Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication




Journal article


Journal of immunology (Baltimore, Md. : 1950)

Publication Date





2824 - 2829


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


CD4-Positive T-Lymphocytes, Th1 Cells, Animals, Mice, Knockout, Mice, Salmonella typhimurium, Salmonella Infections, Animal, Lymphopenia, Signal Transduction, Cell Survival, Lymphocyte Cooperation, Immunity, Cellular, Homeostasis, Receptors, OX40, Ki-1 Antigen