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- W4313351353 abstract "Abstract T cells from tumor-bearing hosts have reduced NF-κB activity. Our previous results indicate that reduced NF-κB activation results in impaired T cell survival, decreased Th1 differentiation and increased iTreg differentiation. We hypothesized that forced activation of NF-κB in T cells should have the opposite effect, which would be beneficial for tumor rejection. We generated mice with constitutively active IKKβ in T cells (CA-IKKβ mice). T cell numbers were comparable to littermate controls, but CA-IKKβ mice had fewer Tregs and increased frequency of activated T cells that produced IFNγ and IL-4 upon re-stimulation. When B16-SIY melanoma cells were injected subcutaneously, tumors grew progressively in control littermates, but were rejected by CA-IKKβ mice. Tumor control was associated with a massive increase in the number of tumor-specific IFNγ-producing CD8+ T cells and IFNγ blockade restored tumor growth. CA-IKKβ+ CD8+ T cells were able to control tumor growth in the absence of CD4+ T cells. Interestingly, CA-IKKβ+ CD4+ T cell help was sufficient to induce tumor control by WT CD8+ T cells. Finally, enhanced tumor control was observed in immune-competent mice when fewer than 5% of T cells expressed CA-IKKβ. Our results suggest that NF-κB is at the cross-roads of major T cell fate decisions that uniquely synergize for control of tumor growth and identify a therapeutic pathway with potential clinical applicability." @default.
- W4313351353 created "2023-01-06" @default.
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- W4313351353 date "2013-05-01" @default.
- W4313351353 modified "2023-10-01" @default.
- W4313351353 title "Forcing NF-κB in T cells promotes tumor rejection (P2042)" @default.
- W4313351353 doi "https://doi.org/10.4049/jimmunol.190.supp.132.11" @default.
- W4313351353 hasPublicationYear "2013" @default.
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