The striking link between the immune system and hair growth

Summary: Regulatory T cells use glucocorticoid hormones with skin cells to form new hair follicles and promote hair growth. Studies may have a positive impact on the development of new therapies for the treatment of alopecia and other hair loss disorders.

A source: Salk Institute

Salk’s scientists have discovered an unexpected molecular goal in the general treatment of alopecia, in which the human immune system attacks hair follicles and causes hair loss.

Results, published Natural immunology On June 23, 2022, describe how immune cells, known as regulatory T cells, interact with skin cells using the hormone as a messenger to create new hair follicles and hair growth.

“For a long time, regulatory T-cells have been studied to reduce excess immune responses in autoimmune diseases,” says Ye Zheng, an associate professor at Salk’s NOMIS Center for Immunobiology and Microbial Pathogenesis.

“We have now identified a hormonal signal and a low growth factor that promotes hair growth and regeneration, completely different from suppressing the immune response.”

Researchers did not start by studying hair loss. They were interested in studying the role of regulatory T cells and glucocorticoid hormones in autoimmune diseases. (Glucocorticoid hormones are steroid hormones derived from cholesterol produced by the adrenal glands and other tissues.) They first studied how these immune components work in multiple sclerosis, Crohn’s disease, and asthma.

They found that glucocorticoids and regulatory T cells do not work together to play an important role in any of these conditions. Thus, they thought that T cells would be more successful in regulatory environments that reflected particularly high levels of glucocorticoid receptors (in response to glucocorticoid hormones), such as in the skin tissue.

The researchers found that normal mice and mice that did not have glucocorticoid receptors in their regulatory T cells lost their hair.

“After two weeks, we found a significant difference between the mice – normal mice had hair growth, but mice without glucocorticoid receptors could barely do it,” said Zhi Liu, the first author of Zheng Laboratory.

“It was very surprising and showed us the right direction to move forward.”

Studies have suggested that there must be some connection between the regulatory T cells and the stem cells of the hair follicle to ensure hair regeneration.

Using a variety of methods to control multicellular communication, the researchers studied the behavior of regulatory T cells and glucocorticoid receptors in skin tissue samples.

They found that glucocorticoids command regulatory T-cells to activate the stem cells of the hair follicle, which leads to hair growth. This intersection between T cells and stem cells depends on a mechanism that induces the production of TGF-beta3 protein inside T cells, which is regulated by glucocorticoid receptors.

Studies have suggested that there must be some connection between the regulatory T cells and the stem cells of the hair follicle to ensure hair regeneration. Image in public domain

TGF-beta3 then activates the stem cells of the hair follicle and differentiates into new hair follicles, which promotes hair growth. Additional analysis confirmed that this pathway is completely independent of T-cells’ ability to maintain immune balance.

However, regulatory T cells do not normally produce TGF-beta3, as is the case here. When researchers scan databases, this phenomenon is found in injured muscle and heart tissue, and in this study, hair removal simulates a skin tissue injury.

“In acute cases of alopecia, immune cells attack the skin tissue and cause hair loss. The usual measure is to use glucocorticoids to suppress the skin’s immune response, so they should not attack the hair follicles, ”said Zheng. “The use of glucocorticoids activates regulatory T-cells in the skin to produce TGF-beta3 and stimulates the activation of hair follicle stem cells.”

This study showed that regulatory T-cells and glucocorticoid hormones have not only immunosuppressants but also regenerative function. The researchers then looked at other injury models and isolated regulatory T cells from damaged tissue to monitor elevated levels of TGF-beta3 and other growth factors.

Funding: This work was supported by the NOMIS Scholarship and the NOMIS Foundation, National Institutes of Health (NCI CCSG P30-014195, NIA P01-454 AG073084, NIA-NMG RF1-AG064049, NIA P30-AG068635, R01-111015, R01-111015 -AI154919 and S10-OD023689), Leona M. and Harry B. Helmsley Charitable Trust, Crown and Colitis Foundation, National Cancer Institute and Salk Cancer Center Key Facilities (P30-CA014195).

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Other authors: Xianting Hu, Yuziong Liang, Jinting Yu and Salk’s Maxim N. Шохирев; and Huabin Lee from Fudan University in Shanghai.

It’s about research on the immune system and hair growth

Author: Press service
A source: Salk Institute
The connection: Press Service – Salk Institute
Photo: Image in public domain

Original study: Closed access.
“Glucocorticoid signaling and regulatory T cells cooperate to maintain the location of the stem cell of the hair follicle,” Ye Zheng et al. Natural immunology


Glucocorticoid signaling and regulatory T cells work together to maintain the location of the stem cell of the hair follicle.

The maintenance of tissue homeostasis depends on the communication between the stem cells in a cell and the supporting cells. Regulatory T cells (T)reg cells) emerge as an important component of the stem cell cell to support their differentiation.

How Treg Cells sense dynamic signals in this microenvironment and their relationship to stem cells is often unknown. In this study, T using hair follicles (HFs)reg At the intersection of the cell and the stem cell, we find that the unrecognized function of the steroid hormone glucocorticoid is skin-resident T.reg to facilitate HF stem cell activation (HFSC) activation and HF regeneration.

Ablation of glucocorticoid receptor (GR) in T.reg The cells inhibit hair regeneration without affecting immune homeostasis. Mechanically GR and Foxp3 Treg to induce transformative growth factor β3 (TGF-β3), which activates Smad2 / 3 in cells HFSCs and facilitates HFSC proliferation.

This study Treg The cells and HFSCs mediate through the GR-TGF-β3 axis, highlighting possible means of T manipulation.reg Cells to support tissue regeneration.

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