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Treg dysfunction is linked to various autoimmune skin diseases, and understanding Treg properties is key for new treatments.

Using special RNA to target a mutant gene fixed hair problems in mice.

A gene mutation worsens skin irritation in mice due to a lack of certain fats.

A protein from certain immune cells is key for new hair growth after skin injury in mice.

A new mutation in the STING protein causes a range of symptoms and its severity may be affected by other genetic variations; treatment with a specific inhibitor showed improvement in one patient.

A new mutation in the TMEM173 gene and a risk allele in IFIH1 cause a unique set of immune-related symptoms.

Certain HLA class II alleles increase or decrease the risk of alopecia areata.

Genetic variations affecting skin structure play a key role in severe acne.

Tofacitinib is a promising treatment for children with rheumatic diseases.

IFN-γ and IL-2 are important for T cell activation in hair loss in mice.

The rs6152 allele is not a good marker for baldness in the Indonesian population, but family history, age, gender, high blood pressure, and body weight are linked to the risk.

Deleting the MAD2L1 gene is tolerated in certain mouse cancer models.

New hair regrowth model proposed, imiquimod found to kill skin cancer cells, T-cadherin loss linked to invasive skin cancer, no clear gene link to skin cancer after transplant, and study on children's hair loss shows male dominance and genetic ties.

CD8+ T cells are involved in alopecia areata and may cause disease relapse.

G allele of AR Stul polymorphism linked to higher hair loss risk, especially in white people.

Finasteride doesn't affect omeprazole metabolism in Japanese people.

Lymphocytes, especially CD8+ T cells, play a key role in causing alopecia areata, and targeting them may lead to new treatments.

Malt1 protease is essential for regulatory T cell function and could be targeted to boost antitumor immunity.

Scientists made a mouse model of a serious skin cancer by changing skin cells with a virus and a specific gene, which is similar to the disease in humans.

CD8+ T cells play a key role in graft-versus-host disease in certain mice models.

Activating TLR9 helps heal wounds and regrow hair by using specific immune cells.

The absence of functional sebaceous glands causes hair follicle destruction and scarring alopecia.

AR polyglycine repeat doesn't cause baldness.

NKG2D gene polymorphism doesn't affect SLE risk but may influence symptoms like rash and hair loss.

Mice treatments didn't grow hair, a patient treatment may affect immune response, and people with hair loss often feel anxious or depressed.

Normal skin cell renewal doesn't need RAR signaling, but vitamin A-related skin thickening does.

A new mouse mutation causes skin and hair defects due to a gene change.

Low serum complement levels in SLE patients don't always match with disease flares; monitoring C3 and C4 is useful, but cell-bound complement products might better indicate disease activity.

Cavity macrophages gather on organ surfaces but don't really invade or help repair the organs after injury.

A woman with a unique syndrome similar to TRPS has a genetic change near the TRPS1 gene, affecting its regulation.