September 2024 in “Journal of the American Academy of Dermatology” Regulatory γδ T cells help protect hair follicles from alopecia areata and promote hair regrowth.
January 2026 in “Medicina” CD34 is absent in most basal cell carcinoma cells but present in surrounding skin.
April 2018 in “Journal of Investigative Dermatology” The role of γδT-cells in causing alopecia areata remains unclear.
February 2025 in “PubMed” CS12192 effectively treats alopecia areata with better safety than current options.
2 citations
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April 2023 in “American Journal of Dermatopathology” CCCA may involve the PD1/PDL1 pathway and increased caspase 3, leading to permanent hair loss.
48 citations
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March 2003 in “International Journal of Cancer” DMBT1 and galectin-3 may help suppress epithelial skin cancer.
60 citations
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September 2015 in “Expert Review of Clinical Immunology” Lymphocytes, especially CD8+ T cells, play a key role in causing alopecia areata, and targeting them may lead to new treatments.
141 citations
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May 2007 in “Cancer Research” CD34 is crucial for skin tumor development in mice.
10 citations
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July 2021 in “Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin” LRIG1 is linked to better survival in Merkel cell carcinoma.
April 2018 in “Journal of Investigative Dermatology” CENPV, a new partner of CYLD, helps regulate ciliary acetylated tubulin and is overexpressed in certain skin tumors.
October 1984 in “Immunology Today” 5 citations
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March 2020 in “Thoracic Cancer” CT-707 is effective and safe for treating certain Chinese lung cancer patients.
23 citations
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July 2023 in “Proceedings of the National Academy of Sciences” CD8+ T cells drive alopecia areata, while regulatory T cells are protective.
April 2023 in “Journal of Investigative Dermatology” IL-17 plays a key role in severe hair loss in chronic alopecia areata.
May 2014 in “Journal of The American Academy of Dermatology” The number of new cases of cutaneous B-cell lymphoma has leveled off since the early 2000s, and survival rates have improved since 1973.
γδTregs may help treat autoimmune diseases like alopecia areata by promoting hair regrowth and reducing immune attacks.
June 2025 in “bioRxiv (Cold Spring Harbor Laboratory)” In alopecia areata, certain immune cells increase and express a protein linked to immune activation.
December 2022 in “KSBB Journal” Activating TLR3 boosts autophagy gene expression in skin cells.
13 citations
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February 2012 in “International Journal of Dermatology” A new genetic mutation in the CDH3 gene causes hair loss and eye problems in young people.
1 citations
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November 2024 in “Blood” PI3Kδ inhibition may effectively treat cutaneous chronic graft-versus-host disease.
January 2010 in “Journal of Animal Science” Transcutaneous vaccination using nanoparticles can enhance immune responses and reduce basal cell carcinomas.
17 citations
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January 2010 in “PubMed” CD10 helps distinguish between basal cell carcinoma and benign hair follicle tumors.
1 citations
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November 2018 in “immuneACCESS” Expanded CD8+ T cells are linked to Alopecia Areata and may cause relapse after treatment.
January 2021 in “American journal of dermatological research and reviews” The muscle damage was caused by T-cell large granular lymphocytic leukemia, not dermatomyositis.
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.
Deleting the MAD2L1 gene in mice led to rapid tumor growth despite chromosomal instability.
23 citations
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July 2016 in “JAMA Ophthalmology” CDH3-related disease causes worsening eye and hair issues.
April 2017 in “The journal of investigative dermatology/Journal of investigative dermatology” Both induced and spontaneous AA lymphocytes can cause alopecia areata in mice.
February 2024 in “International journal of molecular sciences” Type 3 Innate Lymphoid Cells help maintain skin health and balance, and are involved in skin diseases and healing.
Higher PD-1 levels mean fewer CD8+ T cells in alopecia areata hair follicles.