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. 2022 Jul 5;13:947568. doi: 10.3389/fimmu.2022.947568

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Copyright © 2022 Witalisz-Siepracka, Klein, Zdársky and Stoiber

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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STAT3 contribution to NK cell-mediated tumor immune surveillance. NK cell-intrinsic STAT3 (left) inhibits expression of granzyme B and DNAM-1 ( ), increases IFNγ secretion ( ) and seems to upregulate TIGIT and LAG-3 (), while the effect on NCRs and NKG2D expression remain context dependent (). Tumor cell-intrinsic STAT3 (right) inhibits expression of NKG2D ligands (MICA/B, ULBPs) and NK-cell attracting chemokine CCL5 (). STAT3 in tumor cells upregulates surface expression of MHC I and PD-L1 molecules and secretion of immune suppressive TGF-β ( ). NK, natural killer; IFN, interferon; DNAM-1, DNAX accessory molecule; NKG2D, NK-cell receptor natural killer group 2D; NCR, natural cytotoxicity receptor; KIR, killer-cell immunoglobulin-like receptor; CCL5, C-C motif chemokine ligand 5; CD, cluster of differentiation; MICA/B, major histocompatibility complex class I-related sequence A/B; ULBP, UL16-binding protein; MHC I, major histocompatibility complex I; TGF-β, transforming growth factor β, STAT, signal transducer and activator of transcription. TIGIT, T cell immunoreceptor with Ig and ITIM domains; LAG-3, lymphocyte-activation gene 3; PD-(L)1, programmed cell death ligand/protein 1.

Inline graphic — STAT3 contribution to NK cell-mediated tumor immune surveillance. NK cell-intrinsic STAT3 (left) inhibits expression of granzyme B and DNAM-1 ( ), increases IFNγ secretion ( ) and seems to upregulate TIGIT and LAG-3 (), while the effect on NCRs and NKG2D expression remain context dependent (). Tumor cell-intrinsic STAT3 (right) inhibits expression of NKG2D ligands (MICA/B, ULBPs) and NK-cell attracting chemokine CCL5 (). STAT3 in tumor cells upregulates surface expression of MHC I and PD-L1 molecules and secretion of immune suppressive TGF-β ( ). NK, natural killer; IFN, interferon; DNAM-1, DNAX accessory molecule; NKG2D, NK-cell receptor natural killer group 2D; NCR, natural cytotoxicity receptor; KIR, killer-cell immunoglobulin-like receptor; CCL5, C-C motif chemokine ligand 5; CD, cluster of differentiation; MICA/B, major histocompatibility complex class I-related sequence A/B; ULBP, UL16-binding protein; MHC I, major histocompatibility complex I; TGF-β, transforming growth factor β, STAT, signal transducer and activator of transcription. TIGIT, T cell immunoreceptor with Ig and ITIM domains; LAG-3, lymphocyte-activation gene 3; PD-(L)1, programmed cell death ligand/protein 1.