Li Yunyuan, Kilani Ruhangiz T, Leung Gigi, Ghahary Aziz
Department of Surgery, Division of plastic Surgery, University of British Columbia, Vancouver, British Columbia, Canada.
Department of Surgery, Division of plastic Surgery, University of British Columbia, Vancouver, British Columbia, Canada.
J Investig Dermatol Symp Proc. 2020 Nov;20(1):S16-S21. doi: 10.1016/j.jisp.2020.04.001.
Alopecia areata (AA), which is defined as an autoimmune hair loss disease, has a serious impact on the quality of life for patients with AA worldwide. In this study, to our knowledge, a previously unreported method of AA induction in C3H mice has been established and validated. Using this method, we showed that dermal injection of 1-3 million of a mixture of skin cells freshly isolated from AA-affected skin induces AA in more than 80% of healthy mice. Contrary to the previous protocol, the induction of AA by this approach does not need any surgical AA skin grafting, cell manipulation, or high number of activated T cells. We also showed that dermal injection of adherent myeloid cells (mainly CD11b+) in healthy mice is as potent as a mixture of none adherent CD3+ T cells and CD19+ B cells in the induction of AA. Interestingly, most of the mice (7 out of 8) that received non-adherent cells developed AA universalis, whereas most of the mice (5 out of 7) that received adherent cells developed patchy AA. Finally, we found a high number of stage-specific embryonic antigen-expressing cells whose expression in monocytes in an inflammatory disease causes the release of inflammatory cytokines, TNF-α and IL-1β, from these cells in AA-affected skin.
斑秃(AA)被定义为一种自身免疫性脱发疾病,对全球范围内的斑秃患者的生活质量有严重影响。在本研究中,据我们所知,一种此前未报道的在C3H小鼠中诱导斑秃的方法已被建立并验证。使用这种方法,我们发现,向健康小鼠真皮内注射100万至300万个从斑秃病变皮肤新鲜分离的皮肤细胞混合物,可使超过80%的健康小鼠患上斑秃。与之前的方案不同,通过这种方法诱导斑秃不需要任何手术性斑秃皮肤移植、细胞操作或大量活化的T细胞。我们还发现,向健康小鼠真皮内注射贴壁髓样细胞(主要是CD11b+)在诱导斑秃方面与非贴壁CD3+T细胞和CD19+B细胞的混合物效果相当。有趣的是,大多数接受非贴壁细胞的小鼠(8只中的7只)患上了全秃,而大多数接受贴壁细胞的小鼠(7只中的5只)患上了斑秃。最后,我们在斑秃病变皮肤中发现了大量表达阶段特异性胚胎抗原的细胞,这些细胞在炎症性疾病的单核细胞中的表达会导致这些细胞释放炎症细胞因子TNF-α和IL-1β。