term effects on AE2 cells and their lamellar bodies. These data may explain some of the clinical pulmonary consequences of this procedure. The data should also be taken into account when BM-Tx is used as an experimental procedure to investigate the impact of bone marrow-derived cells for the phenotype of a specific genotype in the mouse.
Wang Y, Jenkins SA, Gu C, et al., 2016, Bacillus anthracis Spore Surface Protein BclA Mediates Complement Factor H Binding to Spores and Promotes Spore Persistence, PLOS Pathogens, Vol: 12, ISSN: 1553-7366
Spores of Bacillus anthracis, the causative agent of anthrax, are known to persist in the host lungs for prolonged periods of time, however the underlying mechanism is poorly understood. In this study, we demonstrated that BclA, a major surface protein of B. anthracis spores, mediated direct binding of complement factor H (CFH) to spores. The surface bound CFH retained its regulatory cofactor activity resulting in C3 degradation and inhibition of downstream complement activation. By comparing results from wild type C57BL/6 mice and complement deficient mice, we further showed that BclA significantly contributed to spore persistence in the mouse lungs and dampened antibody responses to spores in a complement C3-dependent manner. In addition, prior exposure to BclA deletion spores (ΔbclA) provided significant protection against lethal challenges by B. anthracis, whereas the isogenic parent spores did not, indicating that BclA may also impair protective immunity. These results describe for the first time an immune inhibition mechanism of B. anthracis mediated by BclA and CFH that promotes spore persistence in vivo. The findings also suggested an important role of complement in persistent infections and thus have broad implications.
Vernon KA, Ruseva MM, Cook HT, et al., 2016, Partial complement factor H deficiency associates with C3 glomerulopathy and thrombotic microangiopathy, Journal of the American Society of Nephrology, Vol: 27, Pages: 1334-1342, ISSN: 1046-6673
The complement–mediated renal diseases C3 glomerulopathy (C3G) and atypical hemolytic uremic syndrome (aHUS) strongly associate with inherited and acquired abnormalities in the regulation of the complement alternative pathway (AP). The major negative regulator of the AP is the plasma protein complement factor H (FH). Abnormalities in FH result in uncontrolled activation of C3 through the AP and associate with susceptibility to both C3G and aHUS. Although previously developed FH–deficient animal models have provided important insights into the mechanisms underlying susceptibility to these unique phenotypes, these models do not entirely reproduce the clinical observations. FH is predominantly synthesized in the liver. We generated mice with hepatocyte–specific FH deficiency and showed that these animals have reduced plasma FH levels with secondary reduction in plasma C3. Unlike mice with complete FH deficiency, hepatocyte–specific FH–deficient animals developed neither plasma C5 depletion nor accumulation of C3 along the glomerular basement membrane. In contrast, subtotal FH deficiency associated with mesangial C3 accumulation consistent with C3G. Although there was no evidence of spontaneous thrombotic microangiopathy, the hepatocyte–specific FH–deficient animals developed severe C5–dependent thrombotic microangiopathy after induction of complement activation within the kidney by accelerated serum nephrotoxic nephritis. Taken together, our data indicate that subtotal FH deficiency can give rise to either spontaneous C3G or aHUS after a complement-activating trigger within the kidney and that the latter is C5 dependent.
