A R Kitching

Summary

Affiliation: Monash University
Country: Australia

Publications

  1. ncbi request reprint IL-12 directs severe renal injury, crescent formation and Th1 responses in murine glomerulonephritis
    A R Kitching
    Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Eur J Immunol 29:1-10. 1999
  2. ncbi request reprint CD100 enhances dendritic cell and CD4+ cell activation leading to pathogenetic humoral responses and immune complex glomerulonephritis
    Ming Li
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Clayton, Victoria, Australia
    J Immunol 177:3406-12. 2006
  3. ncbi request reprint Interleukin-4 and interleukin-10 attenuate established crescentic glomerulonephritis in mice
    A R Kitching
    Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 52:52-9. 1997
  4. ncbi request reprint IL-12p40 and IL-18 in crescentic glomerulonephritis: IL-12p40 is the key Th1-defining cytokine chain, whereas IL-18 promotes local inflammation and leukocyte recruitment
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 16:2023-33. 2005
  5. ncbi request reprint Targeting leukocytes in immune glomerular diseases
    A R Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Rd, Clayton, VIC 3168, Australia
    Curr Med Chem 15:448-58. 2008
  6. ncbi request reprint Endogenous IL-13 limits humoral responses and injury in experimental glomerulonephritis but does not regulate Th1 cell-mediated crescentic glomerulonephritis
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Rd, Clayton, VIC 3168, Australia
    J Am Soc Nephrol 15:2373-82. 2004
  7. ncbi request reprint Experimental autoimmune anti-glomerular basement membrane glomerulonephritis: a protective role for IFN-gamma
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    J Am Soc Nephrol 15:1764-74. 2004
  8. ncbi request reprint Endogenous alpha2-antiplasmin does not enhance glomerular fibrin deposition or injury in glomerulonephritis
    A R Kitching
    Center for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Center, Clayton, Victoria, Australia
    J Thromb Haemost 1:1992-9. 2003
  9. doi request reprint The emergence of TH17 cells as effectors of renal injury
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Center, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 22:235-8. 2011
  10. pmc Effects of CTLA4-Fc on glomerular injury in humorally-mediated glomerulonephritis in BALB/c mice
    A R Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Clin Exp Immunol 128:429-35. 2002

Collaborators

Detail Information

Publications64

  1. ncbi request reprint IL-12 directs severe renal injury, crescent formation and Th1 responses in murine glomerulonephritis
    A R Kitching
    Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Eur J Immunol 29:1-10. 1999
    ..These results establish a central role for IL-12 in severe crescentic GN...
  2. ncbi request reprint CD100 enhances dendritic cell and CD4+ cell activation leading to pathogenetic humoral responses and immune complex glomerulonephritis
    Ming Li
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Clayton, Victoria, Australia
    J Immunol 177:3406-12. 2006
    ..Although T cell-B cell interactions also may be relevant, these studies demonstrate that CD100 enhances pathogenetic humoral immune responses and promotes the activation of APCs by up-regulating CD86 expression...
  3. ncbi request reprint Interleukin-4 and interleukin-10 attenuate established crescentic glomerulonephritis in mice
    A R Kitching
    Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 52:52-9. 1997
    ..Administration of Th2 cytokines, IL-4 and IL-10 to mice with established GN attenuates the development of glomerular crescent formation and protects renal function...
  4. ncbi request reprint IL-12p40 and IL-18 in crescentic glomerulonephritis: IL-12p40 is the key Th1-defining cytokine chain, whereas IL-18 promotes local inflammation and leukocyte recruitment
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 16:2023-33. 2005
    ..These studies demonstrate that in severe experimental crescentic GN, IL-12p40 is the key Th1-defining cytokine chain, whereas IL-18 has local proinflammatory roles...
  5. ncbi request reprint Targeting leukocytes in immune glomerular diseases
    A R Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Rd, Clayton, VIC 3168, Australia
    Curr Med Chem 15:448-58. 2008
    ..Modifying pathogenetic T or B cells also is a promising strategy in both systemic autoimmunity affecting the kidney and organ specific autoimmunity...
  6. ncbi request reprint Endogenous IL-13 limits humoral responses and injury in experimental glomerulonephritis but does not regulate Th1 cell-mediated crescentic glomerulonephritis
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Rd, Clayton, VIC 3168, Australia
    J Am Soc Nephrol 15:2373-82. 2004
    ..They indicate a role for IL-13 in limiting antibody-mediated renal injury, but not in regulating DTH-like cell-mediated responses in the kidney...
