Cutting Edge: Regulation of TLR4-Driven B Cell Proliferation by RP105 Is Not B Cell Autonomous-Reference-Cited by-同舟云学术

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Cutting Edge: Regulation of TLR4-Driven B Cell Proliferation by RP105 Is Not B Cell Autonomous

Published:2012-01-30 Issue:5 Volume:188 Page:2065-2069
ISSN:0022-1767
Container-title:The Journal of Immunology
language:en
Short-container-title:J.I.

Author:

Allen Jessica L.,Flick Leah M.,Divanovic Senad,Jackson Shaun W.,Bram Richard,Rawlings David J.,Finkelman Fred D.,Karp Christopher L.

Publisher

The American Association of Immunologists

Subject

Immunology,Immunology and Allergy

Reference18 articles.

1. Murine B cell proliferation and protection from apoptosis with an antibody against a 105-kD molecule: unresponsiveness of X-linked immunodeficient B cells.

2. Activation mediated by RP105 but not CD40 makes normal B cells susceptible to anti-IgM-induced apoptosis: a role for Fc receptor coligation.

3. The Molecular Mechanism of B Cell Activation by toll-like Receptor Protein RP-105

4. CD19 regulates innate immunity by the toll-like receptor RP105 signaling in B lymphocytes

5. Vav proteins are required for B-lymphocyte responses to LPS

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