The evolution of the immune system is key for the host to mount an efficient defence against pathogens. At the same time, unwanted immune responses against self and innocuous foreign antigens need to be tightly regulated to avoid catastrophic autoimmunity. While self-reactive thymocytes could be eliminated through cell intrinsic mechanisms of central tolerance, an additional layer of immune regulation by the CD4+Foxp3+ Regulatory T (Treg) cells has become a major focus of immune research. Furthermore, due to their capability of dampening anti-tumor immunity, Treg cells have emerged as a prominent cellular population of interest in the cancer microenvironment.
Although identified in the context of dominant tolerance of the immune system, in recent years it is increasingly appreciated that apart from controlling overenthusiastic immune responses, Treg cell activities also assimilate into a broader biological paradigm of tissue and organ homeostasis. Several distinct Treg populations are identified in non-lymphoid tissues such as adipose tissues, lung, skin, intestine, muscle, kidney and brain, where their functional significance are well appreciated in the context of metabolic inflammation, tissue development, regeneration, repair and beyond. Despite such advances our knowledge in relation to the cell intrinsic and extrinsic mechanisms promoting their parenchymal migration, adaptation, maintenance as well as tissue specific targets and functions, have only begun to emerge. Provided that the general principles contributing to such phenotypic diversity are also attributable to their functions in tumors and sites of inflammatory lesions, an in-depth understanding of such aspects of Treg biology may be instrumental in implementing various strategies of therapeutic interventions in clinical settings of autoimmunity and cancer.
In this Research Topic, we welcome submissions of Original Research, Review, Mini Review, Opinion and Perspective articles that address, but are not limited to, the following topics:
• Tissue homing and adaptation mechanisms employed by non-lymphoid Treg cells.
• Metabolic reprogramming strategies contributing to stability and functions of non-lymphoid Treg cells.
• Biochemical and epigenetic mechanisms contributing to phenotypic and functional heterogeneity of non-lymphoid Treg cells.
• “Immune” and “non-immune” strategies employed by Treg cells in tissue homeostasis.
• Functional diversities of Treg cell in the context of tumor immunity and inflammation.
• Therapeutic strategies to harness effector properties of non-lymphoid Treg cells in clinical settings.
The evolution of the immune system is key for the host to mount an efficient defence against pathogens. At the same time, unwanted immune responses against self and innocuous foreign antigens need to be tightly regulated to avoid catastrophic autoimmunity. While self-reactive thymocytes could be eliminated through cell intrinsic mechanisms of central tolerance, an additional layer of immune regulation by the CD4+Foxp3+ Regulatory T (Treg) cells has become a major focus of immune research. Furthermore, due to their capability of dampening anti-tumor immunity, Treg cells have emerged as a prominent cellular population of interest in the cancer microenvironment.
Although identified in the context of dominant tolerance of the immune system, in recent years it is increasingly appreciated that apart from controlling overenthusiastic immune responses, Treg cell activities also assimilate into a broader biological paradigm of tissue and organ homeostasis. Several distinct Treg populations are identified in non-lymphoid tissues such as adipose tissues, lung, skin, intestine, muscle, kidney and brain, where their functional significance are well appreciated in the context of metabolic inflammation, tissue development, regeneration, repair and beyond. Despite such advances our knowledge in relation to the cell intrinsic and extrinsic mechanisms promoting their parenchymal migration, adaptation, maintenance as well as tissue specific targets and functions, have only begun to emerge. Provided that the general principles contributing to such phenotypic diversity are also attributable to their functions in tumors and sites of inflammatory lesions, an in-depth understanding of such aspects of Treg biology may be instrumental in implementing various strategies of therapeutic interventions in clinical settings of autoimmunity and cancer.
In this Research Topic, we welcome submissions of Original Research, Review, Mini Review, Opinion and Perspective articles that address, but are not limited to, the following topics:
• Tissue homing and adaptation mechanisms employed by non-lymphoid Treg cells.
• Metabolic reprogramming strategies contributing to stability and functions of non-lymphoid Treg cells.
• Biochemical and epigenetic mechanisms contributing to phenotypic and functional heterogeneity of non-lymphoid Treg cells.
• “Immune” and “non-immune” strategies employed by Treg cells in tissue homeostasis.
• Functional diversities of Treg cell in the context of tumor immunity and inflammation.
• Therapeutic strategies to harness effector properties of non-lymphoid Treg cells in clinical settings.
