Abstract
CD72, a B cell surface protein of the C-type lectin superfamily, recruits the tyrosine phosphatase SHP-1 through its ITIM motif(s). Using CD72-deficient (CD72(-/-)) mice, we demonstrate that CD72 is a nonredundant regulator of B cell development. In the bone marrow of CD72(-/-) mice, there was a reduction in the number of mature recirculating B cells and an accumulation of pre-B cells. In the periphery of CD72(-/-) mice, there were fewer mature B-2 cells and more B-1 cells. In addition, CD72 is a negative regulator of B cell activation, as CD72(-/-) B cells were hyperproliferative in response to various stimuli and showed enhanced kinetics in their intracellular Ca2+ response following IgM cross-linking.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 495-506 |
| Number of pages | 12 |
| Journal | Immunity |
| Volume | 11 |
| Issue number | 4 |
| DOIs | |
| State | Published - Oct 1999 |
| Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases
- Immunology
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Pan, C., Baumgarth, N., & Parnes, J. R. (1999). CD72-deficient mice reveal nonredundant roles of CD72 in B cell development and activation. Immunity, 11(4), 495-506. https://doi.org/10.1016/S1074-7613(00)80124-7