Immune Regulation in Human Health and Disease

Abstract

The immune system requires a homeostatic equilibrium among the mechanisms that assure self‐tolerance, those that control the capacity to mount life‐long immunity to pathogenic microbes and those that attenuate effector mechanisms from inducing immune pathology. There are multiple processes in place to ensure that healthy immune regulation and FOXP3 + T regulatory (Treg) cells are thought to be the major players. Treg cells exercise their regulatory role through various contact‐dependent and ‐independent mechanisms, and FOXP3 is the master regulator of their various functions such as inhibiting T effector (Teff) cell proliferation and inflammatory cytokine production. Various autoimmune diseases such as IPEX occur when Treg‐cell function or numbers are abrogated. Although there is evidence that supports the involvement of Treg cells in the development of autoimmune disease, there are inconsistencies in the literature owing to the lack of Treg‐cell‐specific markers. Key Concepts The immune system employs multiple tolerance mechanisms to maintain immune homeostasis. Multiple specialised regulatory cells exist, FOXP3+ T regulatory (Treg) cells being one of the major players in the maintenance of immune tolerance. FOXP3 is the master transcription factor of Treg cells, controlling Treg‐cell phenotype and suppressive functions. Autoimmune diseases such as IPEX arise when Treg cells are defective or lacking, which can be due to mutations at the Foxp3 gene locus. Multiple markers are currently being used to study the Treg‐cell population; however, these markers are not specific to Treg cells and therefore are the cause of inconsistencies in the literature on the topic of Treg‐cell function in health and disease. Disturbances in FOXP3+ Treg‐cell development, homeostasis and/or function are thought to occur in many autoimmune and chronic inflammatory diseases in humans.

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