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).



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.

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.

Yaqinuddin, A. and J. Kashir. (2020). Novel therapeutic targets for SARS-CoV-2-induced acute lung injury: Targeting a potential IL-1β/neutrophil extracellular traps feedback loop. Med Hypotheses 143: 109906. [Epub: Ahead of Print]


TC#NameOrganismal TypeExample

Interleukin-1 alpha, IL1α or IL1A, of 271 aas and 0 TMSs. Regulates gap junctional communication in Sertoli cells, which is critical for sertoli cell barrier/blood-testis barrier (BTB) restructuring (Chojnacka et al. 2016). 

IL1α of Homo sapiens


Interleukin 1β, IL1β, IL1beta, IL1B, IL1F2, of 269 aas.  Its release depends on its insertion into the membrane with the formation of a transmembrane pore (Martín-Sánchez et al. 2016). IL-1beta is generated by macrophages upon activation of intracellular NLRP3 (NOD-like, leucine rich repeat domains, and pyrin domain-containing protein 3), part of the functional NLRP3 inflammasome complex that detects pathogenic microorganisms and stressors, while neutrophils are enhanced by increasing levels of IL-1beta (Yaqinuddin and Kashir 2020).

IL1beta of Homo sapiens