Heat shock protein 90, death-associated protein kinase 1 and other cold-induced proteins: Who’s to blame for cold-induced inflammasome activation in familial cold autoinflammatory syndromes?

Abstract

Many advances have been made to understand the pathogenesis of primary autoinflammatory syndromes. Several NOD-like receptors, such as NLRP3, NLRC4 and NLRP12 are at the center stage of the different types of familial cold autoinflammatory syndromes, but the mechanisms that govern their activation after cold exposure still need clarification. Here, I discuss several studies that demonstrate a link between cold-induced proteins and NLRP3, NLRC4 and NLRP12 activation, in particular, heat shock protein (HSP) 90 and death-associated protein kinase 1 (DAPK1). Therefore, I hypothesize that cold-induced proteins lead to inflammasome assembly, and suggest a methodological approach to validate the here proposed hypothesis.