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    Mao et al. showed that phosphorylation and transcriptional upregulation of ASS1 mediated by JAK2 and STAT1, respectively, to deplete citrulline is essential for proinflammatory macrophage activation. High levels of intracellular citrulline resulting from ASS1 inhibition can bind and inhibit JAK2, leading to a blocked innate immune response in macrophages.

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    • 🖊️ Tsinghua University researchers present evidence in @MolecularCell that citrulline depletion by argininosuccinate synthetase is required for proinflammatory #macrophage activation and immune responses. https://t.co/six4FJCuV0 https://t.co/w3lAChqMCp

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    Focus Epithelial tuft cells are major producers of lipid mediators (leukotrienes) that drive allergic inflammation and host defense against worm parasites. (see the related Research Article by Ualiyeva et al.). Reviews …

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    • The new January issue of Science #Immunology is out! The cover article describes 3 tissue-resident #macrophage subsets. Other papers focus on cancer immunotherapy with shielded pro-IL-12 and stromal cells in the spleen. Plus more to come: https://t.co/I7FBgG3QGK https://t.co/S2oi6beLj2

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    The anaphylatoxin C5a is core effector of complement activation. C5a exerts potent proinflammatory and immunomodulatory actions through interacting with its C5a receptors, C5aR1 and C5aR2, modulating multiple signaling and functional activities of immune cells. Native C5a contains a large N -linked

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    • From the Trent Woodruff lab at @UQ_News | Suggest using recombinant human #C5a should be paired with #C5aR1 inhibitors, or purified/synthetic human C5a to confirm relevant findings https://t.co/RmESi8bU8W #ReadTheJI #immunology #complement #innateimmunology #macrophage https://t.co/S3JswTwy23