Interleukin-37

Interleukins (from Latin/Greek inter = between; leukos = white; kinein = to move) are a group of endogenous, short-chain regulatory proteins (cytokines) of the immune system (IL1-IL38). Interleukins are mediators for the induction, progression and control of T-cell-mediated cytotoxic immune reactions and B-cell activation (antibody production). They are mainly produced and secreted by stimulated leukocytes, monocytes and macrophages. To date, around 38 different interleukins have been clearly identified. Each cytokine in the interleukin group is assigned a nomenclatural number for its classification.

Interleukin-37 is a protein that belongs to the interleukin-1 cytokine family. The cytokine is regarded as a ligand for the interleukin-18 receptor (IL18R1/IL-1Rrp) and binds to the beta subunit of the IL18 receptor. The function of interleukin-18 is inhibited via this cytokine-IL-18 receptor complex.

Interleukin-37 is expressed in macrophages, in epithelial cells. The expression leads to a suppression of pro-inflammatory cytokines.

IL-37 is a potent inhibitor of innate immunity. It has been shown that interleukin-37 plays an important immunosuppressive role in the pathogenesis of psoriasis. This leads to a suppression of pro-inflammatory cytokines. Therapeutic consequences remain to be seen.

Interleukin-37 (IL-37) has a broad inhibitory effect on innate immunity functions. IL-37 transgenic mice are protected against lipopolysaccharide-induced shock. In Behçet's disease, it has been shown that reduced IL-37 expression is associated with an increased inflammatory response. The use of systemic glucocorticoids, on the other hand, leads to an increase in IL-37 mRNA.

1. Bouali E et al (2015) Interleukin-37 expression is decreased in Behçet's disease and is associated with inflammation. Immunol Lat. 167:87-94.
2. Dinarello CA et al. (2013) Interleukin-37th Semin Immunol. 25:466-468.
3. Teng X et al (2014) IL-37 ameliorates the inflammatory process in psoriasis by suppressing proinflammatory cytokine production. J Immunol 192:1815-1823.