Evaluation of Serum Toll-Like Receptor 4, Interferon Gamma, and Interleukin-17 Levels in Iraqi Patients with Alopecia Areata
Abstract
Background: Alopecia areata is a non-scarring autoimmune disease and a type of hair loss, where immune responses are disregarded, and thus they are central to the pathogenesis of the disease. There is growing evidence that innate immune receptors, as well as adaptive immune cytokines, are involved in the disease development and progression. Methods: The patients enrolled in this study were 70 Iraqi patients with clinically verified alopecia areata and 50 controls, aged and sex matched. The concentration of Toll-Like Receptor 4 (TLR4), interferon gamma (IFN-γ) and interleukin-17 (IL-17) in serum was determined by employing enzyme-linked immunosorbent assays. The statistical comparison of groups was carried out, as well as analyzing associations with demographic characteristics. Results: The level of TLR4 serum in the cases of alopecia areata patients was significantly higher than that of the control (6.82 ± 1.47 vs. 3.95 ± 1.12 ng/mL; p < 0.001). Similarly, patients exhibited markedly elevated IFN-γ concentrations (24.6 ± 6.8 vs. 14.3 ± 4.9 pg/mL; p < 0.001) and IL-17 levels (18.9 ± 5.2 vs. 9.7 ± 3.6 pg/mL; p < 0.001). The relationship between these immunological markers and age or gender did not show statistically significant relationships (p > 0.05). Conclusion: The substantial increase of TLR4, IFN-γ, and IL-17 in Iraqi patients with alopecia areata highlights the synergy of innate immune stimulation and Th1/Th17-type adaptive immune responses in the pathogenesis of the disease. These biomarkers can be used to provide a good indication of disease activity and ultimately become targets of future immunomodulatory therapies.
Fields of Study & Subjects
Hair Growth and Disorders
Dermatology and Skin Diseases
Nail Diseases and Treatments
Publication details
- Journal / source
- European journal of ecology, biology and agriculture.
- Volume
- 3
- Issue
- 2
- Pages
- 36–43
- Publication date
- 1 March 2026
- Language
- EN