18 citations
,
February 2023 in “eLife” ILC1-like cells can independently cause alopecia areata.
53 citations
,
September 2013 in “Journal of Investigative Dermatology” Hair follicle cells help protect against immune attacks by regulating T-cell activity.
September 2025 in “Figshare” Alopecia areata involves complex immune responses, suggesting broader treatments could help.
γδTregs may help treat autoimmune diseases like alopecia areata by promoting hair regrowth and reducing immune attacks.
November 2022 in “Journal of Investigative Dermatology” ILC1-like cells can cause alopecia areata by affecting hair follicles.
June 2022 in “bioRxiv (Cold Spring Harbor Laboratory)” ILC1-like cells can cause alopecia areata by attacking hair follicles.
14 citations
,
January 2023 in “Nature Immunology” iNKT cells help develop and maintain healthy skin in young mice.
9 citations
,
January 2020 in “Critical Reviews in Immunology” MAIT cells may help fight COVID-19 but also contribute to severe inflammation.
19 citations
,
February 1998 in “Cellular Immunology” Hair growth phase in mice weakens certain immune responses.
5 citations
,
June 2022 in “Frontiers in immunology” Increasing Treg cells in the skin does not cure hair loss from alopecia areata in mice.
August 2021 in “Journal of Investigative Dermatology” ILC1-like cells can cause alopecia areata by disrupting hair follicle immunity, suggesting a new treatment approach.
26 citations
,
May 2020 in “JCI Insight” Alopecia areata involves specific immune cells, offering potential treatment targets.
September 2025 in “Figshare” Alopecia areata involves complex immune responses, suggesting broader treatments could help.
January 2014 in “Repository KITopen (Karlsruhe Institute of Technology)” Autoimmune diseases need combined therapy of tolerance induction and immunosuppression.
July 2024 in “Journal of Investigative Dermatology” IL-13 protein is much higher in the skin of atopic dermatitis patients than in healthy skin.
January 2026 in “Journal of Investigative Dermatology” Special cells can help regrow hair in alopecia areata.
ILC1-like cells may contribute to hair loss in alopecia areata.
33 citations
,
October 2006 in “European Journal of Immunology” The CD44-CD49d complex boosts T cell activation and survival in autoimmune disease.
2 citations
,
June 2025 in “Journal of Investigative Dermatology” CD8+ T cells re-expressing CD45RA may predict treatment resistance in severe alopecia areata.
April 2019 in “Journal of Investigative Dermatology” Wnt-signaling is regulated differently in skin cells and immune responses during wound healing.
April 2023 in “Journal of Investigative Dermatology” Type 1/17 inflammation in psoriasis increases skin cell growth due to a molecule that could be a new treatment target.
November 2024 in “Journal of Investigative Dermatology” 37 citations
,
April 2018 in “Journal of Allergy and Clinical Immunology” A mutation in the IKZF1 gene causes immune system overactivity, linked to autoimmune diseases like lupus.
7 citations
,
February 2012 in “British Journal of Dermatology” TH antibodies in vitiligo and AA patients recognize the same protein parts.
April 2018 in “Journal of Investigative Dermatology” The role of γδT-cells in causing alopecia areata remains unclear.
April 2023 in “The journal of investigative dermatology/Journal of investigative dermatology” Removing certain immune cells in mice causes their hair to enter the growth phase earlier than usual.
September 2025 in “Figshare” Alopecia areata involves complex immune activity, mainly Th1, with potential benefits from broader immune treatments.
April 2018 in “The journal of investigative dermatology/Journal of investigative dermatology” Certain immune cells, when activated by specific signals, can encourage hair growth.
July 2024 in “Journal of Investigative Dermatology” CD8+ T cells expand significantly in alopecia areata, suggesting new treatment targets.
106 citations
,
January 2013 in “Clinical and Developmental Immunology” Alopecia areata is caused by immune system attacks on hair follicles, often triggered by viral infections.