Mechanisms of tissue injury induced with anti-gp70 autoantibodies

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1. Mechanisms of the development of glomerular lesions induced by transplantation of anti-gp70 antibody-producing hybridomas : Purified IgG molecules of the nephritogenic anti-gp70 monoclonal antibodies were injected into NZW and C57BL/6 strains of mice. Glomerular lesions were observed only in NZW mice that express a high level of serum gp70. Thus, gp70-anti-gp70 immune complexes seems to be involved in the development of glomerular lesions.2. Localization of antigenic epitopes recognized by nephritogenic anti-gp70 monoclonal antibodies : By expressing chimeras of xenotropic and polytropic viral env genes, antigenic epitopes recognized by most of the nephritogenic anti-gp70 monoclonal antibodies were mapped to the N-terminal one third of the xenotropic viral gp70.3. Expression of endogenous retroviral env gene products on platelets : Some of the pathogenic anti-gp70 monoclonal antibodies induce thrombocytopenia associated with systemic hemorrhage when injected into normal mice. Therefore, possible expression of endogenous retroviral gp70 on platelets was tested by FACS analysis. Peripheral blood platelets of normal and MRL strains of mice express several different endogenous retroviral env gene products on their surface. Platelets were aggregated in vivo in small vessels as demonstrated by electron microscopic examination of antibody-injected mice.