About this Research Topic

Background

In many disorders including autoimmune, autoinflammatory and metabolic diseases, a prolonged and deranged immune response leads to the development of chronic inflammation which can ultimately lead to severe tissue damage. At the same time, inflammation induces regulatory cell subsets critically involved in limiting the inflammatory response; whilst chemokines, metabolites, and growth factors released by inflammatory cells can facilitate tissue repair and regeneration after injury. Often in genetically predisposed individuals, T cells migrate to the target site of chronic inflammation, where they differentiate into local effectors and develop tissue-selective functional specialization, thereby fueling the recurrence of inflammatory episodes. A fraction of resident T cells can also recirculate to other body sites, thereby aggravating the disease process.

Human diseases characterized by organ-specific chronic inflammation display distinct, although often a-specific signs of inflammation in the periphery. This only provides a partial picture of the mechanisms inducing and sustaining organ-specific inflammation, which could be elucidated by investigating target organs in physiological or pathological conditions. Factors determining T cell tissue immunity include - but are not limited to - the quality of the antigen(s) driving the immune reaction and the local inflammatory milieu (e.g. cytokines and chemotactic factors driving T cell migration between secondary lymphoid organs and peripheral tissues). All these aspects contribute to the generation of antigen-experienced T cells with unique tissue and disease-specific profiles and functions. Accumulating evidence now shows that, in diseases like obesity and type 2 diabetes (T2D), displaying systemic and metabolic organ-selective chronic inflammation, autoreactivity is observed in selective subgroups of patients. However, tissue-resident antigen-specific T cells and their matched auto-antigens have yet to be identified. Elucidation of the mechanisms underlying chronic tissue inflammation in human diseases will help enable us to identify mediators of inflammation with clinical significance, untangle disease heterogeneity, determine prognostic/predictive biomarkers of disease outcome and test therapeutic strategies to modulate tissue inflammation.

In this Research Topic, we welcome the submission of Original Research, Reviews/Mini-reviews, Perspective and Opinion articles on the tissue-specific profile and functional properties of T cell subsets in homeostasis and in the following pathological conditions: autoimmune diseases, autoinflammatory diseases, obesity and T2D. This collection accepts articles focusing on human subject research.
We seek contributions related to, but not limited to, the following themes:

• T cell phenotype and function in chronic tissue inflammation
• Effects of the tissue microenvironment on T cell differentiation and function
• Impact of metabolic dysregulation on tissue-resident T cell profile and functional properties
• Mechanisms of T cell-mediated disease pathogenesis, progression and regulation in human tissues
• Drug-mediated modulation of tissue T cell profile and plasticity
• Interaction of T cells with other resident cell subsets
• Phenotype and function of recirculating T cells
• Contribution of genetic variants to tissue-restricted T cell dynamics


Dr. Van Wijk has received investigator initiated funding from Pfizer and Regeneron, with relation to IBD and eczema treatment studies. Dr. Taams receives funding from Sanofi. The other Topic Editors declare no competing interests with regards to the topic theme.

Keywords: tissue immunity, resident T cells, chronic inflammation, human

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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