The Journal of Immunology, Vol 143, Issue 7 2133-2141, Copyright © 1989 by American Association of Immunologists

ARTICLES

Differential regulation of murine B cell Fc gamma RII expression by CD4+ T helper subsets

CM Snapper, JJ Hooley, U Atasoy, FD Finkelman and WE Paul
Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.

The murine B cell FcR for IgG (Fc gamma RII) is a membrane glycoprotein reported to mediate inhibition of B cell activation and differentiation. We show that IL-4 inhibits the enhanced expression of Fc gamma RII by LPS-stimulated B cells. This activity is completely reversed by anti-IL-4 mAb and is specific, in that multiple other lymphokines tested do not exert a similar effect. This effect of IL-4 is apparent by day 1 of culture, although maximal inhibition occurs on day 4 at a concentration of 500 U/ml. The IL-4-induced inhibition of enhanced Fc gamma RII expression by LPS stimulation observed on day 4 of culture is associated with a significant reduction in the steady state level of Fc gamma RII beta gene-specific mRNA. IFN-gamma which inhibits many of the effects of IL-4 on B cells, does not reverse the IL-4-induced inhibition of Fc gamma RII membrane expression nor the levels of beta gene-specific mRNA. Fc gamma RII expression is significantly increased in B cells stimulated with antigen-specific, CD4+ T cell clones of the Th1 type (i.e., IL-2 and IFN-gamma- producing). By contrast, three different Th2 clones (i.e., IL-4- producing) fail to stimulate an increase in Fc gamma RII levels. Anti- IL-4 mAb significantly enhanced Fc gamma RII expression by Th2- stimulated B cells indicating that IL-4 was the active, inhibitory, substance produced by the Th2 cells. Supernatants from stimulated Th2 clones inhibited the enhanced expression of Fc gamma RII by LPS- stimulated B cells and this activity was completely reversed by anti-IL- 4 mAb. By contrast, supernatants from stimulated Th1 clones further enhanced Fc gamma RII expression by LPS-stimulated B cells. The differential regulation of B cell Fc gamma RII expression by Th subsets may play an important role in the regulation of humoral immunity by altering the sensitivity of B cells to IgG immune complex-mediated inhibition of B cell activation and differentiation in vivo.

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