Barbour TD, Ling GS, Ruseva MM, et al., 2016, Complement receptor 3 mediates renal protection in experimental C3 glomerulopathy, Kidney International, Vol: 89, Pages: 823-832, ISSN: 1523-1755
C3 glomerulopathy is a complement-mediated renal disease that is frequently associated with abnormalities in regulation of the complement alternative pathway. Mice with deficiency of factor H (Cfh–/–), a negative alternative pathway regulator, are an established experimental model of C3 glomerulopathy in which complement C3 fragments including iC3b accumulate along the glomerular basement membrane. Here we show that deficiency of complement receptor 3 (CR3), the main receptor for iC3b, enhances the severity of spontaneous renal disease in Cfh–/– mice. This effect was found to be dependent on CR3 expression on bone marrow–derived cells. CR3 also mediated renal protection outside the setting of factor H deficiency, as shown by the development of enhanced renal injury in CR3-deficient mice during accelerated nephrotoxic nephritis. The iC3b–CR3 interaction downregulated the proinflammatory cytokine response of both murine and human macrophages to lipopolysaccharide stimulation in vitro, suggesting that the protective effect of CR3 on glomerular injury was mediated via modulation of macrophage-derived proinflammatory cytokines. Thus, CR3 has a protective role in glomerulonephritis and suggests that pharmacologic potentiation of the macrophage CR3 interaction with iC3b could be therapeutically beneficial.
Bulla R, Tripodo C, Rami D, et al., 2016, C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation, Nature Communications, Vol: 7, ISSN: 2041-1723
Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa(-/-)) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa(-/-) mice. Bone marrow (BM) chimeras between C1qa(-/-) and WT mice identify non-BM-derived cells as the main local source of C1q that can promote cancer cell adhesion, migration and proliferation. Together these findings support a role for locally synthesized C1q in promoting tumour growth.
Carlucci F, Botto M, Ishaque A, et al., 2016, C1q modulates the response to TLR7 stimulation by pristane-primed macrophages: implications for pristane-induced lupus, Journal of Immunology, Vol: 196, Pages: 1488-1494, ISSN: 1550-6606
The complement component C1q is known to play a controversial role in thepathogenesis of systemic lupus erythematosus (SLE), but the underlying mechanismsremain poorly understood. Intraperitoneal injection of pristane induces a lupus-likesyndrome whose pathogenesis implicates the secretion of type I IFN by CD11b+Ly6Chigh inflammatory monocytes in a TLR7-dependent fashion. C1q has also beenshown to influence the secretion of IFN-α. Herein we explored whether C1qdeficiency could affect pristane-induced lupus (PIL). Surprisingly, C1qa-/- micedeveloped lower titres of circulating antibodies and milder arthritis compared to thecontrols. In keeping with the clinical scores, two weeks after pristane injection theperitoneal recruitment of CD11b+ Ly6Chigh inflammatory monocytes in the C1qa-/-mice was impaired. Furthermore, C1q-deficient pristane-primed resident peritonealmacrophages secreted significantly less CCL3, CCL2, CXCL1 and IL-6 whenstimulated in vitro with TLR7 ligand. Replenishing C1q in vivo during the pristanepriming phase rectified this defect. Conversely, pristane-primed macrophages fromC3-deficient mice did not show any impaired cytokine production. These findingsdemonstrate that C1q deficiency impairs the TLR7-dependent chemokine productionby pristane-primed peritoneal macrophages and suggest that C1q, and not C3, isinvolved in the handling of pristane by phagocytic cells which is required to triggerdisease in this model.
