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. 2013 Jan 1;2(1):e22653.
doi: 10.4161/onci.22653.

Involvement of STAT3 in immune evasion during lung tumorigenesis

Hiroshi Kida  1 , Shoichi Ihara, Atsushi Kumanogoh
Affiliations

Involvement of STAT3 in immune evasion during lung tumorigenesis

Hiroshi Kida et al. Oncoimmunology. .

Abstract

In a recent study, we have shown that STAT3 expressed by tumor cells blunts antitumor immunity during carcinogen-induced lung tumorigenesis. STAT3 inhibits the production of pro-inflammatory chemokines and MHC Class I chain-related gene A. In contrast, STAT3 promotes the expression of MHC class I molecules. Consequently, STAT3 promotes tumor cell resistance to NK cell-mediated cytotoxicity.

Keywords: MHC Class I; MICA; NK cell; STAT3; antitumor immunity; lung; tumorigenesis.

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Figures

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Figure 1. STAT3 activation allows tumor cells to evade antitumor immunity. STAT3 negatively regulates chemokines that play important roles in cancer-related inflammation by acting on various subpopulations of immune effector cells. STAT3 augments the expression of major histocompatibility complex (MHC) Class I molecules, a ligand for inhibitory natural killer (NK)-cell receptors and inhibits the expression of MHC Class I chain-related gene A (MICA), a ligand for activating NK-cell receptors. Consequently, the activation of NK-cell effector functions is inhibited by STAT3 activation in tumor cells.
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