title: Immune reactivity and immunosuppressive intervention (TLI) in experimental nephritis. I. Immunopathologic correlates in the accelerated autologous form of nephrotoxic serum nephritis.
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.
mesh_terms: D000419:Albuminuria / Q000209:etiology / Q000276:immunology / Q000473:pathology; D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000096:biosynthesis / Q000502:physiology / Q000652:urine; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D003176:Complement C3 / Q000032:analysis; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000276:immunology; D007165:Immunosuppression Therapy; D007700:Kinetics; D008213:Lymphocyte Activation / Q000528:radiation effects; D008297:Male; D011817:Rabbits; D051381:Rats; D011917:Rats, Inbred Lew; D011919:Rats, Inbred Strains; D012756:Sheep; D014916:Whole-Body Irradiation
chemical_list: D000888:Antibodies, Anti-Idiotypic; D003176:Complement C3; D007074:Immunoglobulin G