IGA BLOCKS IGM AND IGG-INITIATED IMMUNE LYSIS BY SEPARATE MOLECULAR MECHANISMS

  • 1 January 1983
    • journal article
    • research article
    • Vol. 130  (6) , 2882-2885
Abstract
Circulating IgA which does not bind the 1st component of complement (C) and does not activate the classical C pathway, blocked the initiation of C-mediated immune effector mechanisms. In at least 2 clinical situations, epidemic meningococcal disease and severe hepatic dysfunction, IgA blockade of 1 such mechanism, immune lysis, resulted in susceptibility to hematogenous bacterial [Neisseria meningitidis] dissemination. The presence of strain-specific IgM, but not IgG, in the sera of susceptible patients at the time of dissemination suggested that IgA blockade of IgM-initiated lysis involves a separate mechanism more sensitive to quantitative changes than that involved in IgA blockade of IgG-initiated lysis. Whereas IgA blockade of IgG-initiated immune lysis is a competitive function of the ratio of IgA to IgG, the blocking of IgM-initiated lysis is a noncompetitive function of the ratio of IgA to target cells, independent of the concentration of IgM. In the presence of sufficient IgA to saturate binding sites, IgM is an impotent bystander unable to compete for sites or initiate lysis. Therefore, C-mediated effector mechanisms are more sensitive to quantitative changes in circulating IgA and target cells (binding sites) in the absence of IgG than in its presence. Neither mechanism appears related to binding kinetics.

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