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  • Title: Immune reactivity and immunosuppressive intervention (TLI) in experimental nephritis. I. Immunopathologic correlates in the accelerated autologous form of nephrotoxic serum nephritis.
    Author: Lowry RP, Forbes RD, Blackburn JH.
    Journal: J Immunol; 1984 Feb; 132(2):1001-6. PubMed ID: 6361128.
    Abstract:
    The progression of histologic changes observed in the accelerated autologous form of nephrotoxic serum nephritis (AA-NTSN) in the inbred LEW rat, ranging from minimal endocapillary proliferation to marked endo- and extra-capillary proliferation together with fibrin deposition and necrosis of glomerular tufts, was closely correlated (day 8) with parallel measures of albuminuria (1.6 leads to 280 mg/24 hr). In the induction phase of AA-NTSN (day 0) a direct linear correlation (r = 0.72, p less than 0.05) was obtained between anti-SGG antibody levels and 24-hr urine albumin excretion. Subsequent observations (day 7) yield an inverse correlation between anti-SGG antibody and albuminuria (r = -0.54, p less than 0.01), and this change was shown to be related to the loss of specific antibody in the urine (r = 0.59, p less than 0.025). Although splenic T cells of rats with AA-NTSN manifest a specific proliferative response to the inducing antigen SGG, and although the magnitude of this proliferative response (day 7) correlates directly with parallel measures of urine albumin excretion (r = 0.71, p less than 0.02), delayed-type hypersensitivity (DTH) to SGG measured by radiometric ear assay was inversely correlated with albuminuria in this model of experimental nephritis (r = 0.80, p less than 0.01). Additional data are presented that strongly suggest that persistent albuminuria at 1 mo after induction of AA-NTSN is independent of ongoing immunopathologic processes. Thus, glomerular injury in AA-NTSN, previously linked to prominent glomerular macrophage accumulation, is shown to be primarily dependent on a brisk antibody response to the planted heterologous (sheep) immunoglobulin, whereas cellular immunity, readily demonstrated in the splenic T cell compartment, is likely to be of lesser import in the pathogenesis of this lesion in the intact animal.
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