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Expansion of FOXP3-positive CD4+CD25+ T cells associated with disease activity in atopic dermatitis.
Ito, Yasunori MD, PhD *; Adachi, Yuichi MD, PhD *; Makino, Teruhiko MD, PhD +; Higashiyama, Hiroyuki MD *; Fuchizawa, Tatsuya MD, PhD *; Shimizu, Tadamichi MD, PhD +; Miyawaki, Toshio MD, PhD *
[Article] Annals of Allergy, Asthma, & Immunology. 103(2):160-165, August 2009.

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Background: FOXP3-positive CD4 CD25 T cells are known to have an immunoregulatory function by means of preventing T-cell reactivity to both self- and non-self-antigens. However, the role of these cells in the pathogenesis of allergic diseases is not clear.

Objective: To evaluate the quantity and quality of circulating FOXP3-positive T cells in patients with atopic dermatitis (AD).

Methods: Peripheral blood mononuclear cells were isolated from 35 AD patients (mean [SD] age, 27.1 [7.5] years) and 36 controls (mean [SD] age, 27.5 [10.0] years). Cellular FOXP3 expression was analyzed using flow cytometry. Characteristics of FOXP3-positive T cells were evaluated with respect to cytokine production capability and suppressive function.

Results: Frequencies of circulating FOXP3 CD25 cells in the CD4 T-cell population of AD patients were significantly higher than those in controls (mean [SD], 7.4% [4.6%] vs 4.5% [1.3%]; P = .002) and correlated with their Scoring Atopic Dermatitis (SCORAD) scores (r = 0.74, P = .008) and peripheral blood eosinophil counts (r = 0.72, P < .001). In the patients whose samples were analyzed at intervals of 1 to 2 months, frequencies of FOXP3-positive T cells were decreased as their skin lesions improved, regardless of medicines used. FOXP3-positive CD4 T cells from patients, as well as those from controls, showed little capability to synthesize interferon [gamma] and interleukin 4. No differences were found in suppression abilities of CD4 CD25 T cells between AD patients and controls.

Conclusions: Our data suggest that dynamic fluctuation in numbers of circulating FOXP3-positive regulatory T cells might contribute to the pathogenesis of AD.