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IL-2 family cytokines: new insights into the complex roles of IL-2 as a broad regulator of T helper cell differentiation

Open access
Liao, Wei, Lin, Jian-Xin, Leonard, Warren J·2011·Current Opinion in Immunology

Abstract

Interleukin-2 (IL-2) is a pleiotropic cytokine that drives T-cell growth, augments NK cytolytic activity, induces the differentiation of regulatory T cells, and mediates activation-induced cell death. Along with IL-4, IL-7, IL-9, IL-15, and IL-21, IL-2 shares the common cytokine receptor γ chain, γc, which is mutated in humans with X-linked severe combined immunodeficiency. Herein, we primarily focus on the recently discovered complex roles of IL-2 in broadly modulating T cells for T helper cell differentiation. IL-2 does not specify the type of Th differentiation that occurs; instead, IL-2 modulates expression of receptors for other cytokines and transcription factors, thereby either promoting or inhibiting cytokine cascades that correlate with each Th differentiation state. In this fashion, IL-2 can prime and potentially maintain Th1 and Th2 differentiation as well as expand such populations of cells, whereas it inhibits Th17 differentiation but also can expand Th17 cells.

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Metadata

Authors
Liao, W., Lin, J.-X., & Leonard, W. J.
Venue
Current Opinion in Immunology
Publisher
Elsevier BV
Published
2011-10
Volume
23
Issue
5
Pages
598-604
ISSN
0952-7915 (ISSN-L)
OpenAlex
W2083054031
Cited by
745
References
57
FWCI
2.33
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: IL-2 family cytokines: new insights into the complex roles of IL-2 as a broad regulator of T helper cell differentiation. https://app.cochat.ai/papers/10.1016/j.coi.2011.08.003
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Liao, W., Lin, J.-X., & Leonard, W. J. (2011). IL-2 family cytokines: new insights into the complex roles of IL-2 as a broad regulator of T helper cell differentiation. Current Opinion in Immunology. https://doi.org/10.1016/j.coi.2011.08.003

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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