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Abstract
T cells are a central element of cell-mediated immunity. Host detection of infectious agents leads to antigen presentation and release of cytokines that cause naïve T cells to develop into effector T cells or regulatory T cells (Treg cells). Effector T cells act to control the invading agents and mediate tissue inflammation. Treg cells maintain immune homeostasis by suppressing effector T cell responses to prevent collateral damage. Until recently, T cell differentiation into distinct subsets with different functions had been considered irreversible. However, new evidence suggests that some differentiated T cell subsets are more phenotypically flexible than others. Studying the plasticity of T cells and the underlying signaling mechanisms may lead to important clues for understanding immunity and autoimmunity.
