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Differential Susceptibility to Staphylococcal Superantigen (SsAg)-Induced Apoptosis of CD4⁺ T Cells from Atopic Dermatitis Patients and Healthy Subjects: The Inhibitory Effect of IL-4 on SsAg-Induced Apoptosis¹

Yu-Tsan Lin^*, Chen-Ti Wang, Chen-Tong Hsu^*, Li-Fang Wang, Wen-Yi Shau, Yao-Hsu Yang^* and Bor-Luen Chiang^2,*,

Departments of ^* Pediatrics, Orthopedics, and Dermatology, National Taiwan University Hospital and Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan

This study had two aims: 1) to determine whether there are differences between atopic dermatitis (AD) patients and healthy subjects in staphylococcal superantigen (SsAg)-induced CD4⁺ T cell activation, cytokine production, chemokine receptor expression, and apoptosis; and 2) to investigate the effect of IL-4 on SsAg-induced apoptosis. By using immunofluorescence and annexin V staining, we analyzed PBMC with or without staphylococcal enterotoxin B (SEB) stimulation in the presence or absence of rIL-4 or anti-IL-4-neutralizing Abs in 15 healthy subjects and 27 AD patients. We found that SEB preferentially induced production of Th1 cytokine in SEB-reactive (TCRV3⁺ or V12⁺ or V17⁺) CD4⁺ T cells from healthy subjects and Th2 cytokine in those from AD patients. SEB induced up-regulation of CXCR3⁺ cells in SEB-reactive CD4⁺ T cells from healthy subjects and CCR4⁺ cells in those from AD patients. SEB-reactive CD4⁺ T cells from AD patients were more resistant to SEB-induced apoptosis than those from healthy subjects. There was no significant difference between AD and healthy subjects in SEB-induced activation of CD4⁺ T cells. CXCR3⁺ CD4⁺ T cells were more susceptible to SEB-induced apoptosis than CCR4⁺ CD4⁺ T cells in healthy subjects. Exogenously added IL-4 inhibited SEB-induced apoptosis of SEB-reactive CD4⁺ and CXCR3⁺ CD4⁺ T cells but not of CCR4⁺ CD4⁺ T cells in healthy subjects. Inhibition of endogenous IL-4 increased SEB-induced apoptosis of SEB-reactive CD4⁺ T cells from AD patients. These results might provide new clues to the mechanism that SsAgs contribute to the persistence and exacerbation of allergic skin inflammation in AD.

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