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Critical Synergy of CD30 and OX40 Signals in CD4 T Cell Homeostasis and Th1 Immunity to Salmonella¹

Medical Research Council Centre for Immune Regulation, Division of Immunity and Infection, University of Birmingham, Birmingham, United Kingdom

CD30 and OX40 (CD134) are members of the TNFR superfamily expressed on activated CD4 T cells, and mice deficient in both these molecules harbor a striking defect in the capacity to mount CD4 T cell-dependent memory Ab responses. This article shows that these mice also fail to control Salmonella infection because both CD30 and OX40 signals are required for the survival but not commitment of CD4 Th1 cells. These signals are also needed for the survival of CD4 T cells activated in a lymphopenic environment. Finally, Salmonella and lymphopenia are shown to act synergistically in selectively depleting CD4 T cells deficient in OX40 and CD30. Collectively these findings identify a novel mechanism by which Th1 responses are sustained.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by programme grants from The Wellcome Trust and The U.K. Medical Research Council.

² Address correspondence and reprint requests to Dr. Adam F. Cunningham or Dr. Peter J. Lane, Institute of Biomedical Research, University of Birmingham Medical School, Room 432, Birmingham B15 2TT, U.K. E-mail addresses: a.f.cunningham{at}bham.ac.uk or p.j.l.lane{at}bham.ac.uk

³ Abbreviations used in this paper: _c, -chain; DKO, double knockout; LTI, lymphoid tissue inducer cell; LN, lymph node; WT, wild type.

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