@article{oai:kanazawa-u.repo.nii.ac.jp:00026880,
 author = {Matsushita, Takashi and Fujimoto, Manabu and Hasegawa, Minoru and Matsushita, Yukiyo and Komura, Kazuhiro and Ogawa, Fumihide and Watanabe, Rei and Takehara, Kazuhiko and Sato, Shinichi},
 issue = {12},
 journal = {Journal of Investigative Dermatology},
 month = {Dec},
 note = {The tight-skin (TSK/+) mouse, a genetic model for systemic sclerosis (SSc), develops cutaneous fibrosis and autoimmunity. Although immunological abnormalities have been demonstrated in TSK/+ mice, the roles of B-cell-activating factor belonging to the tumor necrosis factor family (BAFF), a potent B-cell survival factor, have not been investigated. Serum BAFF levels in TSK/+ mice were examined by ELISA. Newborn TSK/+ mice were treated with BAFF antagonist, and then skin fibrosis of 8-week-old mice was assessed. Serum BAFF levels were significantly elevated in TSK/+ mice. Remarkably, BAFF antagonist inhibited the development of skin fibrosis, hyper-γ-globulinemia, and the autoantibody production in TSK/+ mice. The skin from TSK/+ mice showed upregulated expressions of fibrogenic cytokines, such as IL-6 and IL-10, while BAFF antagonist significantly suppressed them. Reciprocally, BAFF antagonist augmented antifibrogenic cytokines, such as IFN-γ, in the skin of TSK/+ mice. Furthermore, TSK/+ B cells with BAFF stimulation had a significantly enhanced ability to produce IL-6. The results suggest that BAFF/BAFF receptor system is critical for the development of skin fibrosis in TSK/+ mice and could be a potent therapeutical target. © 2007 The Society for Investigative Dermatology.},
 pages = {2772--2780},
 title = {BAFF antagonist attenuates the development of skin fibrosis in Tight-Skin Mice},
 volume = {127},
 year = {2007}
}