M J Walport

Summary

Affiliation: Imperial College
Country: UK

Publications

  1. pmc A hierarchical role for classical pathway complement proteins in the clearance of apoptotic cells in vivo
    P R Taylor
    Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom
    J Exp Med 192:359-66. 2000
  2. pmc Complement and systemic lupus erythematosus
    Mark J Walport
    Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK
    Arthritis Res 4:S279-93. 2002
  3. ncbi request reprint Multiple lupus susceptibility loci map to chromosome 1 in BXSB mice
    M B Hogarth
    Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
    J Immunol 161:2753-61. 1998
  4. ncbi request reprint Serum amyloid P component controls chromatin degradation and prevents antinuclear autoimmunity
    M C Bickerstaff
    Immunological Medicine Unit, Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London, UK
    Nat Med 5:694-7. 1999
  5. pmc Antibody-mediated glomerulonephritis in mice: the role of endotoxin, complement and genetic background
    M G Robson
    Division of Medicine and Department Histopathology, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK
    Clin Exp Immunol 133:326-33. 2003
  6. ncbi request reprint Accelerated nephrotoxic nephritis is exacerbated in C1q-deficient mice
    M G Robson
    Division of Medicine, Imperial College School of Science, Technology, and Medicine, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom
    J Immunol 166:6820-8. 2001
  7. ncbi request reprint Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation
    D A Mitchell
    Rheumatology Section and Department of Histopathology, Hammersmith Campus, Imperial College School of Medicine, London, United Kingdom
    J Immunol 162:5676-9. 1999
  8. ncbi request reprint Identification of chromosome intervals from 129 and C57BL/6 mouse strains linked to the development of systemic lupus erythematosus
    Y Heidari
    Molecular Genetics and Rheumatology Section, Faculty of Medicine, Imperial College, Hammersmith Campus, London, UK
    Genes Immun 7:592-9. 2006
  9. ncbi request reprint Autoantigen glycoprotein 70 expression is regulated by a single locus, which acts as a checkpoint for pathogenic anti-glycoprotein 70 autoantibody production and hence for the corresponding development of severe nephritis, in lupus-prone PXSB mice
    M E Haywood
    Rheumatology Section, Imperial College School of Medicine, Hammersnith Campus, Du Cane Road, London, W12 0NN, United Kingdom
    J Immunol 167:1728-33. 2001
  10. pmc Prevention of C5 activation ameliorates spontaneous and experimental glomerulonephritis in factor H-deficient mice
    M C Pickering
    Rheumatology Section and Department of Histopathology, Faculty of Medicine, Imperial College, Hammersmith Campus, Du Cane Road, London W12 0NN, United Kingdom
    Proc Natl Acad Sci U S A 103:9649-54. 2006

Collaborators

Detail Information

Publications62

  1. pmc A hierarchical role for classical pathway complement proteins in the clearance of apoptotic cells in vivo
    P R Taylor
    Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom
    J Exp Med 192:359-66. 2000
    ..Apoptotic cells are thought to be a major source of the autoantigens of SLE, and impairment of their removal by complement may explain the link between hereditary complement deficiency and the development of SLE...
  2. pmc Complement and systemic lupus erythematosus
    Mark J Walport
    Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK
    Arthritis Res 4:S279-93. 2002
    ..In this chapter the role of the complement system in SLE is reviewed and hypotheses are advanced to explain the complex relationships between complement and lupus...
  3. ncbi request reprint Multiple lupus susceptibility loci map to chromosome 1 in BXSB mice
    M B Hogarth
    Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
    J Immunol 161:2753-61. 1998
    ..This implies that, though some loci may be common to a number of mouse models of lupus, different clusters of disease genes confer disease susceptibility in different strains of mice...
  4. ncbi request reprint Serum amyloid P component controls chromatin degradation and prevents antinuclear autoimmunity
    M C Bickerstaff
    Immunological Medicine Unit, Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London, UK
    Nat Med 5:694-7. 1999
    ..These findings indicate that SAP has an important physiological role, inhibiting the formation of pathogenic autoantibodies against chromatin and DNA, probably by binding to chromatin and regulating its degradation...
  5. pmc Antibody-mediated glomerulonephritis in mice: the role of endotoxin, complement and genetic background
    M G Robson
    Division of Medicine and Department Histopathology, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK
    Clin Exp Immunol 133:326-33. 2003
    ..C1q may play a protective role in mixed-strain 129/Sv x C57BL/6 mice, but the data may also be explained by systematic bias in background genes, as there is a large difference in disease susceptibility between C57BL/6 and 129/Sv mice...
