PhD. Raquel Cuevas-Díaz Durán

The immune system and the hair follicle

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Alopecia areata is a condition in which the immune system attacks an individual’s own hair follicles, causing hair loss. The key players in this story are regulatory T cells, whose role has been studied for a long time in the context of autoimmune diseases.

From immunosuppression to regeneration:

However, a study conducted by scientists from the Salk Institute revealed that these immune cells, called Regulatory T cells, are not only immunosuppressive but also interact with skin cells using a hormone to promote hair growth and regeneration.

These unexpected hormones are glucocorticoid hormones, derived from cholesterol and produced in various parts of the body. They are used by regulatory T cells as messengers to stimulate hair regeneration.

This process is a revelation in the field of hair medicine, as it was believed that these cells only suppressed the immune response.

Research at the Salk Institute

Scientists at the Salk Institute began their research without the intention of studying hair loss. However, when they studied mice with glucocorticoid receptors and induced hair loss, they observed surprising results.

Mice with glucocorticoid receptors experienced significant hair growth compared to those lacking these receptors.

This discovery opened up new perspectives in the treatment of alopecia and other conditions related to hair loss.

In cases of acute alopecia, we now know that applying glucocorticoids also has the additional benefit of stimulating the production of TGF-3 by the skin’s regulatory T cells, which promotes the activation of hair follicle stem cells.

Now you know, at CapilarFix, we take pride in staying at the forefront of hair research. We are committed to improving the quality of life of our patients and harnessing these scientific advances for the benefit of those struggling with hair loss.

References:

[1] Glucocorticoids initiate regulatory T cell and stem-cell crosstalk to grow new hair. Nat Immunol 23, 1006–1007 (2022). https://doi.org/10.1038/s41590-022-01250-x