  7. ncbi request reprint Experimental autoimmune anti-glomerular basement membrane glomerulonephritis: a protective role for IFN-gamma
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    J Am Soc Nephrol 15:1764-74. 2004
    ..They lend weight to the hypothesis that depending on the context/severity of the nephritogenic immune response IFN-gamma has different effects...
  8. ncbi request reprint Endogenous alpha2-antiplasmin does not enhance glomerular fibrin deposition or injury in glomerulonephritis
    A R Kitching
    Center for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Center, Clayton, Victoria, Australia
    J Thromb Haemost 1:1992-9. 2003
    ..alpha2-Antiplasmin (alpha2-AP) is the major circulating inhibitor of plasmin and is expressed in the renal tubulointerstitium...
  9. doi request reprint The emergence of TH17 cells as effectors of renal injury
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Center, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 22:235-8. 2011
    ....
  10. pmc Effects of CTLA4-Fc on glomerular injury in humorally-mediated glomerulonephritis in BALB/c mice
    A R Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Clin Exp Immunol 128:429-35. 2002
    ..These results demonstrate that CTLA4-Fc is of benefit in this model of glomerulonephritis by its capacity to attenuate antibody production, without affecting the minor degree of cell-mediated glomerular injury...
  11. pmc Interleukin-10 inhibits experimental mesangial proliferative glomerulonephritis
    A R Kitching
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Clin Exp Immunol 128:36-43. 2002
    ..The effects of IL-10 in inhibiting mesangial cell proliferation are likely to be due to a combination of direct effects of IL-10 on mesangial cells and effects mediated by macrophages...
  12. ncbi request reprint IL-18 has IL-12-independent effects in delayed-type hypersensitivity: studies in cell-mediated crescentic glomerulonephritis
    A R Kitching
    Centre for Inflammatory Diseases, Department of Medicine Monash Medical Centre, Monash University, Clayton, Victoria, Australia
    J Immunol 165:4649-57. 2000
    ..These studies demonstrate that even in the absence of IL-12, IL-18 can induce in vivo DTH responses and up-regulate ICAM-1 without inducing IFN-gamma, GM-CSF, or TNF-alpha production...
  13. ncbi request reprint IFN-gamma mediates crescent formation and cell-mediated immune injury in murine glomerulonephritis
    A R Kitching
    Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    J Am Soc Nephrol 10:752-9. 1999
    ..They support the hypothesis that crescentic glomerulonephritis is a manifestation of a Th1 nephritogenic immune response...
  14. ncbi request reprint Interleukin-4 deficiency enhances Th1 responses and crescentic glomerulonephritis in mice
    A R Kitching
    Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 53:112-8. 1998
    ..They show that IL-4 deficiency promotes crescentic glomerular injury and amplifies local and systemic Th1 responses. They support the hypothesis that crescent formation results from Th1 immune responses to antigens in the glomerulus...
  15. ncbi request reprint Crescentic glomerulonephritis--a manifestation of a nephritogenic Th1 response?
    A R Kitching
    Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Histol Histopathol 15:993-1003. 2000
    ....
  16. ncbi request reprint Endogenous interleukin-10 regulates Th1 responses that induce crescentic glomerulonephritis
    A R Kitching
    Center for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Center, Clayton, Victoria, Australia
    Kidney Int 57:518-25. 2000
    ..To determine the role of endogenous IL-10, the development of the nephritogenic immune response and crescentic GN was compared in IL-10-deficient (IL-10-/-) and normal (IL-10+/+) C57BL/6 mice...
  17. pmc Endogenous interleukin (IL)-17A promotes pristane-induced systemic autoimmunity and lupus nephritis induced by pristane
    S A Summers
    Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, Vic, Australia Department of Nephrology, Monash Health, Melbourne, Vic, Australia
    Clin Exp Immunol 176:341-50. 2014
    ..Therefore, IL-17A is required for the full development of autoimmunity and lupus nephritis in experimental SLE, and early in the development of autoimmunity, innate immune cells produce IL-17A...
  18. ncbi request reprint IFN-gamma production by intrinsic renal cells and bone marrow-derived cells is required for full expression of crescentic glomerulonephritis in mice
    Jennifer R Timoshanko
    Center for Inflammatory Diseases, Monash University, and Department of Medicine, Monash Medical Center, Clayton, Victoria, Australia
    J Immunol 168:4135-41. 2002
    ....
