Scientists discover a surprising connection between immune health and hair growth

LA JOLLA, Calif. — Hair-raising new research has found a surprising link between the human immune system and hair growth. Scientists at the Salk Institute for Biological Studies say they weren’t even trying to find this connection, but the evidence emerged while they were examining autoimmune diseases — like alopecia.

Alopecia is an autoimmune disorder which sees the body attack its own hair follicles, causing them to fall out. Generally, this happens in clumps, leaving patients with large patches of missing hair. Actress Jada Pinkett Smith has become one of the most well-known people dealing with alopecia in recent years.

Now, researchers have uncovered an unexpected molecular target in a common treatment for the condition. Their study discovered that regulatory T cells interact with skin cells to generate and grow new hair.

“For the longest time, regulatory T cells have been studied for how they decrease excessive immune reactions in autoimmune diseases,” says corresponding author Ye Zheng, associate professor in Salk’s NOMIS Center for Immunobiology and Microbial Pathogenesis, in a media release. “Now we’ve identified the upstream hormonal signal and downstream growth factor that actually promote hair growth and regeneration completely separate from suppressing immune response.”

Scientists discover the ability to regenerate hair

Originally, the team was examining the roles these specific immune cells and glucocorticoid hormones play in the development of autoimmune conditions like multiple sclerosis, Crohn’s disease, and asthma. Glucocorticoid hormones are steroid hormones derived from cholesterol and produced by the body’s adrenal gland.

However, researchers found that glucocorticoids and regulatory T cells don’t work together to play any significant role in these conditions. That led the team to examine areas of the body where the T cells do express high levels of glucocorticoid receptors — like the skin. When the study authors triggered hair loss in normal lab mice and mice lacking glucocorticoid receptors in their T cells, they discovered a hair-raising connection.

“After two weeks, we saw a noticeable difference between the mice—the normal mice grew back their hair, but the mice without glucocorticoid receptors barely could,” says first author Zhi Liu, a postdoctoral fellow in the Zheng lab. “It was very striking, and it showed us the right direction for moving forward.”

Researchers add their findings suggest that there is some level of communication going on between the immune system’s regulatory T cells and a person’s hair follicle stem cells which causes hair to grow. Moreover, the research shows regulatory T cells and glucocorticoid hormones are not just immunosuppressants, they also have the ability to trigger regeneration.

T cells work a hair-growing side gig

Specifically, the team found that glucocorticoids instruct the T cells to activate hair follicle stem cells. This process causes your hair to grow. This communication relies on a system where glucocorticoid receptors in the T cells begin producing a protein called TGF-beta3. This protein pushes the stem cells to differentiate into new strands of hair.

Interestingly, the Salk team discovered that this process is completely separate from the T cells’ normal job of maintaining good immune health. Moreover, regulatory T cells don’t normally produce TGF-beta3. The study finds that the cells only do this when sensing an injury to muscle and heart tissue — but this is similar to how removing hair in the study simulates a skin tissue injury.

“In acute cases of alopecia, immune cells attack the skin tissue, causing hair loss. The usual remedy is to use glucocorticoids to inhibit the immune reaction in the skin, so they don’t keep attacking the hair follicles,” Zheng explains. “Applying glucocorticoids has the double benefit of triggering the regulatory T cells in the skin to produce TGF-beta3, stimulating the activation of the hair follicle stem cells.”

The study is published in the journal Nature Immunology.

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