Ligands of surface Ig raise cytoplasmic free Ca++ in human B cells.

With the use of the fluorescent Ca++ indicator Quin-2, we have measured changes in intracellular calcium levels in human B cells in response to anti-Ig antibodies, to Staphylococcus aureus (Staph) or to protein A. Cells of an Epstein-Barr virus-transformed mu lambda-carrying B-cell line, AZU-1, increased free cytosolic calcium after addition of anti-mu or anti-lambda antibodies; F (ab')2 fragments with anti-mu specificity were equally effective. Fab fragments of sheep anti-Ig antibodies only induced a rise in calcium levels after addition of a second anti-sheep Ig antiserum. Cross-linking of non-Ig surface determinants did not influence calcium homeostasis. The calcium channel blockers verapamil (100 microM), nifedipine (20 microM), and LaCl3 (200 microM) inhibited the anti-mu-induced calcium influx. Peripheral blood B cells reacted in essentially the same way in response to anti-mu antibodies. The B cell mitogens protein A and Staph also induced a rise in intracellular calcium. These observations indicate that Ca++ may play a role as a messenger in the activation of human B cells via surface Ig.