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FOXP3(+) Treg Cells and Gender Bias in Autoimmune Diseases.

Nie J, Li YY, Zheng SG, Tsun A, Li B - Front Immunol (2015)

Bottom Line: Genetic deficiency of foxp3 induces dysfunction of Treg cells and immuno-dysregulation, polyendocrinopathy, enteropathy, and X-linked syndrome in humans.In general, females are more susceptible to SLE and MS but less susceptible to AS, where the expression of FOXP3 and its protein complex are perturbed by multiple factors, including hormonal fluctuations, inflammatory cytokines, and danger signals.Therefore, it is critical to explore the potential molecular mechanisms involved and these differences linked to gender.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences , Shanghai , China.

ABSTRACT
CD4(+)CD25(+) regulatory T (Treg) cells play a pivotal role in the maintenance of immune homeostasis, where the X-linked master transcription factor forkhead box P3 (FOXP3) determines Treg cell development and function. Genetic deficiency of foxp3 induces dysfunction of Treg cells and immuno-dysregulation, polyendocrinopathy, enteropathy, and X-linked syndrome in humans. Functionally deficient Treg cells or the development of exTreg cells positively correlate with autoimmune diseases, such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), and ankylosing spondylitis (AS). In general, females are more susceptible to SLE and MS but less susceptible to AS, where the expression of FOXP3 and its protein complex are perturbed by multiple factors, including hormonal fluctuations, inflammatory cytokines, and danger signals. Therefore, it is critical to explore the potential molecular mechanisms involved and these differences linked to gender. Here, we review recent findings on the regulation of FOXP3 activity in Treg cells and also discuss gender difference in the determination of Treg cell function in autoimmune diseases.

No MeSH data available.


Related in: MedlinePlus

The development of Treg cells. Treg cells develop in the thymus and periphery. In the thymus, CD4+CD8+ T cells undergo negative selection and become mature tTreg cells through IL-2, IL-15, and TGF-β signals. In the periphery, naïve CD4+ T cells encounter antigen and differentiate into pTreg cells in the presence of TGF-β and IL-2.
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Figure 1: The development of Treg cells. Treg cells develop in the thymus and periphery. In the thymus, CD4+CD8+ T cells undergo negative selection and become mature tTreg cells through IL-2, IL-15, and TGF-β signals. In the periphery, naïve CD4+ T cells encounter antigen and differentiate into pTreg cells in the presence of TGF-β and IL-2.

Mentions: Treg cells comprise approximately 5–15% of the CD4+ T cell compartment and can be subdivided into two subpopulations, including thymus-derived Treg (tTreg) cells and peripherally derived Treg (pTreg) cells. tTreg (also called natural Treg (nTreg)) cells are generated from Treg precursors at the immature HSAhi CD4SP stage when FOXP3 is induced and Treg lineage commitment established (29). pTreg cells are differentiated from naïve T cells at peripheral sites in the presence of IL-2 and TGF-β (Figure 1). Those generated in vitro through TGF-β signals are known as induced Treg (iTreg) cells (30).


FOXP3(+) Treg Cells and Gender Bias in Autoimmune Diseases.

Nie J, Li YY, Zheng SG, Tsun A, Li B - Front Immunol (2015)

The development of Treg cells. Treg cells develop in the thymus and periphery. In the thymus, CD4+CD8+ T cells undergo negative selection and become mature tTreg cells through IL-2, IL-15, and TGF-β signals. In the periphery, naïve CD4+ T cells encounter antigen and differentiate into pTreg cells in the presence of TGF-β and IL-2.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4585344&req=5

Figure 1: The development of Treg cells. Treg cells develop in the thymus and periphery. In the thymus, CD4+CD8+ T cells undergo negative selection and become mature tTreg cells through IL-2, IL-15, and TGF-β signals. In the periphery, naïve CD4+ T cells encounter antigen and differentiate into pTreg cells in the presence of TGF-β and IL-2.
Mentions: Treg cells comprise approximately 5–15% of the CD4+ T cell compartment and can be subdivided into two subpopulations, including thymus-derived Treg (tTreg) cells and peripherally derived Treg (pTreg) cells. tTreg (also called natural Treg (nTreg)) cells are generated from Treg precursors at the immature HSAhi CD4SP stage when FOXP3 is induced and Treg lineage commitment established (29). pTreg cells are differentiated from naïve T cells at peripheral sites in the presence of IL-2 and TGF-β (Figure 1). Those generated in vitro through TGF-β signals are known as induced Treg (iTreg) cells (30).

Bottom Line: Genetic deficiency of foxp3 induces dysfunction of Treg cells and immuno-dysregulation, polyendocrinopathy, enteropathy, and X-linked syndrome in humans.In general, females are more susceptible to SLE and MS but less susceptible to AS, where the expression of FOXP3 and its protein complex are perturbed by multiple factors, including hormonal fluctuations, inflammatory cytokines, and danger signals.Therefore, it is critical to explore the potential molecular mechanisms involved and these differences linked to gender.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences , Shanghai , China.

ABSTRACT
CD4(+)CD25(+) regulatory T (Treg) cells play a pivotal role in the maintenance of immune homeostasis, where the X-linked master transcription factor forkhead box P3 (FOXP3) determines Treg cell development and function. Genetic deficiency of foxp3 induces dysfunction of Treg cells and immuno-dysregulation, polyendocrinopathy, enteropathy, and X-linked syndrome in humans. Functionally deficient Treg cells or the development of exTreg cells positively correlate with autoimmune diseases, such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), and ankylosing spondylitis (AS). In general, females are more susceptible to SLE and MS but less susceptible to AS, where the expression of FOXP3 and its protein complex are perturbed by multiple factors, including hormonal fluctuations, inflammatory cytokines, and danger signals. Therefore, it is critical to explore the potential molecular mechanisms involved and these differences linked to gender. Here, we review recent findings on the regulation of FOXP3 activity in Treg cells and also discuss gender difference in the determination of Treg cell function in autoimmune diseases.

No MeSH data available.


Related in: MedlinePlus