  19. ncbi request reprint Immunopathogenesis of crescentic glomerulonephritis
    P G Tipping
    Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Curr Opin Nephrol Hypertens 8:281-6. 1999
    ..Accumulating evidence suggests that crescentic glomerulonephritis results from a complex cell-mediated nephritogenic immune response. Interruption of a number of immune and inflammatory mediators can improve the outcome of this disease...
  20. pmc The tumour suppressor gene p53 modulates the severity of antigen-induced arthritis and the systemic immune response
    M Leech
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Melbourne, Australia
    Clin Exp Immunol 152:345-53. 2008
    ..p53 is involved in the modulation of adaptive and innate immune responses relevant to arthritis models and is also involved in the modulation of severity of AIA by both cell-cycle dependent and cell-cycle-independent mechanisms...
  21. ncbi request reprint Endogenous myeloperoxidase promotes neutrophil-mediated renal injury, but attenuates T cell immunity inducing crescentic glomerulonephritis
    Dragana Odobasic
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Level 5 Block E, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 18:760-70. 2007
    ....
  22. ncbi request reprint Th1 and Th2 T helper cell subsets affect patterns of injury and outcomes in glomerulonephritis
    S R Holdsworth
    Monash University Department of Medicine, Monash Medical Center, Clayton, Victoria, Australia
    Kidney Int 55:1198-216. 1999
    ..In particular, the evidence that Th1-predominant nephritogenic immune responses are associated with severe proliferative and crescentic GN is presented...
  23. pmc Signal transducer and activation of transcription 6 (STAT6) regulates T helper type 1 (Th1) and Th17 nephritogenic immunity in experimental crescentic glomerulonephritis
    S A Summers
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Vic, Australia
    Clin Exp Immunol 166:227-34. 2011
    ..We conclude that STAT6 is required for attenuation of Th1 and Th17 nephritogenic immune responses and protection from crescentic glomerulonephritis...
  24. doi request reprint Antimyeloperoxidase antibodies rapidly induce alpha-4-integrin-dependent glomerular neutrophil adhesion
    Michael P Kuligowski
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Clayton, Australia
    Blood 113:6485-94. 2009
    ..Lower doses induce adhesion only after an infection-related stimulus, whereas higher doses are capable of inducing responses in the absence of an additional inflammatory stimulus, via alternative adhesion mechanisms...
  25. ncbi request reprint Leukocyte recruitment to the inflamed glomerulus: a critical role for platelet-derived P-selectin in the absence of rolling
    Michael P Kuligowski
    Centre for Inflammatory Diseases, Department of Medicine, Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia
    J Immunol 176:6991-9. 2006
    ..Together, these data indicate that anti-GBM Ab-induced leukocyte adhesion in glomeruli occurs via a novel pathway involving a nonrolling interaction mediated by platelet-derived P-selectin...
  26. pmc Th17 cells promote autoimmune anti-myeloperoxidase glomerulonephritis
    Poh Yi Gan
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    J Am Soc Nephrol 21:925-31. 2010
    ..In conclusion, IL-17A contributes to the pathophysiology of autoimmune anti-MPO GN, suggesting that it may be a viable therapeutic target for this disease...
  27. pmc T-bet deficiency attenuates renal injury in experimental crescentic glomerulonephritis
    Richard K S Phoon
    Department of Medicine, Monash University, Monash Medical Centre, Level 5 Block E, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 19:477-85. 2008
    ..We conclude that T-bet directs Th1 responses that induce renal injury in experimental crescentic glomerulonephritis...
  28. doi request reprint TLR9 and TLR4 are required for the development of autoimmunity and lupus nephritis in pristane nephropathy
    S A Summers
    Centre for Inflammatory Diseases, Monash University Department of Medicine, 246 Clayton Rd, Clayton, VIC 3168, Australia
    J Autoimmun 35:291-8. 2010
    ..These results demonstrate that both TLR9 and TLR4 are required for 'full-blown' autoimmunity and organ injury in experimental lupus induced by pristane...
  29. ncbi request reprint CD80 and CD86 costimulatory molecules regulate crescentic glomerulonephritis by different mechanisms
    Dragana Odobasic
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 68:584-94. 2005
    ..The aim of the current studies was to define the mechanisms by which CD80 and CD86 regulate the development of this disease...
  30. pmc IL-23, not IL-12, directs autoimmunity to the Goodpasture antigen
    Joshua D Ooi
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    J Am Soc Nephrol 20:980-9. 2009
    ..In conclusion, autoreactivity to the Goodpasture antigen is directed primarily by IL-23, absence of which results in hyporeactivity including but extending beyond a deficient Th17 response...
