The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/12/2057/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 12, December 15, 1997 2057-2062

Brief Definitive Reports

CD4+ T Cell Help Impairs CD8+ T Cell Deletion Induced by Cross-presentation of Self-Antigens and Favors Autoimmunity

Christian Kurts*, Francis R. Carbone{ddagger}, Megan Barnden{ddagger}, Effrossini Blanas*, Janette Allison*, William R. Heath*, and Jacques F.A.P. Miller*

From the * Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Victoria 3050; and {ddagger} The Department of Pathology and Immunology, Monash Medical School, Prahran 3181, Victoria, Australia

Self-antigens expressed in extrathymic tissues such as the pancreas can be transported to draining lymph nodes and presented in a class I–restricted manner by bone marrow-derived antigen-presenting cells. Such cross-presentation of self-antigens leads to CD8+ T cell tolerance induction via deletion. In this report, we investigate the influence of CD4+ T cell help on this process. Small numbers of autoreactive OVA-specific CD8+ T cells were unable to cause diabetes when adoptively transferred into mice expressing ovalbumin in the pancreatic β cells. Coinjection of OVA-specific CD4+ helper T cells, however, led to diabetes in a large proportion of mice (68%), suggesting that provision of help favored induction of autoimmunity. Analysis of the fate of CD8+ T cells indicated that CD4+ T cell help impaired their deletion. These data indicate that control of such help is critical for the maintenance of CD8+ T cell tolerance induced by cross-presentation.

Address correspondence to William R. Heath, Immunology Division, The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Victoria 3050, Australia. Phone: 61-3-9345-2482; FAX: 61-3-9347-0852; E-Mail: heath{at}wehi.edu.au

C. Kurts is supported by a Deutsche Forschungsgemeinschaft fellowship (grant Ku1063/1-2). This work was funded by National Institutes of Health grant AI-29385 and grants from the National Health and Medical Research Council of Australia and the Australian Research Council.


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