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The gamma-interferon pathway describes the cellular signaling events triggered by interferon gamma, a cytokine critical for innate and adaptive immunity. IFN-γ binds to a heterodimeric cell-surface receptor (composed of IFNGR1 and IFNGR2), leading to activation of the JAK/STAT pathway, upregulation of genes involved in immune surveillance and antigen presentation, and modulation of inflammation and cell proliferation. Dysregulation or therapeutic modulation of this pathway plays important roles in infection control, cancer immunology, autoimmunity, and inflammatory diseases. Recombinant interferon gamma and downstream pathway inhibitors (such as JAK inhibitors) exemplify therapeutics that interact directly or indirectly with this pathway.
Cytokine binding to cell-surface receptor (IFNGR1/IFNGR2), activating the JAK/STAT pathway and regulating gene transcription. Some drugs block or downregulate downstream signaling (e.g., JAK inhibitors), others supplement IFN-γ activity (recombinant IFN-γ).
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