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T regulatory cells are a component of the immune system that suppress immune responses of other cells. This is an important "self-check" built into the immune system to prevent excessive reactions. Regulatory T cells come in many forms with the most well-understood being those that express CD4, CD25, and FOXP3 (CD4 + CD25 + regulatory T cells).
Tr1 cells express high levels of regulatory factors, such as glucocorticoid-induced tumor necrosis factor receptor , OX40 , and tumor-necrosis factor receptor . [8] Resting human Tr1 cells express Th1 associated chemokine receptors CXCR3 and CCR5 , and Th2-associated CCR3, CCR4 and CCR8 . [ 8 ]
Regulatory T cells can develop either during normal development in the thymus, and are then known as thymic Treg cells, or can be induced peripherally and are called peripherally derived Treg cells. These two subsets were previously called "naturally occurring" and "adaptive" (or "induced"), respectively. [ 27 ]
These tolerogenic properties are executed by deletion of T cells, induction of Tregs and anergized T cells, then by expression of immunomodulatory molecules such as PD-L1 and PD-L2, heme oxygenase 1, HLA-G, CD95L, TNF-related apoptosis inducing ligands, galectin-1 and DC-SIGN and production of immunosuppressive molecules such as IL-10, TGF-b ...
Deletion of self-reactive T cells in the thymus is only 60-70% efficient, and naive T cell repertoire contains a significant portion of low-avidity self-reactive T cells. These cells can trigger an autoimmune response, and there are several mechanisms of peripheral tolerance to prevent their activation. [ 4 ]
Foxp3 is a specific marker of natural T regulatory cells (nTregs, a lineage of T cells) and adaptive/induced T regulatory cells (a/iTregs), also identified by other less specific markers such as CD25 or CD45RB. [6] [7] [8] In animal studies, Tregs that express Foxp3 are critical in the transfer of immune tolerance, especially self-tolerance. [13]
CD2 was shown to prime naive T cells (T N) even without CD28 or TCR. [2] Also, CD27 is a receptor constitutively expressed on T N (its expression is downregulated upon TCR stimulation) and enhances T cell proliferation. [9] The differentiation of T helper cells (T H) into different subsets also partially depends on their co-stimulatory molecules.
Depletion of regulatory T cells increases immune activation. Glut1 regulation is associated with the activation of CD4+ T cells, thus its expression can be used to track the loss of CD4+ T cells during HIV. [19] Antiretroviral therapy, the most common treatment for patients with HIV, has been shown to restore CD4+ T cell counts. [20]
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