A Meta-Analysis of Chemokines in Alopecia Areata: Recruiting Immune Cells Toward the Hair Follicle

September 2025 in “ Frontiers in Immunology ”

Elise Van Caelenberg, Arno Belpaire, Nanja van Geel, Reinhart Speeckaert

alopecia areata chemokines Th1-associated chemokines CXCL9 CXCL10 CCL5 CXCL11 IFN-γ Th2 chemokine CCL13 CCL17 CCL22 CX3CL1 monocyte recruitment dendritic cell recruitment eosinophil recruitment immune dysregulation immunomodulatory strategies

TLDR Alopecia areata involves complex immune dysregulation, mainly driven by Th1 activity, suggesting broader treatment strategies.

This meta-analysis of 46 studies on alopecia areata (AA) reveals that elevated levels of chemokines such as CXCL9, CXCL10, and CCL5 are present in AA patients, indicating their role in recruiting immune cells to the hair follicle and contributing to the disease's pathogenesis. CXCL9 and CXCL10 levels correlate with disease activity and treatment response, as shown by changes in SALT scores. The study highlights the involvement of Th1, Th2, and Th17-related chemokines, suggesting their potential as biomarkers for disease severity and therapeutic targets. Despite some methodological limitations, the findings underscore the complex immune profile of AA and the potential for chemokine-directed interventions.

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research The AHR Pathway Is Dysregulated in Alopecia Areata

2 citations , March 2025 in “Journal of Translational Autoimmunity”

Targeting the AhR pathway may help treat alopecia areata.

research Humanized CXCL12 Antibody Delays Onset and Modulates Immune Response in Alopecia Areata Mice: Insights from Single-Cell RNA Sequencing

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research Increased CRHR1 Expression on Monocytes from Patients with AA Enables a Pro-Inflammatory Response to Corticotrophin-Releasing Hormone

3 citations , October 2024 in “Experimental Dermatology”

Higher CRHR1 levels in AA patients lead to increased inflammation.

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4 citations , August 2024 in “Skin Research and Technology”

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Copper may protect against alopecia areata, while certain inflammatory markers increase risk.

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20 citations , July 2024 in “Archives of Dermatological Research”

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45 citations , May 2024 in “International Journal of Molecular Sciences”

Alopecia areata is caused by immune attacks on hair follicles, affecting hair growth and quality of life.

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April 2024 in “Bioscience trends”

Higher levels of certain DNAs in blood may indicate hair follicle damage in alopecia areata patients.

research Inhibition of T-Cell Activity in Alopecia Areata: Recent Developments and New Directions

4 citations , November 2023 in “Frontiers in immunology”

New treatments targeting T-cell pathways are needed for better alopecia areata management.

research Scalp Biomarkers During Dupilumab Treatment Support Th2 Pathway Pathogenicity in Alopecia Areata

15 citations , October 2022 in “Allergy”

Dupilumab treatment reduces Th2-related markers and helps hair growth in alopecia areata, showing Th2's role in the condition.

Chemokine C-C Motif Ligand 7 (CCL7), a Biomarker of Atherosclerosis, Is Associated with the Severity of Alopecia Areata: A Preliminary Study

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4 citations , November 2021 in “Journal of Clinical Medicine”

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research Pharmacological Blockade of the CX3CR1/CX3CL1 Fractalkine Axis Prevents Alopecia Areata in C3H/HeJ Mice

April 2021 in “Journal of Investigative Dermatology”

research Pro-Inflammatory Vδ1+ T-Cells Infiltrates Are Present In And Around The Hair Bulbs Of Non-Lesional And Lesional Alopecia Areata Hair Follicles

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134 citations , July 2020 in “Experimental dermatology”

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research Frontal Fibrosing Alopecia Shows Robust T Helper 1 and Janus Kinase 3 Skewing

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Frontal fibrosing alopecia is linked to increased immune system activity and reduced stem cells, suggesting early treatment targeting this pathway might prevent hair follicle damage.

research An Integrated Model of Alopecia Areata Biomarkers Highlights Both TH1 and TH2 Upregulation

58 citations , July 2018 in “Journal of Allergy and Clinical Immunology”

Alopecia areata severity is linked to increased TH1 and TH2 activity.

research CXCR3 Blockade Inhibits T Cell Migration Into the Skin and Prevents Development of Alopecia Areata

64 citations , July 2016 in “Journal of Immunology”

Blocking the CXCR3 receptor reduces T cell accumulation in the skin and prevents hair loss in mice.

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16 citations , December 2015 in “Journal of Investigative Dermatology”

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65 citations , December 2015 in “Experimental dermatology”

Corticosteroid treatment reduces inflammation and alters hair keratins in alopecia areata.

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68 citations , November 2015 in “The Journal of Allergy and Clinical Immunology”

Blocking IL-12/IL-23p40 helped reverse severe hair loss in patients.

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176 citations , August 2015 in “The journal of allergy and clinical immunology/Journal of allergy and clinical immunology/The journal of allergy and clinical immunology”

Alopecia areata involves immune activation in the scalp, suggesting treatments targeting TH1, TH2, and IL-23 pathways.

research Evaluation of the Serum Level of Regulation Upon Activation of Normal T-Cell Expressed and Secreted Protein in Different Types of Alopecia Areata

May 2015 in “Journal of the Egyptian Women's Dermatologic Society /Journal of the Egyptian Women's Dermatologic Society”

Transcriptional Profiling in Alopecia Areata Defines Immune and Cell Cycle Control Related Genes Within Disease-Specific Signatures

research Transcriptional Profiling in Alopecia Areata Defines Immune and Cell Cycle Control Related Genes Within Disease-Specific Signatures

61 citations , September 2010 in “Genomics”

The study found that immune responses disrupt hair growth cycles, causing hair loss in alopecia areata.

research Type 1 Interferon Signature in the Scalp Lesions of Alopecia Areata

52 citations , March 2010 in “British Journal of Dermatology”

Alopecia areata shows a unique type 1 interferon signature, suggesting potential treatment by targeting this pathway.

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58 citations , May 2004 in “British Journal of Dermatology”

Diphenylcyclopropenone treatment helps hair growth in alopecia areata by promoting blood vessel growth and cell survival.