Cd109, a glycosylphosphatidylinositol-anchored glycoprotein, is a member of the α2 -macroglobulin/C3,C4,C5 family of thioester-containing proteins. It associates with transforming growth factor (TGF)-β receptors and negatively regulates TGF-β signaling, and is potentially related to signal transducer and activator of transcription-3 signaling [1]. Cd109's functions span across various biological processes, influencing immune responses, inflammation, and tumor progression [2]. Genetic models, such as knockout mouse models, are valuable for studying its functions.

Cd109 -deficient mice exhibit epidermal hyperplasia and osteopenia, indicating its role in maintaining physiological homeostasis [1]. In asthma, Cd109 -deficient mice had reduced airway hyperreactivity and eosinophilic inflammation, along with lower Th2 cytokine expression. Lung cDC2s from these mice had a poor ability to induce cytokine production, suppressing Th2 differentiation [3]. In bleomycin-induced pulmonary fibrosis, Cd109 -transgenic mice overexpressing Cd109 showed attenuated pulmonary fibrosis, preserved lung function, and reduced lung fibroblasts and myofibroblasts [4].

In conclusion, Cd109 plays crucial roles in maintaining physiological homeostasis, regulating immune responses in asthma, and modulating pulmonary fibrosis. Gene knockout mouse models have been instrumental in revealing these functions, contributing to our understanding of related disease mechanisms and potentially offering new therapeutic strategies for diseases like asthma and pulmonary fibrosis.