Il17b is one of the six members of the interleukin-17 family. Although its functions were once elusive, emerging research shows it plays significant roles in multiple biological processes. It exerts its effects through the Il17b-Il17rb signaling pathway, which has been implicated in various disease-related inflammation processes [1,2].

In a mouse model of DSS-induced colitis, Il17b deficiency led to severe colitis with exaggerated weight loss, shorter colon length, and elevated proinflammatory cytokines in the colon. Recombinant Il17b treatment alleviated the severity. Single-cell transcriptional analyses revealed that loss of Il17b increased neutrophil infiltration and enhanced inflammatory cytokines in intestinal macrophages [5].

In injured peripheral nerves, global or Schwann-cell-specific Il17b deletion reduced macrophage infiltration, myelin clearance, and axon regeneration, indicating its role in macrophage recruitment via the Il17b/Il17rb pathway [3].

In bleomycin-induced mouse lung fibrosis, either lung-microbiota depletion or Il17b deficiency ameliorated disease progression, suggesting a role of Il17b in promoting pulmonary fibrosis [4].

In conclusion, Il17b is crucial in regulating inflammation and tissue repair processes. Studies using gene knockout mouse models have revealed its importance in diseases such as colitis, nerve injury-related repair, and pulmonary fibrosis. Understanding Il17b's functions provides potential therapeutic targets for these disease areas.