EVALUATION OF THE ROLE OF CXCL12 IN CASES OF ALOPECIA AREATA

Document Type : Preliminary preprint short reports of original research

Authors

1 Professor of Dermatology, Venereology and Andrology, Faculty of Medicine, Alexandria University.

2 Lecturer of Dermatology, Venereology and Andrology, Faculty of Medicine, Alexandria University

3 Department of Clinical and Chemical Pathology, Faculty of Medicine University of Alexandria.

4 Dermatology, Venereology and Andrology, Faculty of Medicine, Alexandria University.

Abstract

Introduction
Alopecia areata (AA) is a common immune-mediated disorder that targets anagen hair follicles and causes nonscarring hair loss. The condition most commonly presents with discrete patches of hair loss on the scalp. Other hair-bearing areas may also be affected. In severe cases, patients may experience loss of all scalp or body hair. Patients with alopecia areata typically have smooth, circular, discrete areas of complete hair loss that develop over a period of a few weeks.
CXCL12expression during hair cycle progression have not been characterized. In alopecia areata, a few studies were done and observed different results about the role of CXCL12 in hair growth so it may play dual and complex role in the pathogenesis of alopecia areata.
On one hand, CXCL12 contributes significantly to angiogenesis during adulthood by attracting bone marrow-derived endothelial progenitor cells via a CXCR4 dependent pathway. In AA, decreased CXCL12 levels may impair angiogenesis, potentially disrupting the vascular support of healthy hair follicle , thereby contributing to hair loss. On the other hand, CXCL12 is implicated in the autoimmune mechanisms of AA. Human dermal γδ T cells, known to act as stress sentinels, are recruited to stressed hair follicles through the overexpression of chemoattractants such as CXCL10 and CXCL12. This exacerbates the autoimmune attack on hair follicles, leading to hair loss.

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