Immune complex and complement-mediated leukocyte recruitment in bullous pemphigoid
Gammon, W.R.
Immunology Series 46: 509-525
1989
ISSN/ISBN: 0092-6019 PMID: 2488868 Document Number: 4226
The results of immunohistologic, serologic, and passive transfer studies have provided evidence that BP immune complexes activate C at the BMZ and that C activation contributes to the development or evolution of dermal-epidermal separation. The mechanism whereby C activation contributes to BP lesions is not understood. The results of histologic studies of evolving BP lesions and biochemical studies of BP blister fluids suggest that the pathogenesis of inflammation in BP is not due to C-derived chemotactic factors but rather to mast cell-derived eosinophil chemotactic factors. The results of our studies using the LA assay provide additional functional evidence against a major role for immune complexmediated C activation and production of C-derived chemotactic activity in the initial stages of inflammation and skin injury in BP. These studies have shown that there is little or no production of C-derived chemotactic activity by in vivo deposited BP immune complexes and suggest that what little activity that can be detected may be secondary to tissue injury rather than its cause. Compared to at least two diseases (bullous eruption of SLE and EBA) with BMZ immune complexes composed of BMZ antigen and anti-BMZ antibody and histologic features resembling experimental models of immune complex and C-mediated inflammation, the ability of BP immune complexes to generate C-derived chemotactic activity is relatively insignificant. Furthermore, we have found that BP antibodies are incapable of causing leukocyte recruitment in an in vitro organ culture model of anti-BMZ antibody and C-mediated inflammation.
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