1386 Renal Deposition of Idiotype - Anti - Idiotype

نویسندگان

  • MICHEL GOLDMAN
  • LYNN MASSMAN ROSE
  • AGNES HOCHMANN
  • PAUL HENRI LAMBERT
چکیده

Immune complexes (IC) 1 are thought to play a major role in the pathogenesis of many human glomerulonephritides (1). This has been suggested by immunofluorescence studies showing glomerular deposits of immunoglobulins and complement and by observations of electron-dense deposits around or within the glomerular basement membrane. In addition, glomerulonephritides are a common feature of some autoimmune or infectious diseases associated with the persistence of IC in the circulation (2, 3). Many attempts have been made to identify the antigenic components of the circulating and glomerular IC detected in these diseases. However, in most cases, the nature of the involved antigens remains largely unknown (4). Polyclonal hypergammaglobulinemia is a frequent finding in IC diseases (5-9). This has led to thinking that polyclonal B cell hyperactivity could be involved in the generation of IC. Experimentally, polyclonal B cell activation induced in mice by bacterial lipopolysaccharides (LPS) or other B cell mitogens has been shown to be associated with the occurrence of both circulating and glomerular IC (10, 11). The mechanisms of this association have not been well defined. As activation of the B cell compartment induces the production of various auto-antibodies, including antiimmunoglobulin antibodies (12), some of the complexes might result from the reaction of anti-immunoglobulin antibodies with other immunoglobulin molecules. Idiotypes and corresponding anti-idiotypic auto-antibodies are potential candidates for such immunoglobulin interactions within the B cell repertoire (13). Recently, we were able to demonstrate the simultaneous production of immunoglobulins bearing a known idiotype, the TEPC15 (T 15) idiotype, of corresponding anti-idiotypic antibodies and of circulating T 15 idiotype-anti-T 15-idiotype IC in BALB/c mice injected with LPS 2

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تاریخ انتشار 2003