  31. pmc Th1 and Th17 cells induce proliferative glomerulonephritis
    Shaun A Summers
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 20:2518-24. 2009
    ..In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies...
  32. ncbi request reprint Inducible co-stimulatory molecule ligand is protective during the induction and effector phases of crescentic glomerulonephritis
    Dragana Odobasic
    Department of Medicine, Monash University, Monash Medical Centre, Level 5 Block E, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 17:1044-53. 2006
    ..They also show that ICOSL is upregulated in nephritic glomeruli, where it locally reduces accumulation of T cells and macrophages and attenuates renal injury...
  33. pmc Glomerulonephritis, Th1 and Th2: what's new?
    P G Tipping
    Centre for Inflammatory Diseases, Department of Medicine, Monash University, Clayton, Victoria, Australia
    Clin Exp Immunol 142:207-15. 2005
    ..The challenge remains to understand fully the relevance of T helper cell subset responses to the spectrum of human GN and to apply this new knowledge to the development of more potent and selective therapeutic strategies...
  34. doi request reprint Lymphocytes promote albuminuria, but not renal dysfunction or histological damage in a mouse model of diabetic renal injury
    A K H Lim
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    Diabetologia 53:1772-82. 2010
    ..While the importance of macrophages in diabetic renal injury has been clearly demonstrated, the role of lymphocytes is still unknown. We therefore examined the development of diabetic renal injury in lymphocyte-deficient mice...
  35. ncbi request reprint Intrinsic renal cell expression of CD40 directs Th1 effectors inducing experimental crescentic glomerulonephritis
    Amanda Jane Ruth
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    J Am Soc Nephrol 14:2813-22. 2003
    ..In conclusion, the expression of CD40 by nonimmune renal cells plays a major role in Th1 effector responses by inducing Th1 chemokine production. Therefore, CD40-CD154 interactions are a potential therapeutic target in GN...
  36. ncbi request reprint A pathogenetic role for mast cells in experimental crescentic glomerulonephritis
    Jennifer R Timoshanko
    Center for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Center, 246 Clayton Road, Melbourne, Victoria 3168, Australia
    J Am Soc Nephrol 17:150-9. 2006
    ..These findings suggest that renal mast cells mediate crescentic GN by facilitating effector cell recruitment into glomeruli via augmentation of adhesion molecule expression...
  37. ncbi request reprint Chemokines as therapeutic targets in renal disease
    S R Holdsworth
    Monash University Department of Medicine, Monash Medical Centre, Victoria, Australia
    Curr Opin Nephrol Hypertens 9:505-11. 2000
    ....
  38. ncbi request reprint IL-18 is redundant in T-cell responses and in joint inflammation in antigen-induced arthritis
    Leilani L Santos
    Centre for Inflammatory Diseases, Monash Institute of Medical Research, Monash Medical Centre, Melbourne, Australia
    Immunol Cell Biol 84:166-73. 2006
    ..In conclusion, IL-18 is redundant both as a Th1 response cofactor and inflammatory cytokine, whereas IL-12p40-/- is a key cytokine, in AIA in C57Bl/6 mice...
  39. ncbi request reprint An IL-12-independent role for CD40-CD154 in mediating effector responses: studies in cell-mediated glomerulonephritis and dermal delayed-type hypersensitivity
    Amanda Jane Ruth
    Centre for Inflammatory Diseases, Department of Medicine, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Immunol 173:136-44. 2004
    ..Effector cell activation, renal DTH-like injury, and dermal DTH require direct Th1 CD154/macrophage CD40 interactions...
  40. ncbi request reprint The isolation and purification of biologically active recombinant and native autoantigens for the study of autoimmune disease
    Jim Apostolopoulos
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Level 5 Block E, Monash Medical Centre, 246 Clayton Rd, Clayton, 3168 Victoria, Australia
    J Immunol Methods 308:167-78. 2006
    ..This study also demonstrated that the immunization of myeloperoxidase deficient (Mpo-/-) mice with purified recombinant mouse myeloperoxidase induced a significant antibody response to native myeloperoxidase...
  41. pmc Platelet recruitment to the inflamed glomerulus occurs via an alphaIIbbeta3/GPVI-dependent pathway
    Sapna Devi
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Clayton, Victoria, Australia
    Am J Pathol 177:1131-42. 2010
    ....
