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Quantitative impact of thymic selection on Foxp3 + and Foxp3 − subsets of self-peptide/MHC class II-specific CD4 + T cells
James J. Moon, Pradyot Dash, Thomas H. Oguin III, Jennifer L. McClaren, H. Hamlet Chu, Paul G. Thomas and Marc K. Jenkins
Proceedings of the National Academy of Sciences of the United States of America
Vol. 108, No. 35 (August 30, 2011), pp. 14602-14607
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/27979338
Page Count: 6
You can always find the topics here!Topics: T cell antigen receptors, T lymphocytes, Antigens, Mice, Lymph nodes, Autoantigens, Immunity, Ligands, Transgenic animals, Receptors
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It is currently thought that T cells with specificity for self-peptide/MHC (pMHC) ligands are deleted during thymic development, thereby preventing autoimmunity. In the case of CD4+ T cells, what is unclear is the extent to which self-peptide/MHC class II (pMHCII)-specific T cells are deleted or become Foxp3+ regulatory T cells. We addressed this issue by characterizing a natural polyclonal pMHCII-specific CD4+ T-cell population in mice that either lacked or expressed the relevant antigen in a ubiquitous pattern. Mice expressing the antigen contained one-third the number of pMHCII-specific T cells as mice lacking the antigen, and the remaining cells exhibited low TCR avidity. In mice lacking the antigen, the pMHCII-specific T-cell population was dominated by phenotypically naive Foxp3− cells, but also contained a subset of Foxp3+ regulatory cells. Both Foxp3− and Foxp3+ pMHCII-specific T-cell numbers were reduced in mice expressing the antigen, but the Foxp3+ subset was more resistant to changes in number and TCR repertoire. Therefore, thymic selection of self-pMHCII–specific CD4+ T cells results in incomplete deletion within the normal polyclonal repertoire, especially among regulatory T cells.
Proceedings of the National Academy of Sciences of the United States of America © 2011 National Academy of Sciences