  6. ncbi request reprint Accelerated nephrotoxic nephritis is exacerbated in C1q-deficient mice
    M G Robson
    Division of Medicine, Imperial College School of Science, Technology, and Medicine, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom
    J Immunol 166:6820-8. 2001
    ..The increased IgG deposits and apoptotic cells in the glomeruli of C1q-deficient mice suggest that the exacerbation of disease may be due to a defect in the clearance of immune complexes and/or apoptotic cells from their kidneys...
  7. ncbi request reprint Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation
    D A Mitchell
    Rheumatology Section and Department of Histopathology, Hammersmith Campus, Imperial College School of Medicine, London, United Kingdom
    J Immunol 162:5676-9. 1999
    ....
  8. ncbi request reprint Identification of chromosome intervals from 129 and C57BL/6 mouse strains linked to the development of systemic lupus erythematosus
    Y Heidari
    Molecular Genetics and Rheumatology Section, Faculty of Medicine, Imperial College, Hammersmith Campus, London, UK
    Genes Immun 7:592-9. 2006
    ..They also indicate that some susceptibility genes can be inherited from the genome of non-autoimmune parental strains...
  9. ncbi request reprint Autoantigen glycoprotein 70 expression is regulated by a single locus, which acts as a checkpoint for pathogenic anti-glycoprotein 70 autoantibody production and hence for the corresponding development of severe nephritis, in lupus-prone PXSB mice
    M E Haywood
    Rheumatology Section, Imperial College School of Medicine, Hammersnith Campus, Du Cane Road, London, W12 0NN, United Kingdom
    J Immunol 167:1728-33. 2001
    ..A further mapping study in these two subgroups identified a previously unrecognized interval associated with the production of autoantibodies...
  10. pmc Prevention of C5 activation ameliorates spontaneous and experimental glomerulonephritis in factor H-deficient mice
    M C Pickering
    Rheumatology Section and Department of Histopathology, Faculty of Medicine, Imperial College, Hammersmith Campus, Du Cane Road, London W12 0NN, United Kingdom
    Proc Natl Acad Sci U S A 103:9649-54. 2006
    ....
  11. doi request reprint A lupus-susceptibility C57BL/6 locus on chromosome 3 (Sle18) contributes to autoantibody production in 129 mice
    Y Heidari
    Faculty of Medicine, Molecular Genetics and Rheumatology Section, Imperial College, Hammersmith Campus, London, UK
    Genes Immun 10:47-55. 2009
    ....
  12. ncbi request reprint Intact B cell tolerance in the absence of the first component of the classical complement pathway
    A J Cutler
    Rheumatology Section, Division of Medicine, Imperial College School of Medicine, Hammersmith Campus, Du Cane Road, London, GB, UK
    Eur J Immunol 31:2087-93. 2001
    ....
  13. ncbi request reprint Identification of intervals on chromosomes 1, 3, and 13 linked to the development of lupus in BXSB mice
    M E Haywood
    Imperial College School of Medicine, London, UK
    Arthritis Rheum 43:349-55. 2000
    ..To identify intervals containing systemic lupus erythematosus (SLE) susceptibility alleles in the BXSB strain of mice...
  14. pmc Murine glomerular mesangial cell uptake of apoptotic cells is inefficient and involves serum-mediated but complement-independent mechanisms
    J Cortes-Hernandez
    Rheumatology Section and Histopathology Department, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London, UK
    Clin Exp Immunol 130:459-66. 2002
    ..They also show that serum proteins other than complement components mediate the removal of apoptotic cells by murine mesangial cells in vitro...
  15. ncbi request reprint Ultraviolet-radiation-induced keratinocyte apoptosis in C1q-deficient mice
    M C Pickering
    Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London, UK
    J Invest Dermatol 117:52-8. 2001
    ..Our findings suggest that C1q does not play a critical role in the physiologic clearance of apoptotic murine keratinocytes in vivo...
  16. pmc Immune complex processing in C1q-deficient mice
    J T Nash
    Rheumatology Section, Division of Medicine, Imperial College School of Medicine, London, UK
    Clin Exp Immunol 123:196-202. 2001
    ..These data in mice are consistent with previous observations in humans that confirm that the classical pathway of complement plays an important role in the appropriate processing of IC in vivo...
