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Publication : Murine B cell development and antibody responses to model antigens are not impaired in the absence of the TNF receptor GITR.

First Author  Teodorovic LS Year  2012
Journal  PLoS One Volume  7
Issue  2 Pages  e31632
PubMed ID  22328941 Mgi Jnum  J:185329
Mgi Id  MGI:5428113 Doi  10.1371/journal.pone.0031632
Citation  Sinik Teodorovic L, et al. (2012) Murine B cell development and antibody responses to model antigens are not impaired in the absence of the TNF receptor GITR. PLoS One 7(2):e31632
abstractText  The Glucocorticoid-Induced Tumor necrosis factor Receptor GITR, a member of the tumor necrosis factor receptor superfamily, has been shown to be important in modulating immune responses in the context of T cell immunity. B lymphocytes also express GITR, but a role of GITR in humoral immunity has not been fully explored. To address this question, we performed studies to determine the kinetics of GITR expression on naive and stimulated B cells and the capacity of B cells to develop and mount antibody responses in GITR(-/-) mice. Results of our studies indicate that all mature B cells express GITR on the cell surface, albeit at different levels. Expression of GITR on naive mature B cells is upregulated by BCR signaling, but is counteracted by helper T cell-related factors and other inflammatory signals in vitro. In line with these findings, expression of GITR on germinal center and memory B cells is lower than that on naive B cells. However, the expression of GITR is strongly upregulated in plasma cells. Despite these differences in GITR expression, the absence of GITR has no effect on T cell-dependent and T cell-independent antibody responses to model antigens in GITR(-/-) mice, or on B cell activation and proliferation in vitro. GITR deficiency manifests only with a slight reduction of mature B cell numbers and increased turnover of naive B cells, suggesting that GITR slightly contributes to mature B cell homeostasis. Overall, our data indicate that GITR does not play a significant role in B cell development and antibody responses to T-dependent and independent model antigens within the context of a GITR-deficient genetic background.
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