Cytokine secretion of interferon-gamma and tumor necrosis factor-alpha (None)

Cytokine secretion of interferon-gamma and tumor necrosis factor-alpha refers to the release of these two potent cytokines by immune cells such as Th1 T cells, cytotoxic T cells, NK cells, and macrophages. Both cytokines play pivotal roles in orchestrating immune responses, promoting inflammation, driving effector cell polarization, and mediating both protective and pathogenic processes. They can act synergistically to induce cell activation, immune-mediated killing, apoptosis, necroptosis, and immunosuppression (such as upregulation of PD-L1 in mesenchymal stem cells and some tumor microenvironments). Therapies often target the cytokines themselves or their receptors, especially in chronic inflammatory and autoimmune diseases, or modulate their secretion to enhance antitumor immunity. Overactivity or dysregulation of these cytokines is implicated in a wide range of diseases, from cancer to autoimmunity and infection.

Other names

IFN-γ and TNF-α secretionInterferon-gamma and tumor necrosis factor-alpha releaseTh1 cytokine secretion

Inhibition of cytokine action or secretion: Drugs block cytokines or their receptors, reducing immune activation and inflammation (e.g., anti-TNF biologics prevent TNF-alpha from binding receptor; anti-IFN-γ biologics neutralize IFN-γ). Modulation of cytokine signaling: JAK inhibitors block signaling pathways activated by these cytokines. Enhancement of immune effector function: In cancer, boosting cytokine secretion or signaling can augment antitumor immunity.