Shreya S Sonak, Sharda Ishwarkar, Charu Nimbarte, Vijaykumar D Nimbarte
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引用次数: 0
Abstract
IL-2 agonists significantly modulate T cell regulation, impacting activation, proliferation, differentiation, and immune homeostasis. Interleukin-2 (IL-2) is crucial for T cell growth and function, binding to the IL-2 receptor to trigger signaling pathways that balance immune responses. IL-2 promotes the expansion of effector T cells and enhances regulatory T cells (Tregs), preventing autoimmune responses. This review examines the mechanisms of IL-2 agonists on T cell regulation, including their roles in cytotoxic T cells and Tregs proliferation, and immune homeostasis. Clinically, IL-2 agonists show promise in treating autoimmune diseases by boosting Treg function and in cancer immunotherapy by enhancing cytotoxic T cell activity. Optimizing IL-2 therapies to balance these effects is ongoing. IL-2 agonists are pivotal in modulating T cell responses with significant therapeutic potential for autoimmunity and cancer. Understanding IL-2 signaling is crucial for developing targeted treatments leveraging this cytokine's benefits.
期刊介绍:
Immunology covers a broad spectrum of investigations at the genes, molecular, cellular, organ and system levels to reveal defense mechanisms against pathogens as well as protection against tumors and autoimmune diseases. The great advances in immunology in recent years make this field one of the most dynamic and rapidly growing in medical sciences. Critical ReviewsTM in Immunology (CRI) seeks to present a balanced overview of contemporary adaptive and innate immune responses related to autoimmunity, tumor, microbe, transplantation, neuroimmunology, immune regulation and immunotherapy from basic to translational aspects in health and disease. The articles that appear in CRI are mostly obtained by invitations to active investigators. But the journal will also consider proposals from the scientific community. Interested investigators should send their inquiries to the editor before submitting a manuscript.