Gilhar Amos, Keren Aviad, Paus Ralf
Skin Research Laboratory, Faculty of Medicine, Technion-Israel Institute of Technology and Flieman Medical Center, Haifa, Israel.
J Investig Dermatol Symp Proc. 2013 Dec;16(1):S37-8. doi: 10.1038/jidsymp.2013.11.
Although alopecia areata (AA) is not life threatening, it may lead to severe psychological disturbances, reducing the quality of life in all ages. Thus, a new animal model is needed for shedding more light onto the pathogenesis of this cell-mediated, organ-specific autoimmune disease to identify more effective therapeutic strategies. Recently, we succeeded in developing a new humanized mouse model of AA, which includes transplantation of healthy human scalp skin obtained from normal volunteers on to severe-combined immunodeficient mice. This is followed by intradermal injection of either autologous or allogeneic peripheral blood mononuclear cells, which had been cultured with high dose of IL-2 and enriched for natural killer group 2D-positive (NKG2D+) and CD56+ cells. This protocol leads to rapid and predictable development of focal hair loss, with all the characteristic clinical, histological, and immunohistochemical features of AA. This humanized mouse AA model underscores the functional importance of NKG2D+ and CD56+ cells in AA pathogenesis and promises to be instrumental for identifying novel AA treatment strategies.
尽管斑秃(AA)不会危及生命,但它可能导致严重的心理障碍,降低各年龄段患者的生活质量。因此,需要一种新的动物模型来更深入地了解这种细胞介导的器官特异性自身免疫性疾病的发病机制,以确定更有效的治疗策略。最近,我们成功开发了一种新的AA人源化小鼠模型,该模型包括将从正常志愿者获取的健康人头皮皮肤移植到重度联合免疫缺陷小鼠身上。随后进行皮内注射自体或异体外周血单个核细胞,这些细胞已用高剂量白细胞介素-2培养,并富集了自然杀伤细胞2D阳性(NKG2D+)和CD56+细胞。该方案可导致局灶性脱发快速且可预测地发展,具有AA所有特征性的临床、组织学和免疫组化特征。这种人源化小鼠AA模型强调了NKG2D+和CD56+细胞在AA发病机制中的功能重要性,并有望有助于识别新的AA治疗策略。