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Arch Dermatol Res. 2016 Mar;308(2):115-21. doi: 10.1007/s00403-016-1617-z. Epub 2016 Jan 21.

B cell activating factor and T-helper 17 cells: possible synergistic culprits in the pathogenesis of Alopecia Areata.

Author information

1
Department of Dermatology, Faculty of Medicine, Kasr Al Ainy Hospital, Cairo University, Cairo, Egypt.
2
Department of Dermatology, Faculty of Medicine, Kasr Al Ainy Hospital, Cairo University, Cairo, Egypt. heba.gawdat@yahoo.com.
3
Department of Biochemistry, Faculty of Medicine, Kasr Al Ainy Hospital, Cairo University, Cairo, Egypt.

Abstract

The role of T-helper 17 cells (Th17) and regulatory T-cells (Tregs) in the pathogenesis of alopecia areata (AA) has not been clearly elucidated. B cell activating factor (BAFF) being a regulator of T cell activation could be involved in this pathologic process as well. The current study evaluated the expression of IL-17, IL-22, Foxp3 and BAFF in tissue and sera of AA patients. Forty AA patients and 40 age and sex matched healthy controls were included. Tissue and serum levels of IL-17, IL-22, BAFF as well as serum level of Foxp3 were measured by enzyme-linked immunosorbent assay (ELISA). Immunohistochemical staining was used for assessment of tissue level of Foxp3. Tissue and serum levels of IL-17, tissue levels of IL-22 and BAFF were significantly higher in patients. Serum levels of IL-22, Foxp3 and BAFF were non-significantly higher in patients. Foxp3 immunostaining showed negativity in tissue of patients and controls. A significant positive correlation was found between both tissue levels of IL-17 and BAFF (r = 0.474, P = 0.035) and tissue level of IL-22 and disease duration (r = 0.766, P < 0.001) in AA patients. Th17 cells and BAFF are synergistically involved in the pathogenesis of AA. BAFF represents a promising therapeutic target for such a challenging disease. Defective Tregs number and/or function in AA warrants further studies.

KEYWORDS:

Alopecia Areata; B cell activating factor; Pathogenesis; Regulatory T cells; T Helper 17 cells

PMID:
26796544
DOI:
10.1007/s00403-016-1617-z
[Indexed for MEDLINE]

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