IL-36 beta/IL-1F8 Protein, Human (His)

IL-36 beta (IL-1F8), a subform of IL-36 family, belongs to IL-1 superfamily. IL-36 beta mediates inflammatory response. L-36 beta binds to IL-36R and recruits the co-receptor IL-1RacP, and thereby activating NF-κB and MAPK signaling pathways, but the activation requires N-terminal cleavage by neutrophil granule-derived proteases^[1][2]. IL-36 beta/IL-1F8 Protein, Human (His) is a recombinant human IL-36 beta with N terminal His tag, which is produced in E. coli.

IL-36 beta (IL-1F8), a subform of IL-36 family, belongs to IL-1 superfamily. IL-36 beta is expressed in monocytes, T/B-lymphocytes, bone-marrow, tonsils, heart, lung, testis, colon, neuron cells, glial cells^[3].
The sequence of amino acids in IL-36 beta differs in different species. Human IL-36 beta shares <40% aa sequence identity with mouse.
L-36 beta binds to IL-36R and recruits the co-receptor IL-1RAcP. So that heterodimeric signaling complex brings Toll/IL-1R (TIR) domains of the 2 receptor chains in close proximity, and thereby activating NF-κB and MAPK signaling pathways^[1]. But the activation requires N-terminal cleavage at Arg5 by neutrophil granule-derived proteases, such as cathepsin G, elastase and proteinase-3^[2]. IL-36β plays a role cell maturation in human bone marrow mononuclear cells and DC cells. IL-36β is associated with the development of inflammatory bowel disease (IBD). The serum levels of IL36β are usually higher in patients with IBD^[4].
IL-36 beta is a pro-inflammatory factor. IL-36 beta mediates inflammatory response through the activation of NF-κB and MAPK signaling pathway^[2].

IL-36 beta (human) (1 μg/mL, 24 h) induces the gene expression of themselves and other family members in keratinocytes^[5].
IL-36 beta (human) (1-5 ng/mL) increases IL-36R mRNA level in human blood lymphocytes^[6].
IL-36 beta (human) (1 ng/mL, 48 h) induces early proliferation of IL-36R expressing CD4+ T helper cells^[6].

Human

E. coli

N-His

Q9NZH7-2 (K5-E157)

27177  [NCBI]

Approximately 20 kDa

Greater than 95% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. Bassoy EY, et al. Regulation and function of interleukin-36 cytokines. Immunol Rev. 2018 Jan;281(1):169-178.  [Content Brief]

  [2]. Zhou L,et al. Interleukin-36: Structure, Signaling and Function. Adv Exp Med Biol. 2021;21:191-210.  [Content Brief]

  [3]. Gresnigt MS, et al. Biology of IL-36 cytokines and their role in disease. Semin Immunol. 2013 Dec 15;25(6):458-65.  [Content Brief]

  [4]. Zhu J, et al. Interleukin-36β exacerbates DSS-induce acute colitis via inhibiting Foxp3+ regulatory T cell response and increasing Th2 cell response. Int Immunopharmacol. 2022 Jul;108:108762.  [Content Brief]

  [5]. Carrier Y, et al. Inter-regulation of Th17 cytokines and the IL-36 cytokines in vitro and in vivo: implications in psoriasis pathogenesis. J Invest Dermatol. 2011 Dec;131(12):2428-37.  [Content Brief]

  [6]. Penha R, et al. IL-36 receptor is expressed by human blood and intestinal T lymphocytes and is dose-dependently activated via IL-36β and induces CD4+ lymphocyte proliferation. Cytokine. 2016 Sep;85:18-25.  [Content Brief]