ER stress activates the NLRP3 inflammasome via an UPR-independent pathway

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Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS)

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Blocking interleukin-1β in acute and chronic autoinflammatory diseases

(2010) C. A. Dinarello   JOURNAL OF INTERNAL MEDICINE

A role for mitochondria in NLRP3 inflammasome activation

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How the Noninflammasome NLRs Function in the Innate Immune System

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