YU-TSAN LINCHEN-TI WANGHsu C.-T.Wang L.-F.Shau W.-Y.YAO-HSU YANGBOR-LUEN CHIANG2020-12-182020-12-1820030022-1767https://www.scopus.com/inward/record.uri?eid=2-s2.0-0038785717&doi=10.4049%2fjimmunol.171.2.1102&partnerID=40&md5=c5f138bd4c7b7d50638f8b3dc7aeb4a6https://scholars.lib.ntu.edu.tw/handle/123456789/527303This 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 (TCRVβ3+ or Vβ12+ or Vβ17+) 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.[SDGs]SDG3bacterial antigen; CD4 antigen; chemokine receptor; chemokine receptor CCR4; chemokine receptor CXCR3; cytokine; interleukin 4; lipocortin 5; neutralizing antibody; recombinant interleukin 4; staphylococcal superantigen; Staphylococcus enterotoxin B; superantigen; unclassified drug; adolescent; apoptosis; article; atopic dermatitis; clinical article; controlled study; cytokine production; disease exacerbation; female; gene expression; human; human cell; immunofluorescence; male; mononuclear cell; priority journal; skin allergy; skin inflammation; T lymphocyte; T lymphocyte activation; Th1 cell; Th2 celljournal article10.4049/jimmunol.171.2.1102128472852-s2.0-0038785717