  17. ncbi request reprint Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies
    M Botto
    Rheumatology Section, Hammersmith Campus, Imperial College School of Medicine, London, UK
    Nat Genet 19:56-9. 1998
    ..The phenotype associated with C1q deficiency was modified by background genes. These findings are compatible with the hypothesis that C1q deficiency causes autoimmunity by impairment of the clearance of apoptotic cells...
  18. ncbi request reprint Overlapping BXSB congenic intervals, in combination with microarray gene expression, reveal novel lupus candidate genes
    M E K Haywood
    Rheumatology Section, Division of Medicine, Imperial College Faculty of Medicine, London, UK
    Genes Immun 7:250-63. 2006
    ....
  19. ncbi request reprint A targeted disruption of the murine complement factor B gene resulting in loss of expression of three genes in close proximity, factor B, C2, and D17H6S45
    P R Taylor
    Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
    J Biol Chem 273:1699-704. 1998
    ..The resulting mouse is deficient in both factor B and C2, and hence the alternative and classical pathways of complement activation, and adds to the repertoire of models for studying the in vivo role of complement in the immune system...
  20. ncbi request reprint Altered major histocompatibility complex class II peptide loading in H2-O-deficient mice
    M Perraudeau
    Transplantation Biology Group, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, GB
    Eur J Immunol 30:2871-80. 2000
    ....
  21. pmc Complement contributes to protective immunity against reinfection by Plasmodium chabaudi chabaudi parasites
    P R Taylor
    Rheumatology Section, Division of Medicine, Imperial College School of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom
    Infect Immun 69:3853-9. 2001
    ..In summary, this study indicates that while complement plays only a minor role in the control of the acute phase of parasitemia of a primary infection, it does contribute to parasite control in reinfection...
  22. ncbi request reprint Murine D17H6S45 (Rd) gene: polymorphism and overlap with complement factor B
    P R Taylor
    Rheumatology Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK
    Mamm Genome 8:796-7. 1997
  23. pmc T cell-dependent immune response in C1q-deficient mice: defective interferon gamma production by antigen-specific T cells
    A J Cutler
    Rheumatology Section, Division of Medicine, Imperial College School of Medicine, Hammersmith Hospital, London W12 ONN, United Kingdom
    J Exp Med 187:1789-97. 1998
    ..These data suggest that the classical pathway of complement may influence the cytokine profile of antigen-specific T lymphocytes and the subsequent immune response...
  24. ncbi request reprint Cloning of the mouse homolog of the 126-kDa human C1q/MBL/SP-A receptor, C1qR(p)
    P J Norsworthy
    Rheumatology Section, Imperial College School of Medicine, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK
    Mamm Genome 10:789-93. 1999
    ..The structure of the human gene was found to be similar, with the position of the intron conserved. Cloning of the murine C1qR(p) will facilitate further investigation of the physiological function of this molecule...
  25. ncbi request reprint Clearance pathways of soluble immune complexes in the pig. Insights into the adaptive nature of antigen clearance in humans
    K A Davies
    Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, United Kingdom
    J Immunol 155:5760-8. 1995
    ....
  26. ncbi request reprint Amyloid deposition is delayed in mice with targeted deletion of the serum amyloid P component gene
    M Botto
    Rheumatology Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK
    Nat Med 3:855-9. 1997
    ..This first demonstration of the participation of SAP in pathogenesis of amyloidosis in vivo confirms that inhibition of SAP binding to amyloid fibrils is an attractive therapeutic target in a range of serious human diseases...
  27. ncbi request reprint Polymorphism in the Ly-17 alloantigenic system of the mouse FcgRII gene
    J H Slingsby
    Rheumatology Unit, RPMS, Hammersmith Hospital, Du Cane Road, London, W12 ONN, UK
    Immunogenetics 46:361-2. 1997
  28. ncbi request reprint Immunology: what is the proximal cause of inflammation?
    M J Walport
    Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 0NN, UK
    Curr Biol 7:R41-3. 1997
    ..Knockout mice lacking either the antibody constant region (Fc) receptor or the substance P receptor fail to produce a model inflammatory response, implicating these two receptors in early events of inflammation...
  29. pmc Autoantibodies to the collagenous region of C1q occur in three strains of lupus-prone mice
    M B Hogarth
    Rheumatology Unit, RPMS, London, UK
    Clin Exp Immunol 104:241-6. 1996
    ..This is the first demonstration of anti-C1q (CLR) antibodies in NZB/W and BXSB mice. The pathologic significance and the potential utility of these antibodies for monitoring disease in lupus-prone mice are under evaluation...
