Exp Dermatol. 2012 Mar;21(3):223-6. doi: 10.1111/j.1600-0625.2011.01432.x.
Interferon-γ (IFNγ)-induced collapse of hair follicle (HF) immune privilege (IP) is a key element in the pathogenesis of alopecia areata. In this pilot study, we investigated whether the immunosuppressive neuropeptide, calcitonin gene-related peptide (CGRP), can protect from and/or restore IFNγ-induced HF-IP collapse. After showing that human scalp HFs express CGRP receptor-like receptor (CRLR) immunoreactivity, anagen HFs were cultured in the presence of IFNγ, with CGRP added before or after. Adding CGRP after IFNγ administration ('restoration assay') failed to downregulate IFNγ-induced ectopic MHC class I expression, while MHC class II expression was reduced. However, administering CGRP before IFNγ application ('protection assay') significantly reduced the IFNγ-induced overexpression and ectopic expression of MHC class I and II and reduced the increased degranulation of perifollicular mast cells induced by IFNγ. This suggests that CGRP may not restore HF-IP once it has collapsed, but may protect it from collapsing. Therefore, CRLR stimulation might help to retard AA progression.
干扰素-γ (IFNγ) 诱导的毛囊免疫特权 (IP) 崩溃是斑秃发病机制的关键因素。在这项初步研究中，我们研究了免疫抑制神经肽降钙素基因相关肽 (CGRP) 是否可以预防和/或恢复 IFNγ 诱导的 HF-IP 崩溃。在显示人类头皮毛囊表达 CGRP 受体样受体 (CRLR) 免疫反应性后，将处于生长期的毛囊在 IFNγ 的存在下进行培养，并在 IFNγ 给药之前或之后添加 CGRP。在 IFNγ 给药后添加 CGRP（“恢复测定”）未能下调 IFNγ 诱导的异位 MHC 类 I 表达，而 MHC 类 II 表达减少。然而，在 IFNγ 应用前给予 CGRP（“保护测定”）可显著降低 IFNγ 诱导的 MHC 类 I 和 II 的过度表达和异位表达，并减少 IFNγ 诱导的毛囊周围肥大细胞脱颗粒增加。这表明 CGRP 可能无法在 HF-IP 崩溃后恢复它，但可以保护它免于崩溃。因此，CRLR 刺激可能有助于减缓 AA 的进展。
