The T cell-dependent B cell immune response and germinal center reaction are intact in A-myb-deficient mice

Expression of the protooncogene A-myb is restricted to the developing CNS, adult testes, breasts in late pregnancy, and germinal centers of secondary B cell follicles, The functional relevance of A-myb expression at three of these sites has been demonstrated previously via the generation and analysi s of A-myb-deficient mice, which display behavioral abnormalities, male ste rility, and perturbed breast development during pregnancy, In contrast, her e we show that the germinal center response driven by T cell-dependent Ag i mmunization and the associated processes of Ab V gene somatic hypermutation , affinity maturation, and heavy chain class switching are overtly normal i n A-myb-deficient mice. Nonetheless, these mice display mild splenic white pulp hypoplasia and blunted primary serum Ab responses, suggesting that alt hough A-myb is not directly involved in the regulation of the memory B cell response, it may play a role in enhancing peripheral B cell survival or pr oliferative capacity.