What if a closer look at the immune system could provide a better understanding of hair loss, more specifically alopecia areata, a condition in which a person’s immune system attacks their own hair follicles, causing hair loss? Anyway, that’s the path taken by researchers at the Salk Institute in California who recently shared their discovery in the journal Nature’s immunity. Their study claims that immune cells called regulatory T cells (or T lymphocytes) interact with skin cells using a hormone as a transmitter to generate new hair follicles and grow hair. Regulatory T cells are a subpopulation of immune cells that prevent each individual from provoking immune reactions against its own. In the context of some diseases, these mechanisms may be defective: then we are talking about autoimmune reactions. “ For a very long time, regulatory T cells have been studied to see how they reduce excessive immune responses in autoimmune diseases. ,” explains one of the study’s authors, Professor Yi Cheng.
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He adds: Now we have identified the upstream hormone and downstream growth factor signaling that promote hair growth and regeneration completely separately from inhibiting the immune response.. The scientists did not begin studying hair loss because they wanted to study the roles of regulatory T cells and glucocorticoid hormones in autoimmune diseases, steroid hormones derived from cholesterol produced by the adrenal gland, and other tissues. They first studied the performance of these immune components in multiple sclerosis, Crohn’s disease (a chronic inflammatory disease of the digestive system) and asthma. They found that the glucocorticoids and regulatory T cells did not work together to play a significant role in any of these conditions. Thus, they thought they would have better luck given environments in which regulatory T cells express particularly high levels of glucocorticoid receptors (which respond to glucocorticoid hormones), such as in skin tissue.
A real “regeneration function” has been discovered
To do this, the scientists caused hair loss in normal mice and mice that lacked the glucocorticoid receptors in regulatory T cells. “ After two weeks, we noticed a noticeable difference: normal mice grew their hair back, but mice without glucocorticoid receptors could hardly do so. », says the scientific team. These early results therefore suggested that some kind of communication must occur between regulatory T cells and hair follicle stem cells to enable hair regeneration. The scientists then studied the behavior of regulatory T cells and glucocorticoid receptors in skin tissue samples. There they discovered that glucocorticoids “directed” regulator T cells to activate hair follicle stem cells, which leads to hair growth. It turns out that this interaction between T cells and stem cells depends on a mechanism by which glucocorticoid receptors are stimulated to produce a protein called “TGF-beta3”, all within the regulatory T cells.
Hence it is TGF-beta3 that activates hair follicle stem cells, thus promoting hair growth. However, regulatory T cells do not normally produce TGF-beta3, as they did here. When the scientists scanned databases, they found that the phenomenon occurred in injured heart and muscle tissue, similar to the way hair removal mimics skin tissue damage during this study. “ In severe alopecia areata, immune cells attack the skin tissue, causing hair loss. The usual treatment is glucocorticoids to suppress the skin’s immune reaction, so that it does not continue to attack the hair follicles. Professor Pr Ye Zheng adds. “ The use of glucocorticoids has the dual benefit of stimulating regulatory T cells in the skin to produce TGF-beta3, which stimulates the activation of hair follicle stem cells. Regulatory T cells and glucocorticoid hormones are not only immunosuppressive, but also have a regenerative function. The scientists’ next step will be to isolate regulatory T cells from other affected tissues and monitor TGF-beta3 levels.