  30. ncbi request reprint Homozygous hereditary C1q deficiency and systemic lupus erythematosus. A new family and the molecular basis of C1q deficiency in three families
    J H Slingsby
    Hammersmith Hospital, London, UK
    Arthritis Rheum 39:663-70. 1996
    ..To describe a new kindred with Clq deficiency and to identify the molecular lesions responsible for complete functional C1q deficiency in this and 2 other previously described kindreds...
  31. ncbi request reprint Organ-specific contribution to circulating C7 levels by the bone marrow and liver in humans
    M A Naughton
    Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, GB
    Eur J Immunol 26:2108-12. 1996
    ..These findings provide further support for the concept that locally secreted complement proteins have an important role in inflammation...
  32. ncbi request reprint Eosinophilic myopathic syndromes
    M C Pickering
    Division of Medicine, Imperial College School of Medicine, London, UK
    Curr Opin Rheumatol 10:504-10. 1998
    ..This report describes the various conditions in which eosinophilic myopathy occurs and reviews the current state of knowledge of eosinophilic myopathy...
  33. ncbi request reprint Inherited deficiency of erythrocyte complement receptor type 1 does not cause susceptibility to systemic lupus erythematosus
    F Moldenhauer
    Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK
    Arthritis Rheum 30:961-6. 1987
    ..The low allele for numeric expression of CR1 on erythrocytes is not a disease susceptibility gene for SLE...
  34. ncbi request reprint New microsatellite polymorphisms identified between C57BL/6, C57BL/10, and C57BL/KsJ inbred mouse strains
    J H Slingsby
    Rheumatology Unit, RPMS, Hammersmith Hospital, London, UK
    Immunogenetics 43:72-5. 1996
  35. ncbi request reprint Defective Fc-dependent processing of immune complexes in patients with systemic lupus erythematosus
    Kevin A Davies
    Division of Medicine, Imperial College School of Medicine at Hammersmith Hospital, London, UK
    Arthritis Rheum 46:1028-38. 2002
    ..To explore the Fc receptor-dependent handling of immune complexes (ICs) by the fixed mononuclear phagocytic systems (MPS) in patients with systemic lupus erythematosus (SLE)...
  36. ncbi request reprint Dissection of BXSB lupus phenotype using mice congenic for chromosome 1 demonstrates that separate intervals direct different aspects of disease
    Michelle E K Haywood
    Rheumatology Section, Eric Bywaters Centre, Faculty of Medicine, Imperial College, London, UK
    J Immunol 173:4277-85. 2004
    ..Yaa.BXSB-Bxs1/4. Disease in the Bxs3 mice was delayed in comparison to the BXSB parental strain, emphasizing the necessity for multiple interactions in the production of the full BXSB phenotype...
  37. pmc The in vivo expression of actin/salt-resistant hyperactive DNase I inhibits the development of anti-ssDNA and anti-histone autoantibodies in a murine model of systemic lupus erythematosus
    Anthony P Manderson
    Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, London, UK
    Arthritis Res Ther 8:R68. 2006
    ....
  38. pmc Monocytosis and accelerated activation of lymphocytes in C1q-deficient autoimmune-prone mice
    Marten Trendelenburg
    Rheumatology Section, Eric Bywaters Centre, Faculty of Medicine, Imperial College, Hammersmith Campus, London, UK
    Immunology 113:80-8. 2004
    ..These data show that C1q deficiency causes splenic monocytosis together with accelerated T-cell activation in an autoimmune-prone mouse strain...
  39. pmc The classical pathway is the dominant complement pathway required for innate immunity to Streptococcus pneumoniae infection in mice
    Jeremy S Brown
    Centre for Molecular Microbiology and Infection and Rheumatology Section, Faculty of Medicine, Imperial College London, Flowers Building, Armstrong Road, London SW7 2AZ, United Kingdom
    Proc Natl Acad Sci U S A 99:16969-74. 2002
    ..pneumoniae, loss of which results in rapidly progressing septicemia and impaired macrophage activation. These data demonstrate the vital role of the classical pathway for innate immunity to a bacterial pathogen...
  40. ncbi request reprint Murine CD93 (C1qRp) contributes to the removal of apoptotic cells in vivo but is not required for C1q-mediated enhancement of phagocytosis
    Peter J Norsworthy
    Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London, UK
    J Immunol 172:3406-14. 2004
    ..However, our results suggest that it may contribute to the in vivo clearance of dying cells...