Saja MF, Baudino L, Jackson WD, et al., 2015, Triglyceride-Rich Lipoproteins Modulate the Distribution and Extravasation of Ly6C/Gr1<SUP>low</SUP> Monocytes, CELL REPORTS, Vol: 12, Pages: 1802-1815, ISSN: 2211-1247
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- Citations: 29
Ambrose N, Khan E, Ravindran R, et al., 2015, The exaggerated inflammatory response in behçet's syndrome: Identification of dysfunctional post-transcriptional regulation of the IFN?/CXCL10 (IP-10) pathway, Clinical and Experimental Immunology, Vol: 181, Pages: 427-433, ISSN: 1365-2249
The mechanisms underlying the exaggerated inflammatory response in Behçet's syndrome (BS) remain poorly understood. We investigated the response of CD14+ blood monocytes to interferon (IFN)-γ, focusing on the chemokine CXCL10. Chemokine synthesis and release were analysed at a protein and mRNA level following stimulation with IFN-γ. Findings in BS patients were compared with 25 healthy controls (HC), 15 rheumatoid arthritis (RA) and 15 systemic lupus erythematosus (SLE) disease control patients. BS monocytes produced significantly more CXCL10 protein than HC monocytes from 2 h following IFN-γ stimulation, despite equivalent quantities of mRNA, suggesting more efficient translation. This was significantly more pronounced in BS with high disease activity and in those with ocular and neurological clinical manifestations. The imbalance between CXCL10 protein and mRNA expression was not observed in either RA or SLE patients, and was not seen with other chemokines studied (CXCL9, CXCL11 and CCL2). Furthermore, BS monocytes treated with an alternative stimulant (LPS) did not show abnormal tumour necrosis factor (TNF)-α release. Sucrose density gradients to segregate monocyte CXCL10 mRNA into free RNA or polysome-associated RNA showed equal proportions in BS and HC samples, suggesting that the difference between BS and HC may be due to reduced negative control of CXCL10 translation in BS at a post-initiation level. We conclude that BS monocytes have dysfunctional post-transcriptional regulation of CXCL10 mRNA, resulting in over-expression of CXCL10 protein upon IFN-γ stimulation. As CXCL10 is a chemokine that recruits mononuclear cells, this abnormality may contribute to the exaggerated inflammatory responses that characterizes BS.
Scott D, Botto M, 2015, The paradoxical roles of C1q and C3 in autoimmunity., Immunobiology, Vol: 221, Pages: 719-725, ISSN: 0722-6365
In this review we will focus on the links between complement and autoimmune diseases and will highlight how animal models have provided insights into the manner by which C1q and C3 act to modulate both adaptive and innate immune responses. In particular we will highlight how C1q may not only act as initiator of the classical complement pathway, but can also mediate multiple immune responses in a complement activation independent manner.
Clarke AJ, Ellinghaus U, Cortini A, et al., 2015, Autophagy is activated in systemic lupus erythematosus and required for plasmablast development, Annals of the Rheumatic Diseases, Vol: 74, Pages: 912-920, ISSN: 0003-4967
Background Autophagy has emerged as a critical homeostatic mechanism in T lymphocytes, influencing proliferation and differentiation. Autophagy in B cells has been less studied, but genetic deficiency causes impairment of early and late developmental stagesObjectives To explore the role of autophagy in the pathogenesis of human and murine lupus, a disease in which B cells are critical effectors of pathology.Methods Autophagy was assessed using multiple techniques in NZB/W and control mice, and in patients with systemic lupus erythematosus (SLE) compared to healthy controls. We evaluated the phenotype of the B cell compartment in Vav-Atg7−/− mice in vivo, and examined human and murine plasmablast formation following inhibition of autophagy.Results We found activation of autophagy in early developmental and transitional stages of B cell development in a lupus mouse model even before disease onset, and which progressively increased with age. In human disease, again autophagy was activated compared with healthy controls, principally in naïve B cells. B cells isolated from Vav-Atg7F/F mice failed to effectively differentiate into plasma cells following stimulation in vitro. Similarly, human B cells stimulated in the presence of autophagy inhibition did not differentiate into plasmablasts.Conclusions Our data suggest activation of autophagy is a mechanism for survival of autoreactive B cells, and also demonstrate that it is required for plasmablast differentiation, processes that induce significant cellular stress. The implication of autophagy in two major pathogenic pathways in SLE suggests the potential to use inhibition of autophagy as a novel treatment target in this frequently severe autoimmune disease.
