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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

B cell receptor signal strength determines B cell fate.

B cell receptor (BCR)-mediated antigen recognition is thought to regulate B cell differentiation. BCR signal strength may also influence B cell fate decisions. Here, we used the Epstein-Barr virus protein LMP2A as a constitutively active BCR surrogate to study the contribution of BCR signal strength in B cell differentiation. Mice carrying a targeted replacement of Igh by LMP2A leading to high or low expression of the LMP2A protein developed B-1 or follicular and marginal zone B cells, respectively. These data indicate that BCR signal strength, rather than antigen specificity, determines mature B cell fate. Furthermore, spontaneous germinal centers developed in gut-associated lymphoid tissue of LMP2A mice, indicating that microbial antigens can promote germinal centers independently of BCR-mediated antigen recognition.[1]


  1. B cell receptor signal strength determines B cell fate. Casola, S., Otipoby, K.L., Alimzhanov, M., Humme, S., Uyttersprot, N., Kutok, J.L., Carroll, M.C., Rajewsky, K. Nat. Immunol. (2004) [Pubmed]
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