Abstract
Foxp3+ regulatory T (Treg) cells are a CD4 T cell subset with unique immune regulatory function that are indispensable in immunity and tolerance. Their indisputable importance has been investigated in numerous disease settings and experimental models. Despite the extensive efforts in determining the cellular and molecular mechanisms operating their functions, our understanding their biology especially in vivo remains limited. There is emerging evidence that Treg cells resident in the non-lymphoid tissues play a central role in regulating tissue homeostasis, inflammation, and repair. Furthermore, tissue-specific properties of those Treg cells that allow them to express tissue specific functions have been explored. In this review, we will discuss the potential mechanisms and key cellular/molecular factors responsible for the homeostasis and functions of tissue resident Treg cells under steady-state and inflammatory conditions.
Highlights
The immune system is incessantly confronted by antigens derived from invading foreign pathogens and from self
For those lymphocytes posing a risk of self-reactivity, they are effectively eliminated during the development within the primary lymphoid tissues
Foxp3 expression is acquired in developing T cells within the thymus, and the level of self-reactivity is thought to support the differentiation into tTreg lineage cells [4, 5]
Summary
The immune system is incessantly confronted by antigens derived from invading foreign pathogens and from self. In the skin of adult mice, the proportion of Foxp3+ Treg cells is considerably higher than that of circulation or of lymphoid tissues (~40% vs ~10%) [58]. Gratz et al reported the existence of Treg cells expressing activated effector memory phenotypes that preferentially locate in hair follicles in the skin of mice [59]. Increased methylation levels of the FoxP3 promoter in Ssc patients was found associated with reduced FoxP3 mRNA expression and proportion of CD4+CD25+FoxP3+ Treg cells [79].
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