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Cutting Edge: The Idd3 Genetic Interval Determines Regulatory T Cell Function through CD11b⁺CD11c^– APC¹

Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115

The Idd3 genetic interval confers protection against multiple autoimmune diseases, including type 1 diabetes and experimental autoimmune encephalomyelitis. The favored candidate gene in this interval is Il2, which is polymorphic between susceptible and resistant strains of mice. IL-2 regulates the growth/death of effector T cells as well as the generation/maintenance of regulatory T cells (Tregs), and recent studies have shown that NOD.Idd3 Tregs are more suppressive than their NOD counterparts. We have further dissected the mechanisms underlying the differential suppression by NOD and NOD.Idd3 Tregs and find that it is determined by CD11b⁺CD11c^– APCs. Thus, contrary to what might be expected, our data suggest that the differential suppressive activity of NOD and NOD.Idd3 Tregs is not due to an effect of the Idd3 genetic interval on T cells but rather is due to differences in the APC compartment.

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 National Institutes of Health Grants NS054096 (to A.C.A.) and AI044880 and NS038037 (to V.K.K.). V.K.K. is a recipient of the Javits Neuroscience Investigator Award from National Institutes of Health (NS30843).

² Address correspondence and reprint requests to Dr. Vijay K. Kuchroo or Dr. Ana C. Anderson, Center for Neurologic Diseases, 77 Avenue Louis Pasteur, Harvard Institutes of Medicine, Room 786, Boston, MA 02115. E-mail addresses: vkuchroo{at}rics.bwh.harvard.edu and aanderson{at}rics.bwh.harvard.edu

³ Abbreviations used in this paper: Treg, regulatory T cell; DC, dendritic cell.

⁴ The online version of this article contains supplemental material.

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