title: Pathological conditions re-shape physiological Tregs into pathological Tregs.
abstract: CD4+FOXP3+regulatory T cells (Tregs) are a subset of CD4 T cells that play an essential role in maintaining peripheral immune tolerance, controlling acute and chronic inflammation, allergy, autoimmune diseases, and anti-cancer immune responses. Over the past 20 years, significant progress has been made since Tregs were first characterized in 1995. Many concepts and principles regarding Tregs generation, phenotypic features, subsets (tTregs, pTregs, iTregs, and iTreg35), tissue specificity (central Tregs, effector Tregs, and tissue resident Tregs), homeostasis (highly dynamic and apoptotic), regulation of Tregs by receptors for PAMPs and DAMPs, Treg plasticity (re-differentiation to other CD4 T helper cell subsets, Th1, Th2, Tfh and Th17), and epigenetic regulation of Tregs phenotypes and functions have been innovated. In this concise review, we want to briefly analyze these eight new progresses in the study of Tregs. We have also proposed for the first time a novel concept that "physiological Tregs" have been re-shaped into "pathological Tregs" in various pathological environments. Continuing of the improvement in our understanding on this important cellular component about the immune tolerance and immune suppression, would lead to the future development of novel therapeutics approaches for acute and chronic inflammatory diseases, allergy, allogeneic transplantation-related immunity, sepsis, autoimmune diseases, and cancers.
authors.affiliation: Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors.forename: William Y
authors.initials: WY
authors.lastname: Yang
authors.affiliation: Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors.forename: Ying
authors.initials: Y
authors.lastname: Shao
authors.affiliation: Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors.forename: Jahaira
authors.initials: J
authors.lastname: Lopez-Pastrana
authors.affiliation: Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors.forename: Jietang
authors.initials: J
authors.lastname: Mai
authors.affiliation: Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.affiliation: Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A ; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors.forename: Xiao-Feng
authors.initials: XF
authors.lastname: Yang
keywords: epigenetic mechanisms; histone modifications; immune suppression; metabolic cardiovascular diseases; regulatory T cells