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Ligands of Surface Ig Raise Cytoplasmic Free Ca ++ in Human B Cells
Author(s) -
CLEVERS H. C.,
BLOEM A. C.,
GMELIGMEYLING F.,
BALLIEUX R. E.
Publication year - 1985
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1985.tb01915.x
Subject(s) - calcium , antibody , intracellular , chemistry , verapamil , cytosol , cytoplasm , microbiology and biotechnology , calcium in biology , antiserum , biochemistry , biology , immunology , enzyme , organic chemistry
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 μλ‐carrying B‐cell line, AZU‐1, increased free cytosolic calcium after addition of anti‐μ or anti‐μ antibodies: F (ab′) 2 fragments with anti‐μ 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 μM). nifedipine (20 μM). and LaCl 3 (200 μM) inhibited the anti‐μ‐induced calcium influx. Peripheral blood B cells reacted in essentially the same way in response to anti‐μ 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.