Identification of a B-cell surface structure involved in antigen-dependent triggering: absence of this structure on B cells from CBA/N mutant mice.

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Abstract
CBA/N mice have an X-linked B[bone marrow-derived]cell maturation defect which is reflected in part in an absence or dysfunction of a subclass of mature B cells. The defective .male. offspring of the mating (CBA/N .female. .times. BALB/c .male.) were immunized with BALB/c spleen cells. The resulting antiserum (.alpha.[anti]Lyb3) selectively reacts with a component on the surface of a portion of B cells from a panel of H-2 different mouse strains. Binding of .alpha.Lyb3 serum to this B-cell subclass results in substantial (10 to 20-fold) enhancement of the antibody response to low doses of SRBC [sheep red blood cells]. Binding and enhancement activity are removed by absorption with B cells from B6 and BALB/c, but not CBA/N mice. Absorption of the serum with bone marrow cells, T [thymus-derived] cells or thymocytes from Lyb3+ strains does not remove activity. Since the enhanced plaque-forming cell (PFC) responses are specific for the immunizing antigen, and since no PFC response is produced by injection of the antiserum alone, this enhancement probably reflects a 2nd signal produced by specific interaction between antibody and the surface Lyb3 component. This signal can partially replace the requirement for T cells in the production of antibody to a thymus-dependent antigen. These findings suggest that Lyb3 is a cell surface component expressed selectively on a mature B-cell subclass. This component is important in B-cell triggering by antigen, and it fails to develop in CBA/N mice due to a dysfunction of a regulatory gene on the CBA/N X chromosome.