The role of all-trans retinoic acid in the biology of FOXP3+ regulatory T cells

Zhong Min Liu, Kun Peng Wang, Jilin Ma, Song Guo Zheng

Research output: Contribution to journalReview article

44 Citations (Scopus)

Abstract

Regulatory T (Treg) cells are necessary for immune system homeostasis and the prevention of autoimmune diseases. Foxp3 is specifically expressed in Treg cells and plays a key role in their differentiation and function. FOXP3+ Treg cells are consisted of naturally occurring, thymus-derived Treg (nTreg) and peripheral-induced Treg (iTreg) cells that may have different functional characteristics or synergistic roles. All-trans retinoic acid (atRA), a vitamin A metabolite, regulates a wide range of biological processes, including cell differentiation and proliferation. Recent studies demonstrated that atRA also regulates the differentiation of T helper (Th) cells and Treg cells. Moreover, atRA also sustains nTreg stability under inflammatory conditions. In this review, we summarize the significant progress of our understanding of the role(s) and mechanisms of atRA in Treg biology.

Original languageEnglish (US)
Pages (from-to)553-557
Number of pages5
JournalCellular and Molecular Immunology
Volume12
Issue number5
DOIs
StatePublished - Sep 8 2015

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Regulatory T-Lymphocytes
Tretinoin
Biological Phenomena
Helper-Inducer T-Lymphocytes
Vitamin A
Thymus Gland
Autoimmune Diseases
Cell Differentiation
Immune System
Homeostasis
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Cite this

Liu, Zhong Min ; Wang, Kun Peng ; Ma, Jilin ; Guo Zheng, Song. / The role of all-trans retinoic acid in the biology of FOXP3+ regulatory T cells. In: Cellular and Molecular Immunology. 2015 ; Vol. 12, No. 5. pp. 553-557.
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The role of all-trans retinoic acid in the biology of FOXP3+ regulatory T cells. / Liu, Zhong Min; Wang, Kun Peng; Ma, Jilin; Guo Zheng, Song.

In: Cellular and Molecular Immunology, Vol. 12, No. 5, 08.09.2015, p. 553-557.

Research output: Contribution to journalReview article

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