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- W2052242420 abstract "CBA/N mice, which carry the xid immunodeficiency, lack a mature subpopulation of B cells. The residual B cells in these mice do not make antibodies to type-2 T-independent antigens, nor do they synthesize DNA in response to mitogenic forms of anti-Ig antibodies. It is therefore an attractive hypothesis that the surface immunoglobulin receptors (sIgR) on xid B cells signal abnormally following cross-linking. We show here that anti-Ig antibodies do cause inositol phospholipid hydrolysis and Ca2+ mobilization in xid B cells. However, the responses of these cells are only 40%–50% of those of normal B cells. Studies with permeabilized cells demonstrated that the hyporesponsiveness is not due to ineffective coupling of sIgR to their associated G-protein. Rather it is apparently due to a quantitative and/or qualitative deficiency in the polyphosphoinositide-specific phosphodiesterase which mediates sIgR-induced inositol phospholipid hydrolysis. These observations may provide a biochemical explanation for the immunological abnormalities resulting from the xid mutation." @default.
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- W2052242420 date "1989-11-01" @default.
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- W2052242420 title "Analysis of signaling via surface immunoglobulin receptors on b cells from cba/n mice" @default.
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- W2052242420 doi "https://doi.org/10.1002/eji.1830191117" @default.
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