Gilhar Amos, Landau Marina, Assy Bedia, Ullmann Yehuda, Shalaginov Raya, Serafimovich Sima, Kalish Richard S
Skin Research Laboratories, Flieman Medical Center, Haifa, Israel.
Clin Immunol. 2003 Mar;106(3):181-7. doi: 10.1016/s1521-6616(02)00042-6.
Alopecia areata is an autoimmune condition directed at hair follicles, which results in loss of hair. We have previously demonstrated that it is possible to transfer hair loss, along with the immunohistologic findings of alopecia areata, to human scalp grafts on Prkdc(scid) (SCID) mice by injection of autologous activated lesional T-cells. This study examines the cytokine profile of T-cells and follicular epithelium following transfer of hair loss. Two consistent findings significantly (P < 0.01) associated with hair loss were production of interferon-gamma-inducible protein-10 kDa (IP-10) by follicular epithelium (13/13), and production of INF-gamma by infiltrating T-cells (10/12). Noninjected control grafts regrew hair, and were generally negative for IP-10 (positive 2/9), and INF-gamma (positive 2/9), but expressed of IL-10 on the follicular epithelium (7/9). These data support an INF-gamma TH1 pathogenesis for hair loss in alopecia areata.
斑秃是一种针对毛囊的自身免疫性疾病，可导致脱发。我们之前已经证明，通过注射自体活化的病变T细胞，有可能将脱发以及斑秃的免疫组织学表现转移到Prkdc(scid)（SCID）小鼠的人类头皮移植片上。本研究检测了脱发转移后T细胞和毛囊上皮细胞的细胞因子谱。与脱发显著相关（P < 0.01）的两个一致发现是，毛囊上皮细胞产生γ干扰素诱导蛋白10 kDa（IP-10）（13/13），以及浸润性T细胞产生INF-γ（10/12）。未注射的对照移植片毛发再生，IP-10（阳性2/9）和INF-γ（阳性2/9）通常为阴性，但毛囊上皮细胞表达IL-10（7/9）。这些数据支持γ干扰素TH1型脱发斑秃的发病机制。