  41. ncbi request reprint A novel mechanism for complement activation at the surface of B cells following antigen binding
    Anthony P Manderson
    Cancer and Vascular Biology Group, Division of Immunology and Genetics, John Curtin School of Medical Research, Australian National University, Canberra, Australia
    J Immunol 177:5155-62. 2006
    ..Based on these data, we propose a novel model in which immune complexes can form directly on the surface of the B cell following Ag binding. This model has implications for our understanding of B lymphocyte activation...
  42. ncbi request reprint Predominant role of IgM-dependent activation of the classical pathway in the clearance of dying cells by murine bone marrow-derived macrophages in vitro
    Pierre Quartier
    Rheumatology Section, Imperial College, Hammersmith Campus, London W12 ONN, UK
    Eur J Immunol 35:252-60. 2005
    ..Hence, the efficient uptake of dying cells by BMDM requires IgM antibodies and complement...
  43. ncbi request reprint Increased positive selection of B1 cells and reduced B cell tolerance to intracellular antigens in c1q-deficient mice
    Helen Ferry
    Henry Wellcome Building for Molecular Physiology, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom
    J Immunol 178:2916-22. 2007
    ..We show that exposure of intracellular Ag leads to the activation of conventional B cells, when there is a source of T cell help in vivo...
  44. ncbi request reprint Lupus-prone mice have an abnormal response to thioglycolate and an impaired clearance of apoptotic cells
    Paul K Potter
    Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London, United Kingdom
    J Immunol 170:3223-32. 2003
    ..These findings have implications for the initiation of autoimmunity, as lupus autoantigens are expressed on dying cells, and impaired disposal of these could enhance the development of autoimmunity...
  45. pmc C1q deficiency promotes the production of transgenic-derived IgM and IgG3 autoantibodies in anti-DNA knock-in transgenic mice
    Liliane Fossati-Jimack
    Molecular Genetics and Rheumatology Section, Faculty of Medicine, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
    Mol Immunol 45:787-95. 2008
    ..However, the lack of C1q led to an increased production of Tg IgM and IgG3 antibodies only in VH3H9R mice indicating that additional genetic susceptibility factors are required to break self-tolerance...
  46. pmc Complement activation selectively potentiates the pathogenicity of the IgG2b and IgG3 isotypes of a high affinity anti-erythrocyte autoantibody
    Samareh Azeredo da Silveira
    Department of Pathology, University of Geneva, 1211 Geneva 4, Switzerland
    J Exp Med 195:665-72. 2002
    ....
  47. pmc Regulation of B cell tolerance by 129-derived chromosome 1 loci in C57BL/6 mice
    Liliane Fossati-Jimack
    Molecular Genetics and Rheumatology Section, Faculty of Medicine, Imperial College, London, UK
    Arthritis Rheum 58:2131-41. 2008
    ..The aim of the present study was to elucidate the mechanisms by which this locus contributes to the loss of peripheral tolerance...
  48. ncbi request reprint C1q, autoimmunity and apoptosis
    Marina Botto
    Division of Medicine, Faculty of Medicine, Imperial College, London, UK
    Immunobiology 205:395-406. 2002
    ....
  49. ncbi request reprint Role of surfactant proteins A, D, and C1q in the clearance of apoptotic cells in vivo and in vitro: calreticulin and CD91 as a common collectin receptor complex
    R William Vandivier
    Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine and Pathology, University of Colorado Health Sciences Center, nd Denver, CO, USA
    J Immunol 169:3978-86. 2002
    ....
  50. ncbi request reprint The follicular dendritic cell restricted epitope, FDC-M2, is complement C4; localization of immune complexes in mouse tissues
    Philip R Taylor
    Sir William Dunn School of Pathology, Oxford University, South Parks Road, Oxford, GB
    Eur J Immunol 32:1888-96. 2002
    ..These results demonstrate that mAb209, in addition to its role as an FDC marker, is a valuable reagent for the analysis of complement deposition in vivo...
  51. ncbi request reprint Genetic dissection of spontaneous autoimmunity driven by 129-derived chromosome 1 Loci when expressed on C57BL/6 mice
    Francesco Carlucci
    Rheumatology Section, Faculty of Medicine, Imperial College, London, United Kingdom
    J Immunol 178:2352-60. 2007
    ..These findings have important implication for the interpretation of the autoimmune phenotype associated with gene-targeted models...
  52. ncbi request reprint Restoration of C1q levels by bone marrow transplantation attenuates autoimmune disease associated with C1q deficiency in mice
    Josefina Cortes-Hernandez
    Rheumatology Section, Eric Bywaters Centre, Faculty of Medicine, Imperial College, London, UK
    Eur J Immunol 34:3713-22. 2004
    ..These results provide supporting evidence that BMT may be a therapeutic option in the treatment of autoimmunity associated with human C1q deficiency...
