| First Author | Vences-Catalán F | Year | 2012 |
| Journal | Immunology | Volume | 137 |
| Issue | 1 | Pages | 48-55 |
| PubMed ID | 22564057 | Mgi Jnum | J:189435 |
| Mgi Id | MGI:5445814 | Doi | 10.1111/j.1365-2567.2012.03602.x |
| Citation | Vences-Catalan F, et al. (2012) The CD19/CD81 complex physically interacts with CD38 but is not required to induce proliferation in mouse B lymphocytes. Immunology 137(1):48-55 |
| abstractText | In B lymphocytes, the cell surface receptor CD38 is involved in apoptosis of immature B cells, proliferation and differentiation of mature B cells. Although CD38 has been establish as a receptor, its signaling has been only partially characterized. As a result of the lack of signaling motifs in the cytoplasmic domain, CD38 must use a co-receptor to induce signaling within the cell. Accordingly, CD38 has been associated with different receptors such as the T-cell receptor/CD3 complex on T cells, CD16 on natural killer cells and MHC class II molecules on monocytes. The CD19/CD81 complex has been proposed as a co-receptor for CD38 in human B lymphocytes, but little or no characterization has been performed in mice. In this study the contribution of the CD19/CD81 complex in murine CD38 signaling was evaluated. Proliferation assays were performed using CD19(-/-) or CD81(-/-) deficient mice; CFSE-labeled B lymphocytes from wild-type mice and CD19(-/-) , CD81(-/-) and CD38(-/-) deficient mice were stimulated with agonistic antibodies against CD38. Immunoprecipitation and immunofluorescence were also performed to detect protein-protein interactions. Our results indicate that the CD19/CD81 complex interacts with CD38 but this interaction is not required to induce proliferation in mouse B lymphocytes, suggesting that other receptors may contribute to the proliferation induced by CD38 in B lymphocytes. |
