Stimulation of a B Cell Subset by Anti-Immunoglobulin and T Cell-Derived Regulatory Molecules
B lymphocytes may be divided into distinct subpopulations which differ from one another in the membrane antigens they express, in the immunogens to which they respond, and in their sensitivity to distinct regulatory mechanisms. The appreciation that such subpopulations exist is based, to a very large extent, on studies of mice which have an immunologic defect determined by the xid gene. This X chromosome gene, when present in the hemizygous or homozygous state, leads to a series of B lymphocyte abnormalities among which are unresponsiveness to soluble polysaccharides and other type 2 antigens,1 depressed serum IgM and IgG3 concentrations,2 and failure of B lymphocytes to proliferate upon stimulation with anti-immunoglobulin (Ig) antibodies.3 Mice with the xid defect lack B lymphocytes which bear the Lyb3,4 Lyb5,5 Lyb7,6 and Ia.W397 antigens. These lymphocytes, which are found in all normal strains, will be referred to as Lyb5+ B lymphocytes. The defects of xid-mice can be accounted for by the absence of Lyb5+ B cells.
KeywordsMycosis Fungoides Tritiated Thymidine Thymidine Uptake Distinct Regulatory Mechanism Cell Density Condition
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