The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/11/1343/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 9, November 1, 1999 1343-1350

Original Article

Suppression of T and B Lymphocyte Activation by a Yersinia pseudotuberculosis Virulence Factor, Yoph

Tony Yaoa, Joan Mecsasb, James I. Healya, Stanley Falkowb, and Yueh-hsiu Chiena,b

a Program in Immunology, Stanford University, Stanford, California 94305
b Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
Department of Microbiology and Immunology, Fairchild Bldg. D333, Stanford University, Stanford, CA 94305.650-725-6757650-723-1078

chien{at}leland.stanford.edu

The acquired immune responses are crucial to the survival of Yersinia-infected animals. Mice lacking T cells are sensitive to Yersinia infection, and a humoral response to Yersinia can be protective. Diverse mechanisms for Yersinia to impair and evade the host innate immune defense have been suggested, but the effects of Yersinia on lymphocytes are not known. Here, we demonstrate that after a transient exposure to Y. pseudotuberculosis, T and B cells are impaired in their ability to be activated through their antigen receptors. T cells are inhibited in their ability to produce cytokines, and B cells are unable to upregulate surface expression of the costimulatory molecule, B7.2, in response to antigenic stimulation. The block of lymphocyte activation results from the inhibition of early phosphorylation events of the antigen receptor signaling complex. Through the use of Y. pseudotuberculosis mutants, we show that the inhibitory effect in both T cells and B cells is dependent on the production of Yersinia outermembrane protein (Yop) H, a tyrosine phosphatase. Our results suggest a mechanism by which the pathogenic bacteria may modulate a wide range of T and B cell–mediated immune responses.

Key Words: T cell • B cell • Yersinia pseudotuberculosis • bacterial pathogenesis • YopH

Abbreviations used in this paper: BCR, B cell antigen receptor; FA, focal adhesion; HEL, hen egg lysozyme; MCC, moth cytochrome c; MOI, multiplicity of infection; Yop, Yersinia outermembrane protein.

J. Mecsas and J.I. Healy contributed equally to this work.

© 1999 The Rockefeller University Press


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