May 2023 in “The Journal of Immunology” Alopecia areata involves unique activation of certain immune cells.
30 citations
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July 2019 in “PloS one” Patients with Alopecia areata have fewer specific immune cells that normally regulate the immune system, which may contribute to the condition.
October 2025 in “Science Advances” IFN-γ production by CD4 T cells is crucial for causing alopecia areata.
1 citations
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December 2022 in “Frontiers in Immunology” Tissue environment greatly affects the unique epigenetic makeup of regulatory T cells, which could impact autoimmune disease treatment.
July 2024 in “Journal of Investigative Dermatology” Expanding regulatory T cells may help treat alopecia areata by reducing harmful immune cells.
Using regulatory T cells and Rapamycin together improves chronic graft-versus-host disease treatment outcomes in mice.
May 2023 in “The Journal of Immunology” Expanding CD4+ Tregs can stop hair loss in alopecia areata.
46 citations
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October 2018 in “JCI insight” CD8+ T cells are involved in alopecia areata and may cause disease relapse.
37 citations
,
June 2004 in “Human molecular genetics online/Human molecular genetics” The HCR gene contributes to psoriasis risk.
6 citations
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April 2017 in “Experimental dermatology” CD80CD86 deficiency causes hair loss by disrupting regulatory T cells.
70 citations
,
December 2008 in “Cancer Research” CXCR2 in skin cells promotes tumor growth.
3 citations
,
November 2005 in “Journal of Investigative Dermatology Symposium Proceedings” Enhancing regulatory T cells may help treat autoimmune diseases like alopecia areata.
April 2023 in “Journal of Investigative Dermatology” IL-17 plays a key role in severe hair loss in chronic alopecia areata.
November 2025 in “Journal of Investigative Dermatology” Certain CD8+ T cells attack hair follicles in alopecia areata, suggesting they could be targeted for treatment.
April 2018 in “Journal of Investigative Dermatology” The role of γδT-cells in causing alopecia areata remains unclear.
7 citations
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February 2015 in “Journal of comparative pathology” CD8+ T cells play a key role in graft-versus-host disease in certain mice models.
77 citations
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June 2002 in “Journal of Investigative Dermatology” CD44 variant changes start alopecia areata, but don't maintain it.
July 2024 in “Journal of Investigative Dermatology” A new test helps find drugs to treat head and neck cancer by targeting c-Rel.
5 citations
,
June 2022 in “Frontiers in immunology” Increasing Treg cells in the skin does not cure hair loss from alopecia areata in mice.
3 citations
,
January 2017 in “Acta Dermato Venereologica” Lipid-antigen stimulation may play a role in folliculotropic mycosis fungoides.
127 citations
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January 2000 in “Journal of Investigative Dermatology” Cytotoxic T cells cause hair loss in chronic alopecia areata.
9 citations
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January 2015 in “Medical hypotheses” TCDD disrupts skin stem cells, causing skin issues like chloracne.
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.
July 2025 in “Journal of Investigative Dermatology” Enhancing Tregs can protect against alopecia areata.
April 2017 in “Journal of Investigative Dermatology” The protein CTCF is essential for skin development, maintaining hair follicles, and preventing inflammation.
December 2020 in “bioRxiv (Cold Spring Harbor Laboratory)” Stress can cause a type of hair loss in mice lacking the CCHCR1 gene.
September 1997 in “Journal of the European Academy of Dermatology and Venereology” People with acne have more CD4+ immune cells in their skin than healthy people.
2 citations
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June 2024 in “Medical Journal of Babylon” Higher CD8+ T cell levels are linked to Alopecia areata in Iraqi patients.
December 2023 in “Journal of Investigative Dermatology” A specific type of immune cell plays a key role in causing alopecia areata and could be a target for treatment.
30 citations
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April 2007 in “Journal of Leukocyte Biology” Blocking CD44 can reduce leukocyte migration in autoimmune skin diseases.