  42. ncbi request reprint Glomerular expression of CD80 and CD86 is required for leukocyte accumulation and injury in crescentic glomerulonephritis
    Dragana Odobasic
    Monash University, Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 16:2012-22. 2005
    ..These studies show that CD80 and CD86 are expressed in glomeruli of mice with crescentic anti-GBM GN, in which they play a critical role in facilitating accumulation of Th1 effectors and macrophages, thus exacerbating renal injury...
  43. doi request reprint The cytoplasmic domain of tissue factor in macrophages augments cutaneous delayed-type hypersensitivity
    Jim Apostolopoulos
    Centre for Inflammatory Diseases, Department of Medicine, Monash University, Clayton, Victoria, Australia
    J Leukoc Biol 83:902-11. 2008
    ..These results indicate that leukocyte expression of the cytoplasmic domain of TF contributes to antigen-specific cellular adaptive immune responses via effects on leukocyte recruitment and activation...
  44. ncbi request reprint Plasminogen activator inhibitor-1 is a significant determinant of renal injury in experimental crescentic glomerulonephritis
    A Richard Kitching
    Centre for Inflammatory Diseases, and Department of Medicine, Monash Medical Centre, Monash University, Clayton, Victoria, Australia
    J Am Soc Nephrol 14:1487-95. 2003
    ..These studies demonstrate that PAI-1 is a determinant of glomerular fibrin deposition and renal injury in crescentic glomerulonephritis...
  45. ncbi request reprint Granulocyte macrophage colony-stimulating factor expression by both renal parenchymal and immune cells mediates murine crescentic glomerulonephritis
    Jennifer R Timoshanko
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Center, Clayton, 3168 Victoria, Australia
    J Am Soc Nephrol 16:2646-56. 2005
    ....
  46. ncbi request reprint Anti-neutrophil cytoplasmic antibodies and effector CD4+ cells play nonredundant roles in anti-myeloperoxidase crescentic glomerulonephritis
    Amanda Jane Ruth
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, VIC 3168, Australia
    J Am Soc Nephrol 17:1940-9. 2006
    ..ANCA induces glomerular neutrophil infiltration and MPO deposition. Subsequently, anti-MPO CD4+ cells recognize MPO as a planted glomerular antigen and act with macrophages to amplify severe glomerular injury...
  47. pmc Leukocyte-derived interleukin-1beta interacts with renal interleukin-1 receptor I to promote renal tumor necrosis factor and glomerular injury in murine crescentic glomerulonephritis
    Jennifer R Timoshanko
    Department of Medicine, Centre for Inflammatory Diseases, Monash Medical Centre, Monash University, Clayton, Victoria, Australia
    Am J Pathol 164:1967-77. 2004
    ..These studies demonstrate that leukocytes are the major cellular source of IL-1beta, and that IL-1beta acts principally via the IL-1RI on intrinsic renal cells to induce TNF expression and crescentic glomerular injury...
  48. ncbi request reprint Plasminogen activator inhibitor-1 production is pathogenetic in experimental murine diabetic renal disease
    M Lassila
    The Baker Heart Research Institute, Vascular Division, Danielle Alberti Memorial Centre for Diabetes Complications, Melbourne, Victoria, Australia
    Diabetologia 50:1315-26. 2007
    ..It is upregulated in experimental and human diabetic nephropathy. These studies assessed the effect of PAI-1 deficiency and overproduction on renal disease in experimental diabetes...
  49. ncbi request reprint The requirement for granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in leukocyte-mediated immune glomerular injury
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Australia
    J Am Soc Nephrol 13:350-8. 2002
    ..These studies demonstrate that endogenous GM-CSF plays a role in experimental glomerulonephritis in both the autologous and heterologous phases of injury...
  50. ncbi request reprint Contributions of IL-1beta and IL-1alpha to crescentic glomerulonephritis in mice
    Jennifer R Timoshanko
    Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 15:910-8. 2004
    ..These studies indicate that IL-1beta but not IL-1alpha contributes to crescent formation and inflammatory cell recruitment, whereas IL-1alpha but not IL-1beta contributes to humoral mechanisms of glomerular injury...
  51. doi request reprint Atorvastatin enhances humoral immune responses but does not alter renal injury in experimental crescentic glomerulonephritis
    Richard K S Phoon
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrology (Carlton) 14:650-7. 2009
    ..We sought to evaluate the immunomodulatory effects and therapeutic potential of atorvastatin in experimental crescentic glomerulonephritis, a Th1-predominant animal model of glomerulonephritis...
