Skin-homing CD4+ Foxp3+ T cells exert Th2-like function after staphylococcal superantigen stimulation in atopic dermatitis patients

Authors


Correspondence:
Dr. Bor-Luen Chiang, Department of Pediatrics, National Taiwan University Hospital, No.7, Chung-Shan South Road, Taipei 100, Taiwan. E-mail: gicmbor@ntu.edu.tw

Abstract

Cite this as: Y.-T. Lin, C.-T. Wang, P.-S. Chao, J.-H. Lee, L.-C. Wang, H.-H. Yu, Y.-H. Yang and B.-L. Chiang, Clinical & Experimental Allergy, 2011 (41) 516–525.

Summary

Background The effect of staphylococcal superantigens (SsAgs) on cutaneous lymphocyte-associated antigen (CLA)+ CD4+ Foxp3+ T cells of atopic dermatitis (AD) patients is unknown.

Objective To compare the effects of SsAgs on the ratio, function, and apoptosis of CCR6+ subtype and CCR6 subtype of CLA+ CD4+ Foxp3+ T cells among AD patients, asthma/allergic rhinitis (AR) patients without AD, and healthy subjects.

Methods Using immunofluorescence staining followed by flow cytometric analysis, we analysed peripheral blood mononuclear cells cultured with or without staphylococcal enterotoxin B (SEB) stimulation in 20 AD patients, 20 asthma/AR patients without AD, and 20 healthy subjects.

Results SEB decreased CCR6+/CCR6 ratio in CLA+ CD4+ Foxp3+ T cells from AD patients and increased CCR6+/CCR6 ratio in those from healthy subjects. SEB induced the production of type 2 T helper cell (Th2) cytokine interleukin (IL)-5 in CCR6 subtype and anti-inflammatory cytokine IL-10 in CCR6+ subtype of CLA+ CD4+ Foxp3+ T cells. CLA+ CD4+ Foxp3+ T cells from AD patients produced more IL-5 and less IL-10 after SEB stimulation than those from healthy subjects. CCR6 subtype of CLA+ CD4+ Foxp3+ T cells from AD patients and CCR6+ subtype of those cells from healthy subjects were more resistant to SEB-induced caspase-3 activation than the other subtype and those from other subjects.

Conclusions and Clinical Relevance Despite a phenotype of regulatory T cells, skin-homing CD4+ Foxp3+ T cells of AD patients exert effector Th2-like function after SsAgs stimulation, which may aggravate allergic skin inflammation.

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