Recombinant human IL-17A/F humanized antibody(Livzon Pharmaceutical Group)

The pathobiology of IL‐17 in lung fibrogenesis is controversial. Here we examined the role of IL‐17A/F in bleomycin (BLM) and adenoviral TGF‐β1‐induced lung fibrosis in mice. In both experimental models, WT and IL17af−/− mice showed increased collagen contents and remodeled lung architecture as assessed by histopathological examination, suggesting that IL‐17A/F is dispensable for lung fibrogenesis. However, IL17af−/− mice responded to the BLM challenge with perturbed lung leukocyte subset recruitment. More specifically, bleomycin triggered angiocentric neutrophilic infiltrations of the lung accompanied by increased mortality of IL17af−/− but not WT mice. WT bone marrow transplantation failed to correct this phenotype in BLM‐challenged IL17af−/− mice. Conversely, IL17a/f−/− bone marrow transplantation → WT did not perturb lung leukocytic responses upon BLM. At the same time, IL17af−/− mice treated with recombinant IL‐17A/F showed an attenuated lung inflammatory response to BLM. Together, the data show that the degree of BLM‐driven acute lung injury was critically dependent on the presence of IL‐17A/F, while in both models, the fibrotic remodeling process was not.