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A.F. FOMINA (2020) 'ROLE OF INTRACELLULAR CALCIUM RELEASE CHANNELS IN CALCIUM SIGNALING IN T LYMPHOCYTES' in O.A. Krishtal, E.A. Lukyanetz (Eds.), ESSAYS ON NEUROPHYSIOLOGY BY PLATON KOSTYUK AND HIS STUDENTS, AKADEMPERIODYKA, pp. 141-146


ROLE OF INTRACELLULAR CALCIUM RELEASE CHANNELS IN CALCIUM SIGNALING IN T LYMPHOCYTES

A.F. FOMINA

    University of California, Davis, CA, 95616, USA
DOI: https://doi.org/10.15407/biph.books.EssNeur.141


Abstract

CD4+ helper T (Th) lymphocytes play a crucial role in immune responses, with calcium (Ca²⁺) signaling being essential for their activation and effector functions. Following T cell receptor (TCR) engagement, Ca²⁺ release from intracellular stores via inositol 1,4,5-trisphosphate receptors (IP3R) and ryanodine receptors (RyR) initiates a sustained Ca²⁺ influx through Ca²⁺ release-activated Ca²⁺ (CRAC) channels. This prolonged Ca²⁺ elevation regulates cytokine production, cytoskeletal remodeling, and proliferation. Disruptions in Ca²⁺ homeostasis can lead to immunodeficiency or autoimmunity. Pharmacological targeting of IP3R and RyR offers a potential therapeutic strategy for immune-related disorders. The study highlights the interplay between intracellular Ca²⁺ release channels and CRAC channels in Th cell function and explores the therapeutic implications of modulating these pathways.

Keywords: T cell activation, calcium signaling, CRAC channels, IP3 receptors, ryanodine receptors, cytokine production, immune response, apoptosis, immunosuppression, autoimmune diseases.

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