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Cited by 661

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Anti-inflammatory and pro-inflammatory roles of TGF-β, IL-10, and IL-22 in immunity and autoimmunity

Open access
Sanjabi, Shomyseh, Zenewicz, Lauren A, Kamanaka, Masahito, Flavell, Richard A·2009·Current Opinion in Pharmacology

Abstract

Cytokines play a major role in maintaining lymphocyte homeostasis under both steady-state and inflammatory conditions. Unregulated lymphocytes in steady-state conditions can lead to autoimmunity, whereas during inflammation they can cause excessive tissue damage. Regulatory cytokines function in combination with other environmental signals to properly modulate the function and the extent of lymphocyte activation. Many recent studies have highlighted the importance of regulatory cytokines in controlling the differentiation and function of lymphocytes under steady-state and inflammatory conditions, as well as minimizing tissue damage.

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Registry

Crossref · 10.1016/j.coph.2009.04.008

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Metadata

Authors
Sanjabi, S., Zenewicz, L. A., Kamanaka, M., & Flavell, R. A.
Venue
Current Opinion in Pharmacology
Publisher
Elsevier BV
Published
2009-08
Volume
9
Issue
4
Pages
447-453
ISSN
1471-4892 (ISSN-L)
OpenAlex
W2053367250
Cited by
661
References
16
FWCI
0.94
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Anti-inflammatory and pro-inflammatory roles of TGF-β, IL-10, and IL-22 in immunity and autoimmunity. https://app.cochat.ai/papers/10.1016/j.coph.2009.04.008
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Sanjabi, S., Zenewicz, L. A., Kamanaka, M., & Flavell, R. A. (2009). Anti-inflammatory and pro-inflammatory roles of TGF-β, IL-10, and IL-22 in immunity and autoimmunity. Current Opinion in Pharmacology. https://doi.org/10.1016/j.coph.2009.04.008

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

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.