ABILITY OF COMPLEMENT TO RELEASE SYSTEMIC LUPUS-ERYTHEMATOSUS IMMUNE-COMPLEXES FROM CELL RECEPTORS

  • 1 January 1981
    • journal article
    • research article
    • Vol. 44  (2) , 416-425
Abstract
Endogenous immune complexes [IC] present in sera from 10 different patients with systemic lupus erythematosus (SLE) in an active phase were allowed to bind to Raji [Burkitt lymphoma] cells; the ability of intact complement [c] to release the cell-bound complexes from receptors was then examined. Fresh normal human serum, or, alternatively, zymosan-pretreated serum, was added to the complex-bearing Raji cells. IC remaining bound to Raji cell receptors after increasing times at 37.degree. C were quantitated by addition of 125I-labeled antiglobulin, after removal of serum by washing. In all 10 cases, C-dependent release was observed. In parallel control studies performed under identical conditions. IC prepared in vitro from bovine serum albumin (BSA) and guinea pig anti-BSA antibody were used in place of the endogenous SLE complexes. The experimental complexes were released by fresh serum, but not by zymosan-treated serum, when studied used either 125I-labeled anti-guinea pig Ig or 125I-labeled complexes alone. Apparently, intact C can alter the IC present in SLE sera and influence their interaction with receptors on lymphoid cells. Hypocomplementemia secondarily due to consumption of C by IC may contribute to the persistence of the complexes.