Faculty Research 1990 - 1999

Title

Experimental induction of alopecia areata-like hair loss in C3H/HeJ mice using full-thickness skin grafts.

Document Type

Article

Publication Date

1998

Keywords

Animal, Disease-Models-Animal, Female, Hair-Follicle: im, Human, Immunocompetence, Lymphocyte-Transformation, Male, Mice, Mice-Inbred-C3H, Mice-SCID, Skin-Transplantation: im, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-NON-P-H-S, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes: im

JAX Source

J Invest Dermatol 1998 Nov;111(5):797-803

Grant

AR43801/AR/NIAMS, CA34196/CA/NCI

Abstract

Alopecia areata (AA)-like hair loss in C3H/HeJ mice provides an excellent model for human AA disease research. The potential to induce mouse AA in normal haired C3H/HeJ mice at an early age or serially passage the AA phenotype was investigated by exchange of full-thickness skin grafts. Skin grafts from normal male and female C3H/HeJ, or severe combined immunodeficient C3H/SmnC Prkdc(scid)/J, mice onto AA-affected C3H/HeJ mice became inflamed and lost hair (28 of 28). Successful grafts from AA-affected C3H/HeJ mice induced hair loss in histocompatible C3H/OuJ mice (four of 13) and normal C3H/HeJ mice dependent on age (four of 17 at <31 d and 15 of 15 at >70 d). The AA phenotype was serially transmitted from induced AA mice to normal C3H/HeJ mice (nine of nine). Grafts from AA-affected C3H/HeJ mice onto C3H/SmnC Prkd(scid)/J mice resulted in depigmented hair fiber regrowth and perifollicular neutrophil and eosinophil infiltrates but no hair loss (15 of 15). Sham grafting did not induce AA (none of 10). The finding that AA can be serially transferred from AA-affected C3H/HeJ mice to normal littermates and C3H/ OuJ mice, indicates that an immune response against hair follicles can be induced with suitable stimuli. Conversely, skin grafts from normal C3H/HeJ, or C3H/SmnC Prkd(scid)/J, mice rapidly lose hair due to lymphocyte, but not neutrophil and eosinophil, mediated inflammation. This AA induction method reproducibly provides large numbers of AA-affected mice to study the pathogenesis and treatment of human AA.