金黃色葡萄球菌超級抗原在異位性皮膚炎致病機轉所扮演的角色
Resource
The Journal of Immunology (171),1102–1108
Journal
The Journal of Immunology (171),1102–1108
Pages
-
Date Issued
2004
Date
2004
Author(s)
林于粲
DOI
922314B002224
Abstract
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 (TCRV 3 or V 12 or V 17) 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.
Publisher
臺北市：國立臺灣大學醫學院小兒科
Type
report
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