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Blood, 15 July 2005, Vol. 106, No. 2, pp. 635-640. Prepublished online as a Blood First Edition Paper on April 5, 2005; DOI 10.1182/blood-2004-10-3919. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-3919v1 106/2/635    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hebeis, B. Articles by Turner, M. Search for Related Content PubMed PubMed Citation Articles by Hebeis, B. Articles by Turner, M. Related Collections Immunobiology Signal Transduction Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Vav proteins are required for B-lymphocyte responses to LPS Barbara Hebeis, Elena Vigorito, Dorottya Kovesdi, and Martin Turner From the Laboratory of Lymphocyte Signaling and Development, The Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom. B lymphocytes respond to bacterial lipopolysaccharide (LPS) through Toll-like receptor 4 (TLR4) and CD180 (previously called RP105). We show here that the responses of B lymphocytes to LPS require the function of the Vav family of guanine nucleotide exchange factors. Vav1-mutant mice generate defective humoral immunoglobulin G (IgG) responses following administration of low doses of LPS but respond normally to higher doses, while mice lacking both Vav1 and Vav2 manifest defective responses even after a high dose of LPS. Vav1/2-mutant B cells fail to divide extensively in vitro in response to LPS or CD180, while deficiency of Vav1 alone impairs CD180-but not LPS-driven proliferation. Likewise, activation of Akt (a PI3K [phosphatidylinositol 3-kinase] target) and phosphorylation of IB in response to CD180 or LPS required Vav1 and Vav2, while Vav1 deficiency led to defective responses to CD180. In addition, activation of ERK (extracellular signal regulated kinase) required Vav1 and Vav2 in response to CD180 but was Vav1 and vav2 independent in response to LPS. Induction of CD86 and CD25 by anti-CD180 also required Vav function, as did the induction of the antiapoptotic protein Bcl-xL (B-cell leukemia XL). These data provide evidence for the function for the Vav proteins in regulating the responses of B cells to LPS. (Blood. 2005;106:635-640) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Vav: a newcomer in innate receptor signaling Tomohiro Kurosaki Blood 2005 106: 389-390. [Full Text] [PDF] This article has been cited by other articles: O. Shibolet, C. Giallourakis, I. Rosenberg, T. Mueller, R. J. Xavier, and D. K. Podolsky AKAP13, a RhoA GTPase-specific Guanine Exchange Factor, Is a Novel Regulator of TLR2 Signaling J. Biol. Chem., November 30, 2007; 282(48): 35308 - 35317. [Abstract] [Full Text] [PDF] L. M. Stephenson, A. V. Miletic, T. Kloeppel, S. Kusin, and W. Swat Vav Proteins Regulate the Plasma Cell Program and Secretory Ig Production J. Immunol., December 15, 2006; 177(12): 8620 - 8625. [Abstract] [Full Text] [PDF] A. Utomo, X. Cullere, M. Glogauer, W. Swat, and T. N. Mayadas Vav Proteins in Neutrophils Are Required for Fc{gamma}R-Mediated Signaling to Rac GTPases and Nicotinamide Adenine Dinucleotide Phosphate Oxidase Component p40(phox) J. Immunol., November 1, 2006; 177(9): 6388 - 6397. [Abstract] [Full Text] [PDF]

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