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In Vivo Treatment of Class II MHC-Deficient Mice with Anti-TCR Antibody Restores the Generation of Circulating CD4 T Cells and Optimal Architecture of Thymic Medulla ¹

Mariam Nasreen^*, Tomoo Ueno, Fumi Saito and Yousuke Takahama^2,*,

^* Division of Experimental Immunology, Institute for Genome Research, University of Tokushima, and Laboratory of Immune System Development, The Institute of Physical and Chemical Research (RIKEN), Research Center for Allergy and Immunology, Tokushima, Japan

TCR ligation by the self-peptide-associated MHC molecules is essential for T cell development in the thymus, so that class II MHC-deficient mice do not generate CD4⁺CD8^- T cells. The present results show that the administration of anti-TCR mAb into class II MHC-deficient mice restores the generation of CD4⁺CD8^- T cells in vivo. The CD4 T cells were recovered in the thymus, peripheral blood, and the spleen, indicating that the anti-TCR treatment is sufficient for peripheral supply of newly generated CD4 T cells. Unlike peripheral CD4 T cells that disappeared within 5 wk after the treatment, CD4⁺CD8^- thymocytes remained undiminished even after 5 wk, suggesting that CD4 T cells in the thymus are maintained separately from circulating CD4 T cells and even without class II MHC molecules. It was also found that the mass of medullary region in the thymus, which was reduced in class II MHC-deficient mice, was restored by the anti-TCR administration, suggesting that the medulla for CD4⁺CD8^- thymocytes is formed independently of the medulla for CD4^-CD8⁺ thymocytes. These results indicate that in vivo anti-TCR treatment in class II MHC-deficient mice restores the generation of circulating CD4 T cells and optimal formation of the medulla in the thymus, suggesting that anti-TCR Ab may be useful for clinical treatment of class II MHC deficiencies.

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