Lesional infiltration of mast cells, Langerhans cells, T cells and local cytokine profiles in alopecia areata

Alopecia areata (AA) is a chronic inflammatory disease mediated by an array of cells and cytokines. Immunohistochemistry (IHC) of histological sections with antibodies to mast cell tryptase, CD4, CD8, CD1a and semi-quantitative real-time PCR analysis of Th1- and Th2-type cytokines were performed in 55 patients to investigate the infiltration features of mast cells (MCs), T lymphocytes and Langerhans cells (LCs) in scalp lesions of patients with AA. In AA patients, increased MCs mainly infiltrated the peri-follicular and peri-vascular areas, and correlated positively with numbers of CD8+ T lymphocytes in deep peri-follicular areas (P = 0.04), but negatively with CD4+ T lymphocytes in deep peri-vascular areas (P = 0.031). In patients with active hair loss, LCs in epidermis, deep dermis and peri-vascular were elevated (Ps < 0.05). Infiltration of LCs in upper peri-vascular areas and CD8+ T cell infiltration in deep peri-follicular areas were positively correlated (R = 0.618, P = 0.011), as well as LCs in deep peri-vascular areas with CD8+ T cells in upper peri-follicular areas (R = 0.570, P = 0.017). In patients with active hair loss, Th1-type cytokine (IL-2, IL-8, TNF-α) mRNA expression in deep dermis were higher than in upper dermis (Ps < 0.05). However, in patients with non-active hair loss, Th2-type cytokine (IL-5, IL-10) mRNA expression in deep dermis was higher than that in the upper dermis (Ps < 0.05). Positive correlations were found existing between MCs and CD8+ T cells, as well as between LCs and CD8+ T cells. In conclusion, findings in this study allow us to propose a close relationship between mast cells and CD8+ T cells, as well as between LCs and CD8+ T cells in AA, as well as allergy may interfere with infiltrating T lymphocytes in AA lesional regions. Also, Th1-type cytokine are related to disease activity of alopecia areata, whereas Th2-type cytokines may be associated with persistence of AA.