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Abstract
Previous studies have demonstrated that E proteins induce activation-induced deaminase (AID) expression in activated B cells. Here, we examined the role of Id3 in germinal center (GC) cells. We found that Id3 expression is high in follicular B lineage cells but declines in GC cells. Immunized mice with Id3 expression depleted displayed a block in germinal center B cell maturation, showed reduced numbers of marginal zone B cells and class-switched cells, and were associated with decreased antibody titers and lower numbers of plasma cells. In vitro, Id3-depleted B cells displayed a defect in class switch recombination. Whereas AID levels were not altered in Id3-depleted activated B cells, the expression of a subset of genes encoding signaling components of antigen receptor-, cytokine receptor-, and chemokine receptor-mediated signaling was significantly impaired. We propose that during the GC reaction, Id3 levels decline to activate the expression of genes encoding signaling components that mediate B cell receptor- and or cytokine receptor-mediated signaling to promote the differentiation of GC B cells.
Supplemental material for this article may be found at http://dx.doi.org/10.1128/MCB.00150-16.
ACKNOWLEDGMENTS
We thank members of the Murre laboratory for thoughtful discussion. We thank Yuan Zhuang for the kind gift of Id3f/f and Robert Rickert for CD19-Cre mice.
This study was supported by funding to the CCBB from a CTRI grant (UL1TR001442) and by grants from the NIH to C.M. (AI00880, AI09599, and AI102853).