AI Article Synopsis
- Researchers created mice that lack the TGF-beta receptor specifically in B cells to study its function.
- The results showed that these mice had shorter lifespans for conventional B cells, increased numbers of B-1 cells, and higher serum immunoglobulin levels.
- The findings indicate that TGF-beta plays a key role in regulating B cell responses and suggests it is essential for the production of IgA antibodies in the body.
Article Abstract
To determine the role of the pleiotropic cytokine TGF-beta in B cells, we generated mice lacking the TGF-beta receptor (TbetaR) type II selectively in this cell type through conditional mutagenesis (Cre/loxP). The absence of TbetaRII in B cells leads to a reduced life span of conventional B cells, expansion of peritoneal B-1 cells, B cell hyperplasia in Peyer's patches, elevated serum immunoglobulin, and substantial IgG3 responses to a normally weak immunogen. This B cell hyperresponsiveness is associated with a virtually complete serum IgA deficiency. The data reveal differential roles of TbetaR in homeostasis and antigen responsiveness of B cell subpopulations and establish a critical function of the TGF-beta receptor ligand pair in the induction of IgA responses in vivo.
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| http://dx.doi.org/10.1016/s1074-7613(00)00044-3 | DOI Listing |
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