By Peter F Zipfel
It is obvious faulty or deregulated supplement process leads to kidney illnesses. a huge function of supplement effector and regulatory proteins in pathological settings of the kidney has been validated. a wide panel of distinctive human kidney ailments is because of faulty supplement keep watch over. Genetic analyses have pointed out mutations in supplement regulators which are linked to those illnesses. Mutations were pointed out within the fluid part replacement pathway regulator issue H and the membrane regulator Membrane Cofactor Protein MCP (CD46). The sensible characterization of the mutant proteins permits to outline the pathophysiological occasions on a molecular point. those new ideas and information on ailment mechanisms allowed constructing new diagnostic and promising healing ways for a number of human kidney illnesses. Molecular biology, clinics and treatment are mentioned during this volume.
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J Immunol 162: 4018–4023 Arvieux J, Yssel H, Colomb MG (1988) Antigen-bound C3b and C4b enhance antigenpresenting cell function in activation of human T-cell clones. Immunology 65: 229–235 Erdei A, Kohler V, Schafer H, Burger R (1992) Macrophage-bound C3 fragments as adhesion molecules modulate presentation of exogenous antigens. Immunobiology 185: 314–326 Kerekes K, Prechl J, Bajtay Z, Jozsi M, Erdei A (1998) A further link between innate and adaptive immunity: C3 deposition on antigen-presenting cells enhances the proliferation of antigen-specific T cells.
Nephron 53: 338–342 Zhou W, Marsh JE, Sacks SH (2001) Intrarenal synthesis of complement. Kidney Int 59:1227–1235 Welch TR, Beischel LS, Witte DP (1993) Differential expression of complement C3 and C4 in the human kidney. J Clin Invest 92: 1451–1458 Sacks SH, Zhou W, Andrews PA, Hartley B (1993) Endogenous complement C3 synthesis in immune complex nephritis. Lancet 342: 1273–1274 Andrews PA, Pani A, Zhou W, Sacks SH (1994) Local transcription of complement C3 in human allograft rejection. Evidence for a pathogenic role and correlation to histology and outcome.
Using various complement-deficient mice, we demonstrated that complement plays an important pathogenic role in renal I/R injury . Our study showed that renal injury is reduced up to 50% in C3-defcient mice compared with their wild-type counterparts. Because a similar degree of protection against renal I/R injury is achieved in C3- and C5- or C6-deficient mice, this suggests that products derived from the terminal pathway of complement activation is an important factor in pathogenesis of renal I/R injury.