A novel IL-23p19/Ebi3 (IL-39) cytokine mediates inflammation in Lupus-like mice

By Xiaoqian Wang, Yinxiang Wei, He Xiao, Xiaoling Liu, Yu Zhang, G. Han, Guojiang Chen, C. Hou, N. Ma, B. Shen and 3 more. 2016

167 citations recorded by the source corpus.

Interleukin‐12 family cytokines have emerged as critical regulators of immunity with some members (IL‐12, IL‐23) associated with disease pathogenesis while others (IL‐27, IL‐35) mitigate autoimmune diseases. Each IL‐12 family member is comprised of an α and a β chain, and chain‐sharing is a key feature. Although four bona fide members have thus far been described, promiscuous chain‐pairing between alpha (IL‐23p19, IL‐27p28, IL‐12/IL‐35p35) and beta (IL‐12/IL‐23p40, IL‐27/IL‐35Ebi3) subunits, predicts six possible heterodimeric IL‐12 family cytokines. Here, we describe a new IL‐12 member composed of IL‐23p19 and Ebi3 heterodimer (IL‐39) that is secreted by LPS‐stimulated B cells and GL7+ activated B cells of lupus‐like mice. We further show that IL‐39 mediates inflammatory responses through activation of STAT1/STAT3 in lupus‐like mice. Taken together, our results show that IL‐39 might contribute to immunopathogenic mechanisms of systemic lupus erythematosus, and could be used as a possible target for its treatment.

Subfields: Immunology, Oncology

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Citations in the corpus

Structural activation of pro-inflammatory human cytokine IL-23 by cognate IL-23 receptor enables recruitment of the shared receptor IL-12Rβ1 (2017, background): “For instance, IL-39 has been recently introduced as a pro-inflammatory cytokine comprising the helical subunit IL-23p19 coupled to Epstein-Barr virus-induced protein 3 (EBI3), and has been proposed to signal via IL-23R and gp130 (Wang et al., 2016).”