  53. ncbi request reprint Nephrotoxic nephritis is mediated by Fcgamma receptors on circulating leukocytes and not intrinsic renal cells
    Ruth M Tarzi
    Division of Medicine and Department of Histopathology, Imperial College School of Medicine, Hammersmith Hospital, London, England
    Kidney Int 62:2087-96. 2002
    ..FcRgamma-/- mice were protected from renal inflammation following the induction of accelerated nephrotoxic nephritis using sheep anti-mouse glomerular basement membrane anti-serum in mice sensitized to sheep IgG...
  54. ncbi request reprint Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H
    Matthew C Pickering
    Rheumatology Section, Faculty of Medicine, Imperial College, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
    Nat Genet 31:424-8. 2002
    ..Thus, uncontrolled C3 activation in vivo is essential for the development of MPGN associated with deficiency of factor H...
  55. pmc Both Fcgamma receptor I and Fcgamma receptor III mediate disease in accelerated nephrotoxic nephritis
    Ruth M Tarzi
    Division of Medicine, Hammersmith Hospital, Imperial College School of Medicine, London, United Kingdom
    Am J Pathol 162:1677-83. 2003
    ..Therefore, both FcgammaRI and FcgammaRIII play a role in this active model of glomerulonephritis, because both had to be deficient to protect markedly from disease...
  56. ncbi request reprint C1q deficiency and autoimmunity: the effects of genetic background on disease expression
    Daniel A Mitchell
    Rheumatology Section, Division of Medicine, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London, UK W12 0NN
    J Immunol 168:2538-43. 2002
    ..The work also highlights the potential value of the C1q-deficient MRL/Mp(+/+) strain as a tool with which to dissect further the underlying mechanisms of the autoimmune syndrome associated with C1q deficiency...
  57. ncbi request reprint CD59a deficiency exacerbates accelerated nephrotoxic nephritis in mice
    Daniel Turnberg
    Rheumatology Section and Department of Histopathology, Faculty of Medicine, Hammersmith Campus, Imperial College, London
    J Am Soc Nephrol 14:2271-9. 2003
    ..The lack of CD59a, by allowing unregulated MAC deposition, exacerbates the renal injury in this model of immune complex-mediated glomerulonephritis...
  58. pmc Polymorphism at the C-reactive protein locus influences gene expression and predisposes to systemic lupus erythematosus
    Andrew I Russell
    Rheumatology Section, Imperial College Faculty of Medicine, Hammersmith Hospital, London, UK
    Hum Mol Genet 13:137-47. 2004
    ..The identification of polymorphisms that determine basal CRP levels has implications in ischaemic heart disease, where CRP level is an important predictor of risk...
  59. ncbi request reprint The role of complement in the development of systemic lupus erythematosus
    Anthony P Manderson
    Rheumatology Section, Division of Medicine, Faculty of Medicine, Imperial College, Hammersmith Campus, London W12 0NN, United Kingdom
    Annu Rev Immunol 22:431-56. 2004
    ..These two hypotheses are not mutually exclusive. In addition, there is evidence for a contribution from other genetic factors in determining the phenotype of disease in the absence of complement...
  60. pmc Increased susceptibility of C1q-deficient mice to Salmonella enterica serovar Typhimurium infection
    Joanna Warren
    Rheumatology Section, Division of Medicine, Department of Biochemistry, Imperial College School of Medicine London, University of Cambridge, Cambridge, United Kingdom
    Infect Immun 70:551-7. 2002
    ..The data presented here suggest the possibility of novel pathways by which C1q may modulate the pathogenesis of infectious diseases caused by intracellular pathogens...
  61. pmc CD59a deficiency exacerbates ischemia-reperfusion injury in mice
    Daniel Turnberg
    Rheumatology Section, Eric Bywaters Centre, London, United Kingdom
    Am J Pathol 165:825-32. 2004
    ....
  62. pmc Spontaneous autoimmunity in 129 and C57BL/6 mice-implications for autoimmunity described in gene-targeted mice
    Anne E Bygrave
    Rheumatology Section, Eric Bywaters Centre, Imperial College, London, United Kingdom
    PLoS Biol 2:E243. 2004
    ..These background gene influences may account for some, or even all, of the autoimmune traits described in some gene-targeted models of SLE...