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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.
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.
T-cell anergy can arise when the T-cell does not receive appropriate co-stimulation in the presence of specific antigen recognition. [2] B-cell anergy can be induced by exposure to soluble circulating antigen, and is often marked by a downregulation of surface IgM expression and partial blockade of intracellular signaling pathways.
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.
Interleukin 10 (IL-10) is a protein that inhibits the synthesis of a number of cytokines, including IFN-gamma, IL-2, IL-3, TNF, and GM-CSF produced by activated macrophages and by helper T cells. In structure, IL-10 is a protein of about 160 amino acids that contains four conserved cysteines involved in disulphide bonds. [ 33 ]
This decline in turn reduces IL-2 production [28] [29] and reduction/exhaustion on the number of thymocytes (i.e. immature T cells), thus reducing peripheral naïve T cell output. [30] [31] Once matured and circulating throughout the peripheral system, T cells undergo deleterious age-dependent changes. This leaves the body practically devoid of ...
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 ...
These cells present early in the tissue have higher expression of some genes typical for T RM and at the peak of the T cell response, local T cell population expresses more than 90% of the T RM gene signature. [22] This shows that differentiation process of T RM cells starts early during immune response. [9]