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B cell receptor signal strength determines B cell fate

Stefano Casola1, Kevin L Otipoby, Marat Alimzhanov

  • 1CBR Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115, USA. casola@cbr.med.harvard.edu

Nature Immunology
|February 6, 2004
PubMed

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.

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