Healthy Individuals Genetically At-Risk for the Development of Pemphigus Vulgaris or Alopecia Areata Share Disease-Like Cytokine Dysregulation

January 2025 in “ Frontiers in Immunology ”

Rebekah R. Schwartz, Kristina Seiffert-Sinha, Animesh A. Sinha

Alopecia areata Pemphigus vulgaris cytokine dysregulation Th1 pathway Th17 pathway Th2 pathway IL-8 HLA alleles pro-inflammatory cytokines

TLDR Genetically at-risk healthy people show similar immune issues as those with Pemphigus vulgaris or Alopecia areata.

The study investigates cytokine dysregulation in autoimmune diseases, specifically Pemphigus vulgaris (PV) and Alopecia areata (AA), revealing that healthy individuals genetically predisposed to these conditions exhibit similar immune dysregulation patterns as affected patients. In AA, healthy relatives of patients show Th1 and Th17 pathway dysregulation, while in PV, both patients and healthy individuals with PV-associated HLA alleles display activation of pro-inflammatory cytokines, Th17, Th2 pathways, and IL-8. This suggests that genetic background influences cytokine expression, and there may be protective mechanisms in genetically predisposed individuals that prevent disease onset, supporting the idea of shared genetic factors across autoimmune diseases.

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Healthy Individuals Genetically At-Risk for the Development of Pemphigus Vulgaris or Alopecia Areata Share Disease-Like Cytokine Dysregulation

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research Inheritance-Specific Dysregulation of Th1 and Th17-Associated Cytokines in Alopecia Areata

research The Role of Serum Th1, Th2, and Th17 Cytokines in Patients with Alopecia Areata: Clinical Implications

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research Evaluation of the Level of Serum Interleukins (IL-2, IL-4, IL-15, and IL-17) and Its Relationship with Disease Severity in Patients with Alopecia Areata

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research Alopecia Areata Is Characterized by Dysregulation in Systemic Type 17 and Type 2 Cytokines, Which May Contribute to Disease-Associated Psychological Morbidity

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

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