Abstract
Accumulating evidence indicates that quiescent, murine B lymphocytes have the capacity to respond to multiple physiologic regulatory species. Virtually all small B cells express receptor immunoglobulin of two classes, IgM and IgD which confer responsiveness to antigen. They respond to thymus dependent antigens, and anti-immunoglobulin antibodies which act as antigen surrogates, as determined by an increase in the expression of cell surface Ia (1,2). Under appropriate conditions anti-immunoglobulin antibodies also induce B cell blastogenesis and proliferation (3,4). These mitogenic antibodies mimic the effects of highly polymeric thymus independent antigens generally termed TI type 1 antigens. It appears that the minimal signal generated by mlg crosslinking by TD antigen or anti-Ig antibodies is sufficient for induction of Ia expression. However, the basis by which TIl antigens and certain surrogate antibodies induce proliferation remains unclear. Recent evidence indicates that quiescent B cells also respond to the T cell lymphokine BSF1 resulting in increased expression of surface Ia (5–7). BSF1 also has a general viability promoting effect on quiescent B cells, while nonmitogenic anti-Ig antibodies adversely effect cell viability (J. Cambier, unpublished observations). Studies by Mond et al (8) and ourselves (unpublished observations) indicate that small B cells are responsive to interferony as well as αa and γ endorphins. Cloned IFNγ and endorphins inhibit anti-Ig induction of Ia expression and proliferation.
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Cambier, J.C. et al. (1987). Coupling of B Cell Surface Ig, Ia and BSF1 Receptors to Intracellular “Second Messengers”. In: Gupta, S., Paul, W.E., Fauci, A.S. (eds) Mechanisms of Lymphocyte Activation and Immune Regulation. Advances in Experimental Medicine and Biology, vol 213. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5323-2_19
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DOI: https://doi.org/10.1007/978-1-4684-5323-2_19
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