INHIBITION OF ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY BY ARTIFICIAL IMMUNE-COMPLEXES AND PATHOLOGICAL SERA
- 1 January 1979
- journal article
- research article
- Vol. 37 (2) , 467-475
Abstract
Detection of immune complexes by inhibition of antibody-dependent cellular cytotoxicity (ADCC) is based on the principle that soluble complexes can compete with target cell-bound antibody for receptors (FcR) on cytotoxic lymphocytes. A cytotoxicity system for the determination of soluble immune complexes in the sera of patients with inflammatory bowel disease (IBD) was defined. The conditions under which soluble complexes of rat serum albumin (RSA) and rabbit anti-RSA inhibited human K [antibody-dependent cytoxic] cell mediated lysis of sensitized Chang cells were examined, on the assumption that the behavior in the system of circulating immune complexes putatively present in inflammatory bowel disease, is similar to that of artificial immune complexes. Inhibition of ADCC by a standard amount of artificial complex in different normal human sera was relatively uniform provided that the final concentration of the latter did not exceed 10% of the culture medium. In the absence of extraneous complexes, the effect of both normal and IBD sera on ADCC varied widely. Differential inhibition of ADCC by sera from patients with IBD and normal subjects was expressed as a function of ADCC in a standard batch of fetal bovine serum (FBS). Under these conditions differences between pathological (n = 51) and normal (n = 52) sera were highly significant (P < 0.001), which was not explained by the presence in the patients'' sera of HLA antibodies reactive with the effector cells, nor by a deficit in nutritional support of ADCC. The absence of a correlation between inhibition of ADCC and total serum Ig[immunoglobulin]G or IgM inferred that inhibition was attributable to immune complexes in the IBD sera. The limitations of this assay for assessment of the incidence of immune complexes in pathological sera are discussed.This publication has 23 references indexed in Scilit:
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