Dongjin Jeong, Hye Sung Kim, Hye Young Kim, Min Jueng Kang, Hyeryeon Jung, Yumi Oh, Donghyun Kim, Jaemoon Koh, Sung-Yup Cho, Yoon Kyung Jeon, Eun Bong Lee, Seung Hyo Lee, Eui-Cheol Shin, Ho Min Kim, Eugene C Yi, Doo Hyun Chung
To date, no study has demonstrated that soluble Fas ligand (sFasL)-mediated inflammation is regulated via interaction with Fas in vivo. We found that FasL interacts specifically with tumor necrosis factor receptor superfamily (TNFRSF)10B, also known as death receptor (DR)5. Autoantibody-induced arthritis (AIA) was attenuated in FasL ( Faslgld/gld )- and soluble FasL ( FaslΔs/Δs )-deficient mice, but not in Fas ( Faslpr/lpr and Fas-/- )- or membrane FasL ( FaslΔm/Δm )-deficient mice, suggesting sFasL promotes inflammation by binding to a Fas-independent receptor...
July 5, 2021: ELife