AI Article Synopsis
- IL-1β and IL-18 enhance the immune system's ability to fight infections by boosting the antimicrobial functions of phagocytes and activating Th1 and Th17 adaptive immune responses.
- Inflammasomes are protein complexes that trigger the activation of caspase-1, which processes inactive forms of IL-1β and IL-18 into their active forms.
- The review examines debates surrounding how inflammasomes are activated during infections and suggests that other mechanisms, such as proteases from neutrophils or cytotoxic T cells, may also play a role in processing IL-1β and IL-18.
Article Abstract
Interleukin-1β (IL-1β) and IL-18 contribute to host defense against infection by augmenting antimicrobial properties of phagocytes and initiating Th1 and Th17 adaptive immune responses. Protein complexes called inflammasomes activate intracellular caspase-1 autocatalytically, which cleaves the inactive precursors of IL-1β and IL-18 into bioactive cytokines. In this review, we discuss the controversies regarding inflammasome activation and the role of the inflammasome during infection. We highlight alternative mechanisms for processing IL-1β and IL-18 during infection, which involve extracellular cleavage of the inactive cytokines by neutrophil-derived serine proteases or proteases released from cytotoxic T cells.
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| http://dx.doi.org/10.1016/j.it.2011.01.003 | DOI Listing |
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