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

First Author  Vora KA Year  2001
Journal  J Immunol Volume  166
Issue  5 Pages  3226-30
PubMed ID  11207276 Mgi Jnum  J:67604
Mgi Id  MGI:1930904 Doi  10.4049/jimmunol.166.5.3226
Citation  Vora KA, et al. (2001) The t cell-dependent b cell immune response and germinal center reaction are intact in a-myb-deficient mice. J Immunol 166(5):3226-30
abstractText  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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