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1.A.109.  The Interleukin 1 (IL1) Family 

Interleukin 1α, IL1A or IL1α, is produced by activated macrophages, and IL-1 isoforms stimulate thymocyte proliferation by inducing IL-2 release. IL-1 proteins are involved in the inflammatory response, being identified as endogenous pyrogens, and are reported to stimulate the release of prostaglandin and collagenase from synovial cells.  They also disrupt the sertoli cell barrier/blood-testis barrier by blocking Cx43 (TC# 1.A.24.1.1)-dependent gap junction communication (Chojnacka et al. 2016)

Extracellular Interleukin-1β (IL-1β, IL1B, IL1F2), which regulates of the inflammatory response, is secreted depending on the processing of a precursor form following the activation of the multimolecular inflammasome complex (see TC# 9.A.48). The secretion of IL-1β after inflammasome activation requires membrane permeabilization and occurs in parallel with the death of the secreting cell. In macrophages, the release of IL-1β in response to inflammasome activation appears to be a secretory process independent of nonspecific leakage of proteins during cell death. The mechanism of membrane permeabilization leading to IL-1β release is distinct from the unconventional secretory mechanism employed by its structural homologues fibroblast growth factor 2 (FGF2) or IL-1α, a process that involves the formation of membrane pores but does not result in cell death (Martín-Sánchez et al. 2016).

References associated with 1.A.109 family:

Chojnacka, K., B. Bilinska, and D.D. Mruk. (2016). Interleukin 1α-induced disruption of the Sertoli cell cytoskeleton affects gap junctional communication. Cell Signal 28: 469-480. 26879129
Martín-Sánchez, F., C. Diamond, M. Zeitler, A.I. Gomez, A. Baroja-Mazo, J. Bagnall, D. Spiller, M. White, M.J. Daniels, A. Mortellaro, M. Peñalver, P. Paszek, J.P. Steringer, W. Nickel, D. Brough, and P. Pelegrín. (2016). Inflammasome-dependent IL-1β release depends upon membrane permeabilisation. Cell Death Differ 23: 1219-1231. 26868913