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 Blood, 15 April 2007, Vol. 109, No. 8, pp. 3360-3368.
Prepublished online as a Blood First Edition Paper on December 7, 2006; DOI 10.1182/blood-2006-07-033662.

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IMMUNOBIOLOGY

Vav proteins control MyD88-dependent oxidative burst

Ana V. Miletic1, Daniel B. Graham1, Vivianne Montgrain1, Keiko Fujikawa2, Tracie Kloeppel1, Karry Brim1, Brian Weaver1, Robert Schreiber1, Ramnik Xavier3, and Wojciech Swat1

1 Department of Pathology and Immunology, Washington University School of Medicine and Siteman Cancer Center, St Louis, MO; 2 Department of Biochemistry, Hokkaido University School of Medicine, Sapporo, Japan; 3 Department of Medicine, Massachusetts General Hospital, Boston, MA

The importance of reactive oxygen intermediate (ROI) production in antimicrobial responses is demonstrated in human patients who suffer from chronic granulomatous disease (CGD) due to defective NADPH oxidase function. Exactly how bacterial products activating Toll-like receptors (TLRs) induce oxidative burst is unknown. Here, we identify the Vav family of Rho guanine nucleotide exchange factors (GEFs) as critical mediators of LPS-induced MyD88-dependent activation of Rac2, NADPH oxidase, and ROI production using mice deficient in Vav1, Vav2, and Vav3. Vav proteins are also required for p38 MAPK activation and for normal regulation of proinflammatory cytokine production, but not for other MyD88-controlled effector pathways such as those involving JNK, COX2, or iNOS and the production of reactive nitrogen intermediates (RNIs). Thus, our data indicate that Vav specifically transduces a subset of signals emanating from MyD88.


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