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The T Cell-Dependent B Cell Immune Response and Germinal Center Reaction Are Intact in A-myb-Deficient Mice¹

Kalpit A. Vora^2,*, Vicky M. Lentz^*, William Monsell^*, Sambasiva P. Rao^*, Richard Mettus, Antonio Toscani, E. Premkumar Reddy and Tim Manser^3,*

^* Kimmel Cancer Center and Department of Microbiology and Immunology, Jefferson Medical College, Philadelphia, PA 19107; and Fels Institute for Cancer Research and Department of Biochemistry, Temple University Medical School, Philadelphia, PA 19140

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 analysis of A-myb-deficient mice, which display behavioral abnormalities, male sterility, and perturbed breast development during pregnancy. In contrast, here we show that the germinal center response driven by T cell-dependent Ag immunization and the associated processes of Ab V gene somatic hypermutation, affinity maturation, and heavy chain class switching are overtly normal in A-myb-deficient mice. Nonetheless, these mice display mild splenic white pulp hypoplasia and blunted primary serum Ab responses, suggesting that although 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 proliferative capacity.

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				K. A. Vora, L. C. Wang, S. P. Rao, Z.-Y. Liu, G. R. Majeau, A. H. Cutler, P. S. Hochman, M. L. Scott, and S. L. Kalled Cutting Edge: Germinal Centers Formed in the Absence of B Cell-Activating Factor Belonging to the TNF Family Exhibit Impaired Maturation and Function J. Immunol., July 15, 2003; 171(2): 547 - 551. [Abstract] [Full Text] [PDF]