Ligands of Surface Ig Raise Cytoplasmic Free Ca++ in Human B Cells

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Abstract
With the use of the fluorescence Ca2+ 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 freagments 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 anti-sheep Ig antiserum. Cross-linking of non-linking of non-Ig surface determinants did not influence calcium homeostatis. The calcium channel lockers verapamil (100 .MU.) nifedipine (20 .mu.M), and LaCl3 (200 .mu.M) 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 Ca2+ may play a role as a messenger in the activation of human B cells via surface Ig.