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 Blood, 1 October 2005, Vol. 106, No. 7, pp. 2391-2398.
Prepublished online as a Blood First Edition Paper on June 7, 2005; DOI 10.1182/blood-2004-12-4894.

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IMMUNOBIOLOGY

Vav proteins regulate peripheral B-cell survival

Elena Vigorito, Laure Gambardella, Francesco Colucci, Simon McAdam, and Martin Turner

From the Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge United Kingdom.

Mice lacking all 3 Vav proteins fail to produce significant numbers of recirculating follicular or marginal zone B cells. Those B cells that do mature have shortened lifespans. The constitutive nuclear factor-kappaB (NF-{kappa}B) activity of resting naive B cells required Vav function and expression of cellular reticuloendotheliosis (c-Rel). Rel-A was reduced in Vav-deficient B cells. Furthermore, expression of the NF-{kappa}B-regulated antiapoptotic genes A1 and Bcl-2 was reduced in mature Vav-deficient B cells. Overexpression of Bcl-2 restored the number of mature follicular B cells in the spleens of Vav-deficient mice. When activated by B-cell receptor (BCR) cross-linking, Vav-deficient B cells failed to activate NF-{kappa}B. Vav proteins thus regulate an NF-{kappa}B-dependent survival signal in naive B cells and are required for NF-{kappa}B function after BCR cross-linking.


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