Signaling and Function of Interleukin-2 in T Lymphocytes

Research output: Contribution to journalArticle

22 Citations (Scopus)
125 Downloads (Pure)

Abstract

The discovery of interleukin-2 (IL-2) changed the molecular understanding of how the immune system is controlled. IL-2 is a pleiotropic cytokine, and dissecting the signaling pathways that allow IL-2 to control the differentiation and homeostasis of both pro- and anti-inflammatory T cells is fundamental to determining the molecular details of immune regulation. The IL-2 receptor couples to JAK tyrosine kinases and activates the STAT5 transcription factors. However, IL-2 does much more than control transcriptional programs; it is a key regulator of T cell metabolic programs. The development of global phosphoproteomic approaches has expanded the understanding of IL-2 signaling further, revealing the diversity of phosphoproteins that may be influenced by IL-2 in T cells. However, it is increasingly clear that within each T cell subset, IL-2 will signal within a framework of other signal transduction networks that together will shape the transcriptional and metabolic programs that determine T cell fate.

Original languageEnglish
Pages (from-to)411-433
Number of pages23
JournalAnnual Review of Immunology
Volume36
DOIs
Publication statusPublished - 26 Apr 2018

Fingerprint

Interleukin-2
T-Lymphocytes
STAT5 Transcription Factor
Janus Kinases
Interleukin-2 Receptors
Phosphoproteins
T-Lymphocyte Subsets
Protein-Tyrosine Kinases
Immune System
Signal Transduction
Homeostasis
Anti-Inflammatory Agents
Cytokines

Keywords

  • Interleukin-2
  • JAK1/3
  • PI3K
  • cytokine signaling

Cite this

@article{0a39b27caac24403b95c2d4d8d9dbdcc,
title = "Signaling and Function of Interleukin-2 in T Lymphocytes",
abstract = "The discovery of interleukin-2 (IL-2) changed the molecular understanding of how the immune system is controlled. IL-2 is a pleiotropic cytokine, and dissecting the signaling pathways that allow IL-2 to control the differentiation and homeostasis of both pro- and anti-inflammatory T cells is fundamental to determining the molecular details of immune regulation. The IL-2 receptor couples to JAK tyrosine kinases and activates the STAT5 transcription factors. However, IL-2 does much more than control transcriptional programs; it is a key regulator of T cell metabolic programs. The development of global phosphoproteomic approaches has expanded the understanding of IL-2 signaling further, revealing the diversity of phosphoproteins that may be influenced by IL-2 in T cells. However, it is increasingly clear that within each T cell subset, IL-2 will signal within a framework of other signal transduction networks that together will shape the transcriptional and metabolic programs that determine T cell fate.",
keywords = "Interleukin-2, JAK1/3, PI3K, cytokine signaling",
author = "Ross, {Sarah H} and Cantrell, {Doreen A}",
note = "This work was supported by the Wellcome Trust (Principal Research Fellowship 097418/Z/11/Z and 205023/Z/16/Z to D.A.C.) and Tenovus Scotland (S.H.R.). We would like to thank other members of the Cantrell group for critical reading of the manuscript.",
year = "2018",
month = "4",
day = "26",
doi = "10.1146/annurev-immunol-042617-053352",
language = "English",
volume = "36",
pages = "411--433",
journal = "Annual Review of Immunology",
issn = "0732-0582",
publisher = "Annual Reviews",

}

Signaling and Function of Interleukin-2 in T Lymphocytes. / Ross, Sarah H; Cantrell, Doreen A.

In: Annual Review of Immunology, Vol. 36, 26.04.2018, p. 411-433.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Signaling and Function of Interleukin-2 in T Lymphocytes

AU - Ross, Sarah H

AU - Cantrell, Doreen A

N1 - This work was supported by the Wellcome Trust (Principal Research Fellowship 097418/Z/11/Z and 205023/Z/16/Z to D.A.C.) and Tenovus Scotland (S.H.R.). We would like to thank other members of the Cantrell group for critical reading of the manuscript.

PY - 2018/4/26

Y1 - 2018/4/26

N2 - The discovery of interleukin-2 (IL-2) changed the molecular understanding of how the immune system is controlled. IL-2 is a pleiotropic cytokine, and dissecting the signaling pathways that allow IL-2 to control the differentiation and homeostasis of both pro- and anti-inflammatory T cells is fundamental to determining the molecular details of immune regulation. The IL-2 receptor couples to JAK tyrosine kinases and activates the STAT5 transcription factors. However, IL-2 does much more than control transcriptional programs; it is a key regulator of T cell metabolic programs. The development of global phosphoproteomic approaches has expanded the understanding of IL-2 signaling further, revealing the diversity of phosphoproteins that may be influenced by IL-2 in T cells. However, it is increasingly clear that within each T cell subset, IL-2 will signal within a framework of other signal transduction networks that together will shape the transcriptional and metabolic programs that determine T cell fate.

AB - The discovery of interleukin-2 (IL-2) changed the molecular understanding of how the immune system is controlled. IL-2 is a pleiotropic cytokine, and dissecting the signaling pathways that allow IL-2 to control the differentiation and homeostasis of both pro- and anti-inflammatory T cells is fundamental to determining the molecular details of immune regulation. The IL-2 receptor couples to JAK tyrosine kinases and activates the STAT5 transcription factors. However, IL-2 does much more than control transcriptional programs; it is a key regulator of T cell metabolic programs. The development of global phosphoproteomic approaches has expanded the understanding of IL-2 signaling further, revealing the diversity of phosphoproteins that may be influenced by IL-2 in T cells. However, it is increasingly clear that within each T cell subset, IL-2 will signal within a framework of other signal transduction networks that together will shape the transcriptional and metabolic programs that determine T cell fate.

KW - Interleukin-2

KW - JAK1/3

KW - PI3K

KW - cytokine signaling

U2 - 10.1146/annurev-immunol-042617-053352

DO - 10.1146/annurev-immunol-042617-053352

M3 - Article

C2 - 29677473

VL - 36

SP - 411

EP - 433

JO - Annual Review of Immunology

JF - Annual Review of Immunology

SN - 0732-0582

ER -