  52. ncbi request reprint Macrophage migration inhibitory factor deficiency attenuates macrophage recruitment, glomerulonephritis, and lethality in MRL/lpr mice
    Alberta Y Hoi
    Department of Medicine, Centre for Inflammatory Diseases, Monash Institute of Medical Research, Monash University, Melbourne, Australia
    J Immunol 177:5687-96. 2006
    ..Taken together, these data suggest MIF as a critical effector of organ injury in SLE...
  53. doi request reprint Advances in the pathogenesis of Goodpasture's disease: from epitopes to autoantibodies to effector T cells
    Joshua D Ooi
    Monash University Department of Medicine, Monash Medical Centre, Clayton, VIC 3168, Australia
    J Autoimmun 31:295-300. 2008
    ..Observations in humans suggest that regulatory T cells are associated with the development of self-immunoregulation in the convalescent phase of disease...
  54. doi request reprint Targeting renal macrophage accumulation via c-fms kinase reduces tubular apoptosis but fails to modify progressive fibrosis in the obstructed rat kidney
    Frank Y Ma
    Dept of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    Am J Physiol Renal Physiol 296:F177-85. 2009
    ..In conclusion, c-fms blockade was shown to selectively prevent interstitial macrophage accumulation and to reduce tubular apoptosis in the obstructed kidney, but it had no significant impact on the development of interstitial fibrosis...
  55. pmc Intrarenal antigens activate CD4+ cells via co-stimulatory signals from dendritic cells
    Kristy L Edgtton
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    J Am Soc Nephrol 19:515-26. 2008
    ....
  56. ncbi request reprint Experimental autoimmune Goodpasture's disease: a pathogenetic role for both effector cells and antibody in injury
    Elizabeth G Dean
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 67:566-75. 2005
    ..However, observational human studies and studies in experimental systems also imply a role for cell-mediated effector injury...
  57. doi request reprint In vivo imaging of leukocyte recruitment to glomeruli in mice using intravital microscopy
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Clayton, Melbourne, Victoria, Australia
    Methods Mol Biol 466:109-117. 2009
    ..The process of hydronephrosis does not alter the ability of anti-GBM-antibody to induce a glomerular inflammatory response. This approach allows detailed investigation of the mechanisms of leukocyte recruitment within glomeruli...
  58. doi request reprint Review: T helper 17 cells: their role in glomerulonephritis
    Joshua D Ooi
    Centre for Inflammatory Diseases, Department of Medicine, Monash Medical Centre, Monash University, Clayton, VIC 3168, Australia
    Nephrology (Carlton) 15:513-21. 2010
    ..This review will review the discovery of the Th17 subset, its properties, its relationship with other Th subsets and assess the current evidence implicating Th17 cells in glomerulonephritis...
  59. ncbi request reprint Fibrin independent proinflammatory effects of tissue factor in experimental crescentic glomerulonephritis
    Malcolm A Cunningham
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Victoria, Australia
    Kidney Int 66:647-54. 2004
    ..Tissue factor initiated glomerular fibrin deposition is an important mediator of injury in crescentic glomerulonephritis. Recent data have suggested noncoagulant roles for tissue factor in inflammation...
  60. ncbi request reprint The role of flow cytometric ANCA detection in screening for acute pauci-immune crescentic glomerulonephritis
    A Richard Kitching
    Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrol Dial Transplant 19:365-70. 2004
    ..This article studied the sensitivity and specificity of serum ANCA, determined by flow cytometry and indirect immunofluorescence (IIF), to identify patients with acute PICGN...
  61. doi request reprint IL-1RI deficiency ameliorates early experimental renal interstitial fibrosis
    Lynelle K Jones
    Department of Medicine, Centre for Inflammatory Diseases, Monash University, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrol Dial Transplant 24:3024-32. 2009
    ....
  62. ncbi request reprint Plasmin is not protective in experimental renal interstitial fibrosis
    Kristy L Edgtton
    Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 66:68-76. 2004
    ..The plasminogen-plasmin system has potential beneficial or deleterious effects in the context of renal fibrosis. Recent studies have implicated plasminogen activators or their inhibitors in this process...
  63. pmc The Th17-defining transcription factor RORγt promotes glomerulonephritis
    Oliver M Steinmetz
    Centre for Inflammatory Diseases, Monash University Department of Medicine, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 22:472-83. 2011
    ..Taken together, this study demonstrates that RORγt promotes the development of crescentic glomerulonephritis by directing nephritogenic Th17 responses...
  64. ncbi request reprint A new approach to idiopathic nephrotic syndrome
    Joshua Y Kausman
    J Am Soc Nephrol 18:2621-2. 2007