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Invariant NKT (iNKT) cells can prevent diabetes by inhibiting the differentiation of anti-islet T cells. We recently showed that neither iNKT cell protection against diabetes nor iNKT cell inhibition of T cell differentiation in vitro requires cytokines such as IL-4, IL-10, IL-13, and TGF-beta. In contrast, cell-cell contacts were required for iNKT cell inhibition of T cell differentiation in vitro. The present study was designed to determine whether the CD1d molecule is involved in the inhibitory function of iNKT cells. Experiments were performed in vitro and in vivo, using cells lacking CD1d expression. The in vivo experiments used CD1d-deficient mice that were either reconstituted with iNKT cells or expressed a CD1d transgene exclusively in the thymus. Both mouse models had functional iNKT cells in the periphery, even though CD1d was not expressed in peripheral tissues. Surprisingly, both in vitro inhibition of T cell differentiation by iNKT cells and mouse protection against diabetes by iNKT cells were CD1d-independent. These results reveal that iNKT cells can exert critical immunoregulatory effects in the absence of CD1d recognition and that different molecular interactions are involved in iNKT cell functions.

Original publication

DOI

10.4049/jimmunol.178.3.1332

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

02/2007

Volume

178

Pages

1332 - 1340

Addresses

Institut National de la Santé et de la Recherche Médicale Unité 561, University René Descartes Hôpital Cochin-Saint Vincent de Paul, Paris, France.

Keywords

Islets of Langerhans, Thymus Gland, Killer Cells, Natural, T-Lymphocytes, Animals, Mice, Knockout, Mice, Diabetes Mellitus, Type 1, Antigens, CD1, Cell Differentiation, Transgenes, Antigens, CD1d