Pekkarinen PT, Heikkila N, Kisand K, et al., 2015, Dysregulation of adaptive immune responses in complement C3-deficient patients, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 45, Pages: 915-921, ISSN: 0014-2980
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- Citations: 9
Sumida T, Naito AT, Nomura S, et al., 2015, Complement C1q-induced activation of β-catenin signalling causes hypertensive arterial remodelling, NATURE COMMUNICATIONS, Vol: 6
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- Citations: 44
Karpus ON, Kiener HP, Niederreiter B, et al., 2015, CD55 deposited on synovial collagen fibers protects from immune complex-mediated arthritis, ARTHRITIS RESEARCH & THERAPY, Vol: 17, ISSN: 1478-6354
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- Citations: 16
Fossati-Jimack L, Ling GS, Baudino L, et al., 2015, Intranasal peptide-induced tolerance and linked suppression: consequences of complement deficiency, IMMUNOLOGY, Vol: 144, Pages: 149-157, ISSN: 0019-2805
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- Citations: 5
Giacomassi C, Ling GS, Strid J, et al., 2014, Complement C3 exacerbates skin inflammation in a murine model of imiquimod-induced psoriasis, IMMUNOLOGY, Vol: 143, Pages: 120-120, ISSN: 0019-2805
Banda NK, Mehta G, Chao Y, et al., 2014, Mechanisms of complement activation by dextran-coated superparamagnetic iron oxide (SPIO) nanoworms in mouse versus human serum, PARTICLE AND FIBRE TOXICOLOGY, Vol: 11, ISSN: 1743-8977
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- Citations: 73
Sattler S, Ling G-S, Xu D, et al., 2014, IL-10-producing regulatory B cells induced by IL-33 (Breg(IL-33)) effectively attenuate mucosal inflammatory responses in the gut, Journal of Autoimmunity, Vol: 50, Pages: 107-122, ISSN: 0896-8411
Regulatory B cells (Breg) have attracted increasing attention for their roles in maintaining peripheral tolerance. Interleukin 33 (IL-33) is a recently identified IL-1 family member, which leads a double-life with both pro- and anti-inflammatory properties. We report here that peritoneal injection of IL-33 exacerbated inflammatory bowel disease in IL-10-deficient (IL-10−/−) mice, whereas IL-33-treated IL-10-sufficient (wild type) mice were protected from the disease induction. A phenotypically unconventional subset(s) (CD19+CD25+CD1dhiIgMhiCD5-CD23-Tim-1-) of IL-10 producing Breg-like cells (BregIL-33) was identified responsible for the protection. We demonstrated further that BregIL-33 isolated from these mice could suppress immune effector cell expansion and functions and, upon adoptive transfer, effectively blocked the development of spontaneous colitis in IL-10−/− mice. Our findings indicate an essential protective role, hence therapeutic potential, of BregIL-33 against mucosal inflammatory disorders in the gut.
Bossi F, Tripodo C, Rizzi L, et al., 2014, C1q as a unique player in angiogenesis with therapeutic implication in wound healing, Proceedings of the National Academy of Sciences of the United States of America, Vol: 111, Pages: 4209-4214, ISSN: 0027-8424
We have previously shown that C1q is expressed on endothelial cells (ECs) of newly formed decidual tissue. Here we demonstrate that C1q is deposited in wound-healing skin in the absence of C4 and C3 and that C1q mRNA is locally expressed as revealed by real-time PCR and in situ hybridization. C1q was found to induce permeability of the EC monolayer, to stimulate EC proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aortic ring assay. Using a murine model of wound healing we observed that vessel formation was defective in C1qa−/− mice and was restored to normal after local application of C1q. The mean vessel density of wound-healing tissue and the healed wound area were significantly increased in C1q-treated rats. On the basis of these results we suggest that C1q may represent a valuable therapeutic agent that can be used to treat chronic ulcers or other pathological conditions in which angiogenesis is impaired, such as myocardial ischemia.
