A research team at the Korea Advanced Institute of Science and Technology (KAIST) has found new immune T-cells responsible for alopecia areata, also known as circular hair loss.

When virtual memory T-cells are activated by antigen-unspecific cytokine stimulation, they differentiate into new immune cells with high cytotoxicity, which release cytotoxic substances to destroy hair follicles and cause alopecia areata.
When virtual memory T-cells are activated by antigen-unspecific cytokine stimulation, they differentiate into new immune cells with high cytotoxicity, which release cytotoxic substances to destroy hair follicles and cause alopecia areata.

Alopecia areata is a relatively common condition with a 1-2 percent prevalence, an inflammatory disease that invades the hair follicles.

It is a non-scarring autoimmune hair loss disease characterized by circular bald patches and can affect the hair on the head or any part of the body, causing a great deal of stress due to the changes in appearance.

While alopecia areata is known to be an autoimmune disease caused by immune cells, its pathogenesis has not been clearly understood until now.

To discover the pathogenesis of alopecia areata and propose new treatment strategies, the team, led by Professors Park Su-hyung and Shin Eui-cheol at KAIST Graduate School of Medical Science and Engineering, and Seok Joon of the Department of Dermatology at Chung-Ang University Hospital, analyzed the skin tissue and blood of alopecia areata patients and the skin and lymph nodes of mice induced with alopecia areata.

As a result, the researchers identified a new immune cell family derived from virtual memory T cells as the key to the development of alopecia areata for the first time.

Virtual memory T cells are a group of cells that already have an active immune function, despite not receiving antigen-specific stimulation and have been known to help control viral, bacterial, and parasitic infections and eliminate cancer cells.

The researchers found that cytokines (IL-12, IL-15, and IL-18) secreted from the skin activate virtual memory T cells, causing them to differentiate into a class of immune cells with high cytotoxic capacity, and these activated immune cells destroy hair follicle cells through antigen non-specific cytotoxicity via a receptor (NKG2D), causing alopecia areata.

Furthermore, the researchers found that the development of alopecia areata could be prevented by inhibiting the function of cytokines and the receptor (NKG2D).

The team said the findings of this study are significant in that they identify and characterize a new immune cell that can cause chronic inflammation in the human body, allowing doctors to look at the pathogenesis and treatment of chronic inflammatory and autoimmune diseases from a new perspective.

“The findings are scientifically and medically significant because they are the first to show that virtual memory T cells are not protective, but can be activated by antigen non-specific stimuli and cause inflammatory diseases,” Professor Park said. “Further research and development of new antibody therapeutics may provide new therapeutic strategies for the development of various chronic inflammatory diseases.”

The results of the research were published in Nature Immunology.

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