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Interleukin 21 (IL-21) is a protein that in humans is encoded by the IL21 gene. [5] [6] [7]Interleukin-21 is a cytokine that has potent regulatory effects on cells of the immune system, including natural killer (NK) cells and cytotoxic T cells that can destroy virally infected or cancerous cells.
CD1–restricted T cells produce T H 1, IFN-γ and TNF-α cytokines and are cytolytic. They can induce TNF-α dependent dentritic cells maturation. Many group 1 CD1–restricted T cells are autoreactive, and autoreactivity is enhanced by stimulation through pattern recognition receptors . CD1a-restricted T cells are among the most frequent self ...
IL-27, together with TGF-β induces IL-10–producing regulatory T cells with Tr1-like properties cells. [16] [17] IL-27 alone can induce IL-10-producing Tr1 cells, but in the absence of TGF-β, the cells produce large quantities of both IFN-γ and IL-10. [18] IL-6 and IL-21 also plays a role in differentiation as they regulate expression of ...
Interleukin 21 receptor is a type I cytokine receptor. IL21R is its human gene. [5]The protein encoded by this gene is a cytokine receptor for interleukin 21 (IL21). It belongs to the type I cytokine receptors, and has been shown to form a heterodimeric receptor complex with the common gamma chain (γc), a receptor subunit also shared by the receptors for interleukin 2 (IL2), interleukin 7 ...
Pathogen-specific T SCM cells have been identified in a number of studies of human acute and chronic infections caused by viruses, bacteria and parasites. The presence of T SCM might be essential for the control of persisting infections, in which effector T cells undergo exhaustion and need to be restored; this was supported by the evidence of a negative correlation between the severity of ...
Treg cells can be a source of IL-10 and TGF-β and therefore they can play a role in T cell exhaustion. [70] Furthermore, T cell exhaustion is reverted after depletion of Treg cells and blockade of PD1. [71] T cell exhaustion can also occur during sepsis as a result of cytokine storm.
Unlike the other types, it is not humoral (not antibody-mediated) but rather is a type of cell-mediated response. This response involves the interaction of T cells, monocytes, and macrophages. This reaction is caused when CD4 + T h 1 cells recognize foreign antigen in a complex with the MHC class II on the surface of antigen-presenting cells.
In Th17 response probably NFATc2 plays a key role since mice with NFATc2 knockout show reduction in RORγ as well as in IL-17A, IL-17F, and IL-21. Treg cells are the only exceptions to the NFAT:AP-1 complex formation since after their TCR stimulation NFAT binds to SMAD3 instead of AP-1.