- 原著論文
論文発表:A CD4+ T cell-fibroblast crosstalk exacerbates autoimmunity in a mouse model of primary Sjögren disease.
安友康二先生、九十九伸一先生らの論文「A CD4+ T cell-fibroblast crosstalk exacerbates autoimmunity in a mouse model of primary Sjögren disease.」が掲載されました。
掲載誌等:Nature Communications, 17, 6325, 2026.
DOI:10.1038/s41467-026-72975-8
著者:Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Daisuke Kurotaki, Kei-Ichiro Yasunaga, Aya Ushio, Ruka Nagao, Keiko Aota, Yoshiaki Kitamura, Takaaki Tsunematsu, Hideo Yagita, Naozumi Ishimaru, Junko Morimoto and Koji Yasutomo
DOI:10.1038/s41467-026-72975-8
著者:Kunihiro Otsuka, Hiroyuki Kondo, Shin-ichi Tsukumo, Daisuke Kurotaki, Kei-Ichiro Yasunaga, Aya Ushio, Ruka Nagao, Keiko Aota, Yoshiaki Kitamura, Takaaki Tsunematsu, Hideo Yagita, Naozumi Ishimaru, Junko Morimoto and Koji Yasutomo
要約:CD4+ T cells are key drivers of immune-mediated tissue damage and participate in complex cellular interactions that perpetuate chronic inflammation. However, the specific subsets of pathogenic CD4+ T cells and their non-immune cell partners are less well characterized. Here, we use a mouse model of primary Sjögren disease (pSjD) and identify CD153+CD4+ T cells as critical drivers of inflammation during the early stages of autoimmune pathology. We describe a CD153+CD4+ T cell-CD30+ tissue-resident fibroblast interaction that promotes fibroblast proliferation and chemokine secretion, further driving immune cell infiltration and thereby amplifying the autoimmune response. Importantly, deletion of CD153 in CD4+ T cells or neutralization of fibroblast-derived chemokines reduces lymphocytic infiltration and significantly halts autoimmune-like pathology. The CD153-CD30 axis positively correlates with disease severity in human patients. Thus, our results describe a pathogenic, therapeutically targetable CD153+CD4+ T cell-CD30+ fibroblast axis that perpetuates chronic inflammation in pSjD.



