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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Autoreactive T cells escape clonal deletion in the thymus by a CD24-dependent pathway.

Despite negative selection in the thymus, significant numbers of autoreactive T cells still escape to the periphery and cause autoimmune diseases when immune regulation goes awry. It is largely unknown how these T cells escape clonal deletion. In this study, we report that CD24 deficiency caused deletion of autoreactive T cells that normally escape negative selection. Restoration of CD24 expression on T cells alone did not prevent autoreactive T cells from deletion; bone marrow chimera experiments suggest that CD24 on radio-resistant stromal cells is necessary for preventing deletion of autoreactive T cells. CD24 deficiency abrogated the development of experimental autoimmune encephalomyelitis in transgenic mice with a TCR specific for a pathogenic autoantigen. The role of CD24 in negative selection provides a novel explanation for its control of genetic susceptibility to autoimmune diseases in mice and humans.[1]

References

  1. Autoreactive T cells escape clonal deletion in the thymus by a CD24-dependent pathway. Carl, J.W., Liu, J.Q., Joshi, P.S., El-Omrani, H.Y., Yin, L., Zheng, X., Whitacre, C.C., Liu, Y., Bai, X.F. J. Immunol. (2008) [Pubmed]
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