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Interleukin 1α and the inflammatory process

Abstract

Inflammation occurs after disruption of tissue homeostasis by cell stress, injury or infection and ultimately involves the recruitment and retention of cells of hematopoietic origin, which arrive at the affected sites to resolve damage and initiate repair. Interleukin 1α (IL-1α) and IL-1β are equally potent inflammatory cytokines that activate the inflammatory process, and their deregulated signaling causes devastating diseases manifested by severe acute or chronic inflammation. Although much attention has been given to understanding the biogenesis of IL-1β, the biogenesis of IL-1α and its distinctive role in the inflammatory process remain poorly defined. In this review we examine key aspects of IL-1α biology and regulation and discuss its emerging importance in the initiation and maintenance of inflammation that underlie the pathology of many human diseases.

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Figure 1: Molecular modifications of IL-1α that regulate its intracellular distribution and bioavailability.
Figure 2: Biological contexts of IL-1α-mediated signaling.
Figure 3: IL-1α-driven inflammatory loop model.

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Acknowledgements

Supported by the US National Institutes of Health (NIH) grants AI065429, AI126816 and AI107960 (D.M.S.), AI123126 (N.C.D.P.) and the Children's Healthcare of Atlanta Research Trust (D.M.S.).

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Di Paolo, N., Shayakhmetov, D. Interleukin 1α and the inflammatory process. Nat Immunol 17, 906–913 (2016). https://doi.org/10.1038/ni.3503

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