Studies of surface immunoglobulin-dependent B cell activation
1Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia.
Studies from a number of laboratories have firmly established the potential of surface immunoglobulin-generated signals in B lymphocyte activation. While clearly there are multiple ways of activating B lymphocytes, some of which may not involve surface immunoglobulin, it is clear that crosslinking of surface immunoglobulin whether by antigen or antireceptor antibody can generate signals relevant to B cell activation. Although considerable insight into the mechanism of transduction of mIg-generated signals across the plasma membrane has been realized, a molecular explanation for linking inositol phospholipid hydrolysis to changes within the cytoplasm and nucleus of the B cell is still speculative. A more rigorous definition of the PKC and calcium components of the mIg signal transduction pathway are critical for a thorough understanding of the mechanism of signal transduction by this receptor. The use of tumor cell models allowing selection of mutants within the signalling pathway(s) will be invaluable to fully defining the critical molecular and biochemical events involved in B cell activation.
Studies from a number of laboratories have firmly established the potential of surface immunoglobulin-generated signals in B lymphocyte activation. While clearly there are multiple ways of activating B lymphocytes, some of which may not involve surface immunoglobulin, it is clear that crosslinking of surface immunoglobulin whether by antigen or antireceptor antibody can generate signals relevant to B cell activation. Although considerable insight into the mechanism of transduction of mIg-generated signals across the plasma membrane has been realized, a molecular explanation for linking inositol phospholipid hydrolysis to changes within the cytoplasm and nucleus of the B cell is still speculative. A more rigorous definition of the PKC and calcium components of the mIg signal transduction pathway are critical for a thorough understanding of the mechanism of signal transduction by this receptor. The use of tumor cell models allowing selection of mutants within the signalling pathway(s) will be invaluable to fully defining the critical molecular and biochemical events involved in B cell activation.
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