4.7 Article

Interferons and inflammasomes: Cooperation and counterregulation in disease

期刊

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MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2016.05.010

关键词

Interferon; IL-1 beta; IL-18; gram-negative bacteria; inflammasome; NLRP3; caspase-1; caspase-11; guanylate-binding protein; pyroptosis; AIM2; tuberculosis; multiple sclerosis; experimental autoimmune encephalomyelitis

资金

  1. German Research Foundation (DFG) [SFB 670, SFB 704, SFB 1123, SFB 645, TRR83, TRR57]
  2. European Research Council ERC Inflammact

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Interferons and the IL-1 family of cytokines have important roles in host defense against invading viruses and bacteria. Inflammasomes, multimeric cytosolic sensors of infection, are required for IL-1 beta and IL-18 processing and release. Interferons, IL-1 beta, and IL-18 are also implicated in autoimmune disease and chronic inflammation. Although independent but complementary pathways induce these cytokine subsets during infection, in some circumstances the cross-talk between these key inflammatory mediators is a particular requirement for effective host defense. In this review we will summarize recent discoveries concerning the potentiation of inflammasome responses by type I interferons, particularly in patients with gram-negative bacterial infections, and reflect on the molecular mechanisms of IFN-beta's immunosuppressive effects through modulation of inflammasome and IL-1 beta signaling in patients with tuberculosis and multiple sclerosis.

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