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Mitochondrial reactive oxygen is critical for IL-12/IL-18-induced IFN

Por um escritor misterioso

Last updated 20 setembro 2024

Frontiers Reactive oxygen species formation and its effect on CD4+ T cell-mediated inflammation

IL-33 regulates M1/M2 chemokine expression via mitochondrial redox-related mitophagy in human monocytes - ScienceDirect

Frontiers Interleukin-18 in Inflammatory Kidney Disease

Mitochondrial control of inflammation

Mitochondrial respiration contributes to the interferon gamma response in antigen-presenting cells

Mitochondrial oxidative stress drives IL-12/IL-18-induced IFN-γ production by CD4+ T cells and is controlled by Fas

Mitochondrial-derived damage-associated molecular patterns amplify neuroinflammation in neurodegenerative diseases

IJMS, Free Full-Text

PDF) Mitochondrial reactive oxygen is critical for IL-12/IL-18-induced IFN-γ production by CD4+ T cells and is regulated by Fas/FasL signaling

Mitochondrial reactive oxygen is critical for IL-12/IL-18-induced IFN-γ production by CD4+ T cells and is regulated by Fas/FasL signaling

Mitochondrial reactive oxygen species regulate the induction of CD8+ T cells by plasmacytoid dendritic cells

Journal of Cellular Physiology, Cell Biology Journal

IJMS, Free Full-Text

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