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Nuclear factor of activated T cells (NFAT) 2 null mutant mice die  in utero  of cardiac failure, precluding analysis of the role of NFAT2 in lymphocyte responses. Only the NFAT2 −/− /Rag-1 −/−  chimeric mice model gave insight into the role of NFAT2 transcription factor in T lymphocyte development, activation, and differentiation. As reports are mainly focused on the role of NFAT2 in CD4 +  T lymphocytes activation and differentiation, we decided to investigate NFAT2’s impact on CD8 +  T lymphocyte responses. We report that NFAT2 is phosphorylated and inactive in the cytoplasm of naive CD8 +  T cells, and upon TCR stimulation, it is dephosphorylated and translocated into the nucleus. To study the role of NFAT2 in CD8 +  T responses, we employed NFAT2 fl/fl CD4-Cre mice with NFAT2 deletion specifically in T cells. Interestingly, the absence of NFAT2 in T cells resulted in increased percentage of non-conventional innate-like CD8 +  T cells. These cells were CD122 + , rapid producer of interferon gamma (IFN-γ) and had characteristics of conventional memory CD8 +  T cells. We also observed an expansion of PLZF +  expressing CD3 +  thymocyte population in the absence of NFAT2 and increased IL-4 production. Furthermore, we found that CD8 +  T lymphocytes deficient in NFAT2 had reduced activation, proliferation, and IFN-γ and IL-2 production at suboptimal TCR strength. NFAT2 absence did not significantly influence differentiation of CD8 +  T cells into cytotoxic effector cells but reduced their IFN-γ production. This work documents NFAT2 as a negative regulator of innate-like CD8 +  T cells development. NFAT2 is required for complete CD8 +  T cell responses at suboptimal TCR stimulation and regulates IFN-γ production by cytotoxic CD8 +  T cells  in vitro .

NFAT2 Regulates Generation of Innate-Like CD8+ T Lymphocytes and CD8+ T Lymphocytes Responses