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IL-12 binds to the IL-12 receptor, which is a heterodimeric receptor formed by IL-12Rβ1 and IL-12Rβ2. [6] IL-12Rβ2 is considered to play a key role in IL-12 function, since it is found on activated T cells and is stimulated by cytokines that promote Th1 cells development and inhibited by those that promote Th2 cells development.
When used as drugs, the International Nonproprietary Names ... myostatin inhibitor Bimekizumab [10] Bimzelx: mab: ... IL-12, IL-23: Y:
Ustekinumab, sold under the brand name Stelara among others, is a monoclonal antibody medication used for the treatment of Crohn's disease, ulcerative colitis, plaque psoriasis and psoriatic arthritis, [31] targeting both IL-12 and IL-23. [32] It is administered either by intravenous infusion or subcutaneous injection. [31]
Interleukin-12 receptor, beta 1, or IL-12Rβ1 in short, is a subunit of the interleukin 12 receptor and the interleukin 23 receptor. IL12RB1 , is the name of its human gene . [ 5 ] IL-12Rβ1 is also known as CD212 ( cluster of differentiation 212).
Apilimod (STA-5326) is a drug that was initially identified as an inhibitor of production of the interleukins IL-12 and IL-23, and developed for the oral treatment of autoimmune conditions such as Crohn's disease and rheumatoid arthritis, [1] though clinical trial results were disappointing and development for these applications was not continued.
Interleukin 23 (IL-23) is a heterodimeric cytokine composed of an IL-12B (IL-12p40) subunit (which is shared with IL-12) and an IL-23A (IL-23p19) subunit. [1] IL-23 is part of the IL-12 family of cytokines. [2] The functional receptor for IL-23 (the IL-23 receptor) consists of a heterodimer between IL-12Rβ1 and IL-23R. [3]
These drugs act by binding the IL-2a receptor's α chain, preventing the IL-2 induced clonal expansion of activated lymphocytes and shortening their survival. They are used in the prophylaxis of the acute organ rejection after bilateral kidney transplantation , both being similarly effective and with only few side-effects.
In fact, eccentric exercise may result in a delayed peak and a much slower decrease of plasma IL-6 during recovery. [23] Anti-IL-6 therapies should therefore take into consideration the (beneficial) anti-inflammatory effects of myokines generally, including the now-established multiple benefits of muscle-derived Interleukin 6. [23]