Changes in Populations of HLA- DR+CD3+ Cells and CD57–CD16+ Cells in Alopecia areata after Corticosteroid Therapy

Abstract

We investigated the populations of activated T (HLA-DR+CD3+) cells and natural killer (CD57–CD16+) cells in the peripheral blood of patients with various types of alopecia areata (AA) and noted any changes that occurred in the said populations after administration of local and systemic corticosteroid therapy. In type 2 (severe multiple AA and alopecia totalis) and type 3 (alopecia universalis), the mean percentages of HLA-DR+CD3+ cells and CD57–CD16+ cells were significantly higher when compared with those of the normal controls. The percentages of both subsets in type 1 (mild AA) and the normal controls were consistent. Twenty-four patients in types 2 and 3 had received corticosteroid treatment, and all patients experienced new hair growth. With the changes in disease activity, the populations of HLA-DR+CD3+ cells in these patients after corticosteroid therapy significantly decreased when compared with those recorded prior to treatment. Subsequent to treatment, the mean percentages of CD57–CD16+ cells decreased to levels that were not significant relative to that of the normal controls. These findings indicate that HLA-DR+CD3+ and CD57–CD16+ cells in the peripheral blood of patients with AA may be correlated with the disease activity of AA.

Maintenance of Hair Follicle Immune Privilege Is Linked to Prevention of NK Cell Attack

“…Second, we show that stimulation-sensitive (that is, NKG2D þ ) CD56 þ NK cells prominently aggregate around AA HFs. This is in line with the previous study by Imai et al (1994), who found that patients with severe multifocal AA, AA totalis, or AA universalis had significantly more CD57 À CD16 þ NK cells in the PBMCs compared to normal controls. This suggests that, under physiological conditions, the immunoprivileged HF escapes from NK cell attack, and this cannot be prevented any longer when HF-IP collapses.…”

Peripheral blood gene expression in alopecia areata reveals molecular pathways distinguishing heritability, disease and severity

“…Several of these genes and pathways have a previously described role in AA pathogenesis, validating that our experimental approach is sufficiently sensitive to capture disease-relevant processes. 10,33 Although it has been shown that NK cells aggregate perifollicularly in AA lesional skin 3,4,34 and peripheral blood, 35,36 there is limited data regarding the role of NK cells in AA pathogenesis. Our data show an upregulation of NK-cell cytotoxicity in AA peripheral blood that, as suggested by others, 11,12,37 may promote the failure of hair follicle immune privilege.…”

Androgenetic alopecia and microinflammation

“… 78 By contrast, in humans, betamethasone treatment over 19 weeks stimulated hair regrowth in AA patients, indicating that corticosteroids are not intrinsically detrimental for scalp hair growth in humans. 79 These observations outline the differences between murine pelage and human scalp hair follicles with respect to growth regulation. Whether glucocorticoids may be beneficial for AGA in humans remains to be established.…”