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Review
. 2002 Nov;110(10):1407-9.
doi: 10.1172/JCI17209.

IFN-gamma suspends the killing license of anti-tumor CTLs

Aron E Lukacher  1
Affiliations
Review

IFN-gamma suspends the killing license of anti-tumor CTLs

Aron E Lukacher. J Clin Invest. 2002 Nov.
No abstract available

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Figures

Figure 1
Figure 1
Model for IFN-γ–mediated inhibition of NKs and anti-tumor CTLs. Tumor-infiltrating macrophages present MHC class II:tumor peptide ligands to antigen-specific Th1 cells and induce them to produce IFN-γ. In addition, by upregulating CD40 ligand, these activated Th1 cells ligate CD40 receptors on the macrophages and induce them to secrete IL-12; IL-12 then triggers IFN-γ production by NKs. Low MHC class I–expressing tumor cells also activate high-avidity tumor-specific CTLs and NKs (unengaged iNKRs + activated aNKRs) to produce IFN-γ. By upregulating classical and nonclassical MHC class I surface expression by tumor cells, IFN-γ, either endogenously produced or injected, promotes activation of iNKRs on NKs and anti-tumor CTLs and turns off their cytotoxic effector function.
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Comment on

References

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