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Overexpression of Bcl-2 Differentially Restores Development of Thymus-Derived CD4^-8⁺ T Cells and Intestinal Intraepithelial T Cells in IFN-Regulatory Factor-1-Deficient Mice¹

Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan

Mice lacking IFN-regulatory factor (IRF)-1 have reduced numbers of mature CD8⁺ T cells within the thymus and peripheral lymphoid organs, suggesting a critical role of IRF-1 in CD8⁺ T cell differentiation. Here we show that endogenous Bcl-2 expression is substantially reduced in IRF-1^-/-CD8⁺ thymocytes and that introduction of a human Bcl-2 transgene driven by Eµ or lck promoter in IRF-1^-/- mice restores the CD8⁺ T cell development. Restored CD8⁺ T cells are functionally mature in terms of allogeneic MLR and cytokine production. In contrast to thymus-derived CD8⁺ T cells, other lymphocyte subsets including NK, NK T, and TCR-⁺ intestinal intraepithelial lymphocytes, which are also impaired in IRF-1^-/- mice, are not rescued by expressing human Bcl-2. Our results indicate that IRF-1 differentially regulates the development of these lymphocyte subsets and that survival signals involving Bcl-2 are critical for the development of thymus-dependent CD8⁺ T cells.

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