The Journal of Immunology, Vol 140, Issue 8 2495-2499, Copyright © 1988 by American Association of Immunologists

ARTICLES

Phorbol myristate acetate inhibits increases in membrane fluidity induced by anti-IgM in B cells

J Mizuguchi, N Utsunomiya, M Nakanishi and Y Arata
Department of Applied Immunology, National Institute of Health, Tokyo, Japan.

Anti-IgM or anti-IgD stimulates B cells to induce increases in inositol phospholipid metabolism and intracellular free calcium concentration [( Ca2+]i). Anti-IgM also causes increases in membrane fluidity that occur more promptly than those in [Ca2+]i in resting B cells as well as BAL17 B lymphoma cells. However, other B cell activators such as LPS or PMA did not induce the membrane fluidity changes. Furthermore, sodium fluoride, which is considered to be an activator of the guanine nucleotide-binding protein, caused increases in membrane fluidity as well as increased [Ca2+]i or inositol phospholipid metabolism. Anti-IgM- or sodium fluoride-induced increases in membrane fluidity were inhibited by 20-min pretreatment of cells with PMA, but not by 24-h pretreatment. These results indicate that membrane fluidity changes are closely associated with increased [Ca2+]i after cross-linkage of membrane Ig and are regulated by protein kinase C in B cells.

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