The Journal of Experimental Medicine
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*Diabetes Type 1
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© The Rockefeller University Press, 0022-1007/1996/12/2393/ $5.00
The Journal of Experimental Medicine, Volume 184, Number 6, December 1, 1996 2393-2398

Brief Definitive Reports

The Thymus Contains a High Frequency of Cells that Prevent Autoimmune Diabetes on Transfer into Prediabetic Recipients

Abdelhadi Saoudi{ddagger}, Benedict Seddon*, Debbie Fowell§, and Don Mason*

From the * Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE United Kingdom; {ddagger} Institute National de la Santé et de la Recherche Médicale U28, Hôpital Purpan, 31059, Toulouse, France; and § Infectious Disease Division, University of California, San Francisco, California 94143-0654

Rats of the PVG.RT1u strain develop autoimmune diabetes when thymectomized at 6 wk of age and are rendered relatively lymphopenic by a cumulative dose of 1,000 rads 137Cs {gamma}-irradiation given in four split doses. Previous studies have shown that the disease is prevented by the intravenous injection of 5 x 106 CD4+ CD45RC– TCR{alpha}β+ RT6+ peripheral T cells from normal syngeneic donors. These cells have a memory phenotype and are presumably primed to some extrathymic antigen. However, we now report that the CD4+ CD8– population of mature thymocytes is a very potent source of cells, with the capacity to prevent diabetes in our lymphopenic animals. As few as 6 x 105 of these cells protect ~50% of recipients and the level of protection increases with cell dose. It appears that one characteristic of the intrathymic selection of the T cell repertoire is the generation of cells that regulate the autoimmune potential of peripheral T cells that have been neither clonally deleted intrathymically nor rendered irreversibly anergic in the periphery.

Address correspondence to Ben Seddon, MRC Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.

A. Saoudi is supported by a postdoctoral fellowship from the Wellcome Trust and from the Fondation pour la Recherche Medicale of France. B. Seddon is supported by a Wellcome Trust Prize Studentship.

A. Saoudi and B. Seddon contributed equally to this work.


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