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Inflammatory Features of Frontal Fibrosing Alopecia.

Inflammatory Features of Frontal Fibrosing Alopecia.
Author Information (click to view)

Ma SA, Imadojemu S, Beer K, Seykora JT,


Ma SA, Imadojemu S, Beer K, Seykora JT, (click to view)

Ma SA, Imadojemu S, Beer K, Seykora JT,

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Journal of cutaneous pathology 2017 04 21() doi 10.1111/cup.12955

Abstract
INTRODUCTION
Frontal fibrosing alopecia (FFA) is a cicatricial alopecia typically occurring in post-menopausal women. The etiology and pathophysiology of FFA is poorly understood but thought to be immune mediated. This study aims to further explore the extent of fibrosis and the inflammatory microenvironment by characterizing Langerhans cells (LCs), helper T cells, cytotoxic T cells, and B cells near hair follicles in FFA.

METHODS
11 paraffin-embedded tissues from patients with a clinical and histopathologic diagnosis of FFA were selected for immunohistochemical studies using CD3, CD4, CD8, CD1a, and CD20. The lymphocytes and LCs were counted around involved follicles. The CD4/CD8 T lymphocyte ratios were calculated and compared to the CD4/CD8 T lymphocyte ratios in uninvolved areas.

RESULTS
On histopathologic review, at least 35% of follicles in each case were affected by the disease with concentric perifollicular fibrosis and a perifollicular lichenoid lymphocytic infiltrate around the infundibuloisthmic portion of the hair follicle. There was an increase of perifollicular LCs (mean of 18, standard deviation of 5.5) and intrafollicular LCs (mean of 14, standard deviation of 4.3) in involved follicles compared to uninvolved follicles (p < 0.0001). The involved follicles also showed a relative decrease in the CD4/CD8 ratio indicating increased numbers of CD8+ T cells; a finding distinct from the CD4-predominant population in uninvolved follicles (p < 0.0001). CONCLUSION
The inflammatory features of FFA demonstrate a CD8-biased T cell infiltrate with increased numbers of LCs in the infundibuloisthmic region. The increased LCs may represent an aberrant immune reaction promoting a CD8+ T cell response.

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