Baudino L, Sardini A, Ruseva MM, et al., 2014, C3 opsonization regulates endocytic handling of apoptotic cells resulting in enhanced T-cell responses to cargo-derived antigens, Proceedings of the National Academy of Sciences of the United States of America, Vol: 111, Pages: 1503-1508, ISSN: 0027-8424
Ling GS, Bennett J, Woollard KJ, et al., 2014, Integrin CD11b positively regulates TLR4-induced signalling pathways in dendritic cells but not in macrophages, Nature Communications, Vol: 5, Pages: 1-12, ISSN: 2041-1723
Tuned and distinct responses of macrophages and dendritic cells to Toll-like receptor 4 (TLR4) activation induced by lipopolysaccharide (LPS) underpin the balance between innate and adaptive immunity. However, the molecule(s) that confer these cell-type-specific LPS-induced effects remain poorly understood. Here we report that the integrin αM (CD11b) positively regulates LPS-induced signalling pathways selectively in myeloid dendritic cells but not in macrophages. In dendritic cells, which express lower levels of CD14 and TLR4 than macrophages, CD11b promotes MyD88-dependent and MyD88-independent signalling pathways. In particular, in dendritic cells CD11b facilitates LPS-induced TLR4 endocytosis and is required for the subsequent signalling in the endosomes. Consistent with this, CD11b deficiency dampens dendritic cell-mediated TLR4-triggered responses in vivo leading to impaired T-cell activation. Thus, by modulating the trafficking and signalling functions of TLR4 in a cell-type-specific manner CD11b fine tunes the balance between adaptive and innate immune responses initiated by LPS.
Kraivong R, Vasanawathana S, Limpitikul W, et al., 2013, Complement alternative pathway genetic variation and Dengue infection in the Thai population, Clinical and Experimental Immunology, Vol: 174, Pages: 326-334, ISSN: 1365-2249
Dengue disease is a mosquito-borne infection caused by Dengue virus. Infection may be asymptomatic or variably manifest as mild Dengue fever (DF) to the most severe form, Dengue haemorrhagic fever (DHF). Mechanisms that influence disease severity are not understood. Complement, an integral component of the immune system, is activated during Dengue infection and the degree of activation increases with disease severity. Activation of the complement alternative pathway is influenced by polymorphisms within activation (factor B rs12614/rs641153, C3 rs2230199) and regulatory [complement factor H (CFH) rs800292] proteins, collectively termed a complotype. Here, we tested the hypothesis that the complotype influences disease severity during secondary Dengue infection. In addition to the complotype, we also assessed two other disease-associated CFH polymorphisms (rs1061170, rs3753394) and a structural polymorphism within the CFH protein family. We did not detect any significant association between the examined polymorphisms and Dengue infection severity in the Thai population. However, the minor allele frequencies of the factor B and C3 polymorphisms were less than 10%, so our study was not sufficiently powered to detect an association at these loci. We were also unable to detect a direct interaction between CFH and Dengue NS1 using both recombinant NS1 and DV2-infected culture supernatants. We conclude that the complotype does not influence secondary Dengue infection severity in the Thai population.
Fossati-Jimack L, Ling GS, Cortini A, et al., 2013, Phagocytosis Is the Main CR3-Mediated Function Affected by the Lupus-Associated Variant of CD11b in Human Myeloid Cells, PLOS ONE, Vol: 8, ISSN: 1932-6203
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- Citations: 50
Ruseva MM, Vernon KA, Lesher AM, et al., 2013, Loss of Properdin Exacerbates C3 Glomerulopathy Resulting from Factor H Deficiency, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 24, Pages: 43-52, ISSN: 1046-6673
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- Citations: 58
Lewis MJ, Malik TH, Fossati-Jimack L, et al., 2012, Distinct roles for complement in glomerulonephritis and atherosclerosis revealed in mice with a combination of lupus and hyperlipidemia, ARTHRITIS AND RHEUMATISM, Vol: 64, Pages: 2707-2718, ISSN: 0004-3591
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- Citations: 17
Naito AT, Sumida T, Nomura S, et al., 2012, Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes, CELL, Vol: 149, Pages: 1298-1313, ISSN: 0092-8674
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- Citations: 219
Humphries MM, Kenna PF, Campbell M, et al., 2012, C1q enhances cone photoreceptor survival in a mouse model of autosomal recessive retinitis pigmentosa, EUROPEAN JOURNAL OF HUMAN GENETICS, Vol: 20, Pages: 64-68, ISSN: 1018-4813
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- Citations: 12
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