Suppressors of cytokine signaling: Potential immune checkpoint molecules for cancer immunotherapy

Shunsuke Chikuma, Mitsuhiro Kanamori, Setsuko Mise-Omata, Akihiko Yoshimura

Research output: Research - peer-reviewReview article

  • 4 Citations

Abstract

Inhibition of immune checkpoint molecules, PD-1 and CTLA4, has been shown to be a promising cancer treatment. PD-1 and CTLA4 inhibit TCR and co-stimulatory signals. The third T cell activation signal represents the signals from the cytokine receptors. The cytokine interferon-γ (IFNγ) plays an important role in anti-tumor immunity by activating cytotoxic T cells (CTLs). Most cytokines use the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and the suppressors of cytokine signaling (SOCS) family of proteins are major negative regulators of the JAK/STAT pathway. Among SOCS proteins, CIS, SOCS1, and SOCS3 proteins can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4+ T cells and the maturation of CD8+ T cells. This review summarizes recent progress on CIS, SOCS1, and SOCS3 in terms of their anti-tumor immunity and potential applications.

LanguageEnglish
Pages574-580
Number of pages7
JournalCancer Science
Volume108
Issue number4
DOIs
StatePublished - 2017 Apr 1

Fingerprint

Immunotherapy
Cytokines
T-Lymphocytes
Neoplasms
Suppressor of Cytokine Signaling Proteins
Janus Kinases
Transducers
Immunity
Cytokine Receptors
Interferon-gamma
Therapeutics
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling 1 Protein

Keywords

  • Immune checkpoint
  • JAK-STAT
  • kinase inhibitory region
  • suppressors of cytokine signaling
  • T cell

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Suppressors of cytokine signaling : Potential immune checkpoint molecules for cancer immunotherapy. / Chikuma, Shunsuke; Kanamori, Mitsuhiro; Mise-Omata, Setsuko; Yoshimura, Akihiko.

In: Cancer Science, Vol. 108, No. 4, 01.04.2017, p. 574-580.

Research output: Research - peer-reviewReview article

@article{51a10b7bbb8f40b2954cd2c896f3781c,
title = "Suppressors of cytokine signaling: Potential immune checkpoint molecules for cancer immunotherapy",
abstract = "Inhibition of immune checkpoint molecules, PD-1 and CTLA4, has been shown to be a promising cancer treatment. PD-1 and CTLA4 inhibit TCR and co-stimulatory signals. The third T cell activation signal represents the signals from the cytokine receptors. The cytokine interferon-γ (IFNγ) plays an important role in anti-tumor immunity by activating cytotoxic T cells (CTLs). Most cytokines use the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and the suppressors of cytokine signaling (SOCS) family of proteins are major negative regulators of the JAK/STAT pathway. Among SOCS proteins, CIS, SOCS1, and SOCS3 proteins can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4+ T cells and the maturation of CD8+ T cells. This review summarizes recent progress on CIS, SOCS1, and SOCS3 in terms of their anti-tumor immunity and potential applications.",
keywords = "Immune checkpoint, JAK-STAT, kinase inhibitory region, suppressors of cytokine signaling, T cell",
author = "Shunsuke Chikuma and Mitsuhiro Kanamori and Setsuko Mise-Omata and Akihiko Yoshimura",
year = "2017",
month = "4",
doi = "10.1111/cas.13194",
volume = "108",
pages = "574--580",
journal = "Cancer Science",
issn = "1347-9032",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Suppressors of cytokine signaling

T2 - Cancer Science

AU - Chikuma,Shunsuke

AU - Kanamori,Mitsuhiro

AU - Mise-Omata,Setsuko

AU - Yoshimura,Akihiko

PY - 2017/4/1

Y1 - 2017/4/1

N2 - Inhibition of immune checkpoint molecules, PD-1 and CTLA4, has been shown to be a promising cancer treatment. PD-1 and CTLA4 inhibit TCR and co-stimulatory signals. The third T cell activation signal represents the signals from the cytokine receptors. The cytokine interferon-γ (IFNγ) plays an important role in anti-tumor immunity by activating cytotoxic T cells (CTLs). Most cytokines use the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and the suppressors of cytokine signaling (SOCS) family of proteins are major negative regulators of the JAK/STAT pathway. Among SOCS proteins, CIS, SOCS1, and SOCS3 proteins can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4+ T cells and the maturation of CD8+ T cells. This review summarizes recent progress on CIS, SOCS1, and SOCS3 in terms of their anti-tumor immunity and potential applications.

AB - Inhibition of immune checkpoint molecules, PD-1 and CTLA4, has been shown to be a promising cancer treatment. PD-1 and CTLA4 inhibit TCR and co-stimulatory signals. The third T cell activation signal represents the signals from the cytokine receptors. The cytokine interferon-γ (IFNγ) plays an important role in anti-tumor immunity by activating cytotoxic T cells (CTLs). Most cytokines use the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and the suppressors of cytokine signaling (SOCS) family of proteins are major negative regulators of the JAK/STAT pathway. Among SOCS proteins, CIS, SOCS1, and SOCS3 proteins can be considered the third immunocheckpoint molecules since they regulate cytokine signals that control the polarization of CD4+ T cells and the maturation of CD8+ T cells. This review summarizes recent progress on CIS, SOCS1, and SOCS3 in terms of their anti-tumor immunity and potential applications.

KW - Immune checkpoint

KW - JAK-STAT

KW - kinase inhibitory region

KW - suppressors of cytokine signaling

KW - T cell

UR - http://www.scopus.com/inward/record.url?scp=85018674661&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85018674661&partnerID=8YFLogxK

U2 - 10.1111/cas.13194

DO - 10.1111/cas.13194

M3 - Review article

VL - 108

SP - 574

EP - 580

JO - Cancer Science

JF - Cancer Science

SN - 1347-9032

IS - 4

ER -