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J Immunol. 2013 Jan 15;190(2):578-85. doi: 10.4049/jimmunol.1103794. Epub 2012 Dec 19.

Induction of rapid T cell death and phagocytic activity by Fas-deficient lpr macrophages.

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  • 1Department of Oral Molecular Pathology, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima 770-8504, Japan.


Peripheral T cells are maintained by the apoptosis of activated T cells through the Fas-Fas ligand system. Although it is well known that normal T cells fail to survive in the Fas-deficient immune condition, the molecular mechanism for the phenomenon has yet to be elucidated. In this study, we demonstrate that rapid cell death and clearance of normal T cells were induced by Fas-deficient lpr macrophages. Transfer of normal T cells into lpr mice revealed that Fas expression on donor T cells was promptly enhanced through the IFN-γ/IFN-γR. In addition, Fas ligand expression and phagocytic activity of lpr macrophages were promoted through increased NF-κB activation. Controlling Fas expression on macrophages plays an essential role in maintaining T cell homeostasis in the peripheral immune system. Our data suggest a critical implication to the therapeutic strategies such as transplantation and immunotherapy for immune disorder or autoimmunity related to abnormal Fas expression.

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