Regression of Alopecia Areata by Heat Shock Protein Inhibition and Novel Protection of Chemotherapy-Alopecia

Regression of Alopecia Areata by Heat Shock Protein Inhibition and Novel Protection of Chemotherapy-Alopecia, Dr. Joaquin J.  Jimenez, M.D., Ph.D.

Animal models such as the C3H/HeJ mouse model have facilitated the study of AA. C3H/HeJ mice spontaneously develop AA in a pattern similar to humans.  AA is characterized inflammation of the hair follicle by specific cells of the immune system including, CD4+ and CD8+ white blood cells.  Despite knowing that an association exists between the immune system and alopecia areata; the precise molecular mechanisms mediating the development of this disease is still poorly understood. 

One area that has received attention in the medical literature is that of Heat Shock Proteins (HSP).  HSP are a group of proteins ubiquitously expressed in cells which react to physical stresses such as heat stress, radiation, hypoxia or chemical stimuli. Modulation of HSPs provides cells increased resistance to stress. We therefore hypothesized that HSPs, most specifically, HSP70 may play a role in the development of AA by affecting hair follicles. We then proceeded to locally administer heat in C3H/HeJ mice (48°C, for 20 minutes) daily starting at 6 months of age. At six months of age only 1-5% of animals develop AA.

We randomized the C3H/HeJ mice into two groups: 35 mice received treatment while 40 did not. After 6 weeks, we observed a statistically significant (p=0.000006) increase in the incidence of AA in the group receiving heat.  In conclusion, our results indicate that expression of HSP70 induced by localized heat application exacerbates the development of AA in C3H/HeJ mice and may be involved in the molecular pathway of AA in humans. 

Futher study is needed to confirm a similar mechanism in humans.