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pubmed:abstractText |
Although found predominantly in the peritoneal and pleural cavities, B-1 cells are also present in other peripheral tissues such as spleen and lung. While similar in surface phenotypes, such as CD5, all B-1 cells are not equivalent in their response to stimuli. Here, we report that the src family kinase Lck is required to confer the BCR hyporesponsiveness typical of CD5+ B-1 cells and appears involved in the maintenance of their unique function. Splenic B-1 cells express CD5 but not Lck and are not hyporesponsive; however, within the peritoneum, these B-1 cells are induced to express Lck and acquire a hyporesponsive phenotype. Peritoneal B-1 cells from lck-deficient mice, while CD5+, no longer exhibit attenuated BCR signaling. Interestingly, lck-null mice exhibited increased natural antibody levels characteristic of B-1 cells. Taken together, these results demonstrate a key role for Lck in modulating the signaling and cellular fate of B-1 B cells.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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