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Cytokine receptors on T cells and NK cells are a diverse group of cell-surface glycoproteins that mediate the effects of various interleukins and interferons on immune cell behavior. These receptors, such as the IL-2, IL-7, and IL-15 receptors, are typically multi-subunit complexes that signal through the Janus kinase (JAK) and Signal Transducer and Activator of Transcription (STAT) pathways [1][2]. They play a fundamental role in the activation, proliferation, and survival of T lymphocytes and Natural Killer (NK) cells, making them central to both innate and adaptive immunity [3]. In clinical practice, these receptors are major therapeutic targets for a variety of conditions. In oncology, agonists like recombinant IL-2 (Aldesleukin) or IL-15 superagonists are used to stimulate anti-tumor immune responses by expanding cytotoxic T and NK cell populations [4]. Conversely, monoclonal antibodies that block these receptors, such as Basiliximab (targeting CD25), are employed to prevent organ transplant rejection or treat autoimmune diseases by dampening excessive immune activity [5]. However, modulating these pathways carries risks, including cytokine release syndrome and systemic toxicity, due to the potent and widespread nature of cytokine signaling [1].
Agonism of cytokine receptors to stimulate immune cell proliferation and effector function, or antagonism/blockade of cytokine receptors to inhibit immune activation and inflammation.
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