ILC1-like cells may contribute to hair loss in alopecia areata.
5 citations
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February 2008 in “Histopathology” 4 citations
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January 2016 in “Methods in molecular biology” Hair follicle stem cells can become nerve cells using specific treatments.
August 2021 in “The journal of investigative dermatology/Journal of investigative dermatology” TAGX-0003 protected hair follicles and reversed alopecia areata in a mouse model.
September 2019 in “Journal of Investigative Dermatology” Researchers developed a 3D skin model with its own immune and blood vessel cells to better understand skin health and disease.
4 citations
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January 2023 in “Proteomes” Tumor proteins can both promote and suppress cancer, depending on the situation.
6 citations
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December 2021 in “Journal of Cancer Research and Therapeutics” The treatment improved survival and controlled cancer spread but required managing side effects like rashes.
May 2025 in “Journal of Inflammation Research” Natural killer and CD8+ T cells play a key role in hair loss in androgenetic alopecia.
April 2019 in “Journal of Investigative Dermatology” The humanized AA mouse model is better for testing new alopecia areata treatments.
7 citations
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May 1993 in “Journal of the European Academy of Dermatology and Venereology” Cell adhesion molecules are important in the development of certain skin diseases.
26 citations
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July 2016 in “PLOS ONE” Activating β-catenin in certain skin cells speeds up hair growth in mice.
September 2019 in “The journal of investigative dermatology/Journal of investigative dermatology” Mononuclear cells may protect against certain chemotherapy-induced hair loss.
September 2019 in “The journal of investigative dermatology/Journal of investigative dermatology” PPARγ signaling modulation can protect hair follicle stem cells from chemotherapy-induced damage.
Controlling Tslp can improve health in AEC syndrome patients.
2 citations
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January 2014 in “Journal of Cytology & Histology” Rapamycin and anti-EGFR antibody reduce LAM/TSC cell migration and blood vessel growth in the uterus.
April 2019 in “The journal of investigative dermatology/Journal of investigative dermatology” Targeting cholesterol, fatty acids, fibrosis, and mast cells may help treat CCCA.
48 citations
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March 2003 in “International Journal of Cancer” DMBT1 and galectin-3 may help suppress epithelial skin cancer.
57 citations
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June 2003 in “American Journal of Physiology-cell Physiology” Cyclosporin A helps mice grow hair by blocking a specific protein activity in skin cells.
April 2023 in “Journal of Investigative Dermatology” CD206+ macrophages are crucial for hair growth in alopecia areata treatment.
Neutrophils are key in causing chronic itch in atopic dermatitis, and blocking CXCR3 could reduce this itch.
July 2024 in “Journal of Investigative Dermatology” July 2024 in “Journal of Investigative Dermatology” IL-13 protein is much higher in the skin of atopic dermatitis patients than in healthy skin.
8 citations
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September 2017 in “Scientific Reports” MAD2B slows down the growth of skin cells that are important for hair development by interacting with TCF4.
June 2017 in “Experimental and Therapeutic Medicine” The anti-CXCL4 antibody helps mice grow hair faster and prevents hair loss.
2 citations
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December 2016 in “Experimental cell research” The research found a way to identify and study skin cells with stem cell traits, revealing they behave differently in culture and questioning current stemness assessment methods.
May 2023 in “Frontiers in Endocrinology” Blocking CRF1 receptors improved male hormone levels and reduced testicular tumor size in men with a specific adrenal condition.
Ca²⁺-mediated protein citrullination controls cell growth in the CNS and may help treat brain tumors.
11 citations
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January 1999 in “Dermatology” 1 citations
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January 1998 in “International journal of cancer” Rubbing vitamin D3 on skin can help prevent hair loss from chemotherapy and slow breast tumor growth in mice.
Alopecia areata involves immune system changes, especially in severe cases, with potential new treatment targets identified.