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

Christian Kurts(Walter and Eliza Hall Institute of Medical Research), Federico Carbone(Walter and Eliza Hall Institute of Medical Research), Megan Barnden(Walter and Eliza Hall Institute of Medical Research), Effrossini Blanas(Walter and Eliza Hall Institute of Medical Research), Janette Allison(Walter and Eliza Hall Institute of Medical Research), William R. Heath(Walter and Eliza Hall Institute of Medical Research), Jacques F.A.P. Miller(Walter and Eliza Hall Institute of Medical Research)
The Journal of Experimental Medicine
December 15, 1997
Cited by 316Open Access
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Abstract

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 beta 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.


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