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The CD19/CD81 complex physically interacts with CD38 but is not required to induce proliferation in mouse B lymphocytes
Author(s) -
VencesCatalán Felipe,
Rajapaksa Ranjani,
Levy Shoshana,
SantosArgumedo Leopoldo
Publication year - 2012
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2012.03602.x
Subject(s) - cd19 , cd38 , microbiology and biotechnology , biology , receptor , b cell receptor , b cell , antibody , flow cytometry , immunology , biochemistry , stem cell , cd34
Summary 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.

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