Foxp3 programs the development and function of CD4+CD25+ regulatory T cells

Fontenot, Jason D.; Gavin, Marc A.; Rudensky, Alexander Y.

doi:10.1038/ni904

Cited by 6,641 publications

(5,602 citation statements)

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“…Some authors believe that Treg cells are involved in the suppression of Mtb-specific Th1 cells ( Chen et al 2007 , Roberts et al 2007 ). Human CD4 + Treg cells can be distinguished from recently activated T cells (CD25 + ) by their expression of the nuclear transcription factor FOXP3 ( Fontenot et al 2003 , Roberts et al 2007 , Ellner 2010 ). Treg cells have been shown to regulate effector T cells ( Ribeiro-Rodrigues et al 2006 , Chen et al 2007 ).…”

Section: Resultsmentioning

confidence: 99%

The use of Mycobacterium tuberculosis HspX and GlcB proteins to identify latent tuberculosis in rheumatoid arthritis patients

Silva

Tannus-Silva

Rabahi

et al. 2014

Mem. Inst. Oswaldo Cruz

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Rheumatoid arthritis (RA) is an autoimmune disease characterised by the destruction of articular cartilage and bone damage. The chronic treatment of RA patients causes a higher susceptibility to infectious diseases such as tuberculosis (TB); one-third of the world’s population is latently infected (LTBI) with Mycobacterium tuberculosis (Mtb). The tuberculin skin test is used to identify individuals LTBI, but many studies have shown that this test is not suitable for RA patients. The goal of this work was to test the specific cellular immune responses to the Mtb malate synthase (GlcB) and heat shock protein X (HspX) antigens of RA patients and to correlate those responses with LTBI status. The T-helper (Th)1, Th17 and Treg-specific immune responses to the GlcB and HspX Mtb antigens were analysed in RA patients candidates for tumour necrosis factor-α blocker treatment. Our results demonstrated that LTBI RA patients had Th1-specific immune responses to GlcB and HspX. Patients were followed up over two years and 14.3% developed active TB. After the development of active TB, RA patients had increased numbers of Th17 and Treg cells, similar to TB patients. These results demonstrate that a GlcB and HspX antigen assay can be used as a diagnostic test to identify LTBI RA patients.

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Section: Resultsmentioning

confidence: 99%

The use of Mycobacterium tuberculosis HspX and GlcB proteins to identify latent tuberculosis in rheumatoid arthritis patients

Silva

Tannus-Silva

Rabahi

et al. 2014

Mem. Inst. Oswaldo Cruz

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“…down-regulates T cell activation and cytokine genes (e.g., encoding IL-2, IL-4), and upregulates immunosuppressive cell-surface molecules (e.g., CD25, CTLA-4) and, in doing so, contributes to both the hyporesponsive and suppressive Treg cell phenotype [31,32]. FoxP3 suppresses the effector functions of T helper cells by directly inhibiting the activity of two key transcription factors, nuclear factor of activated T cells (NFAT) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B , which are essential for cytokine gene expression and T cell functions [30].…”

Section: Forkhead Box P3mentioning

confidence: 99%

Regulatory T cells in vitiligo: Implications for pathogenesis and therapeutics

Dwivedi

Kemp

Laddha

et al. 2015

Autoimmunity Reviews

101

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Vitiligo is a hypomelanotic autoimmune skin disease arising from a breakdown in immunological self-tolerance, which leads to aberrant immune responses against melanocytes.Regulatory T cells (Tregs) are crucial to the development of self-tolerance and so are major foci in the study of autoimmune pathogenesis of vitiligo. This review will summarise recent findings concerning the role of Tregs in the pathogenesis of vitiligo. In addition, as antigen-specific Tregs are a potential route for the reinstatement of immune tolerance, new strategies that expand or induce de novo generation of Tregs and which are currently being investigated as therapies for other autoimmune diseases, will be discussed. These approaches will highlight the opportunities for Treg cell-based therapeutics in vitiligo.4

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“…The importance of FOXP3 in the development and function of nTreg is demonstrated by experiments of nature in which spontaneous mutations of the FOXP3 gene cause severe X-linked autoimmune lymphoproliferative disorders. The scurfy mutation in mice, which is associated with a null mutation of the foxp3 gene, results in complete loss of nTreg, autoimmunity, and premature death [3,5]. Similarly, mutations of FOXP3 in humans are responsible for a diseasecalled immuno dysfunction polyendocrinopathy enteropathy X-linked syndrome (IPEX) -in which the impairment of nTreg function is associated with several autoimmune disorders such as enteropathy and type 1 diabetes [6,7].…”

Section: Foxp3 Expression In T Cellsmentioning

confidence: 99%

Is FOXP3 a bona fide marker for human regulatory T cells?

2008

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FOXP3 is a specific marker for naturally occurring regulatory T cells (nTreg). FOXP3 expression is correlated with development and function of nTreg. Recent evidence suggests that, upon activation, human effector T (Teff) cells and type 1 regulatory T (Tr1) cells can express FOXP3, albeit transiently. While the role of transient FOXP3 expression in Teff cells is poorly understood, it is becoming clear that it does not correlate with suppressor function. Furthermore, FOXP3‐independent mechanisms, mediated by IL‐10, contribute to the induction and suppressor functions of Tr1 cells. See accompanying commentary:

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Foxp3 programs the development and function of CD4+CD25+ regulatory T cells

Cited by 6,641 publications

References 26 publications

The use of Mycobacterium tuberculosis HspX and GlcB proteins to identify latent tuberculosis in rheumatoid arthritis patients

The use of Mycobacterium tuberculosis HspX and GlcB proteins to identify latent tuberculosis in rheumatoid arthritis patients

Regulatory T cells in vitiligo: Implications for pathogenesis and therapeutics

Is FOXP3 a bona fide marker for human regulatory T cells?

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