Calcitonin gene-related peptide (CGRP) may award relative protection from interferon-γ-induced collapse of human hair follicle immune privilege.

Exp Dermatol. 2012 Mar;21(3):223-6. doi: 10.1111/j.1600-0625.2011.01432.x.
Calcitonin gene-related peptide (CGRP) may award relative protection from interferon-γ-induced collapse of human hair follicle immune privilege.
Kinori M, Bertolini M, Funk W, Samuelov L, Meyer KC, Emelianov VU, Hasse S, Paus R.

Department of Ophthalmology, Sheba Medical Center, Tel Hashomer, Israel Department of Dermatology, University of Lübeck, Luebeck, Germany Klinik Dr. Kozlowski, Munich, Germany Department of Dermatology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel School of Translational Medicine, University of Manchester, Manchester, UK.

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.

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