1996
DOI: 10.1001/archderm.132.1.27
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Staphylococcal enterotoxin B applied on intact normal and intact atopic skin induces dermatitis

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Cited by 110 publications

(88 citation statements)
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“…In keeping with our findings, it has previously been shown that staphylococcal superantigens can induce T-cell-mediated polyclonal B-cell differentiation without discernible T-cell proliferation [17]. Previous studies have shown that even TCR Vb skewing, a more sensitive marker of superantigen activity than overall proliferative responses, was only observed in CD4 1 T lymphocytes expressing cutaneous Although the application of staphylococcal toxins to the skin surface can result in an eczematous-type reaction [7,8,27], the relative importance of staphylococcal toxins in the pathogenesis of AD remains open to question, since staphylococcal toxins are present on the skin of many individuals who do not have AD [27,28] and, as we found here, over 40% of patients with comparatively severe AD do not carry T 1 S. aureus on their skin surface or nares [5,6,29,30]. It may be that it is the invasion of staphylococcal toxins through the partially-disrupted epidermal barrier in AD, rather than just the carriage of T 1 S. aureus on the intact skin, which stimulates the immune response and causes an exacerbation of AD.…”
Section: Discussion
supporting
confidence: 90%
How this paper cites the one you are viewing
“…In keeping with our findings, it has previously been shown that staphylococcal superantigens can induce T-cell-mediated polyclonal B-cell differentiation without discernible T-cell proliferation [17]. Previous studies have shown that even TCR Vb skewing, a more sensitive marker of superantigen activity than overall proliferative responses, was only observed in CD4 1 T lymphocytes expressing cutaneous Although the application of staphylococcal toxins to the skin surface can result in an eczematous-type reaction [7,8,27], the relative importance of staphylococcal toxins in the pathogenesis of AD remains open to question, since staphylococcal toxins are present on the skin of many individuals who do not have AD [27,28] and, as we found here, over 40% of patients with comparatively severe AD do not carry T 1 S. aureus on their skin surface or nares [5,6,29,30]. It may be that it is the invasion of staphylococcal toxins through the partially-disrupted epidermal barrier in AD, rather than just the carriage of T 1 S. aureus on the intact skin, which stimulates the immune response and causes an exacerbation of AD.…”
Section: Discussion
supporting
confidence: 90%
How this paper cites the one you are viewing
“…Our results suggest an increasing importance of CD8 ϩ T cells in atopic skin, especially when colonized with SEB-producing strains of S. aureus. In line with earlier reports (9,15,18,30), we also found that cutaneous SEB exposure can trigger allergic inflammation. Laouini et al (15) reported previously that repeated epicutaneous SEB exposure in the murine model of AD induces Th2-type skin inflammation in the skin.…”
Section: Figure 2 Immunohistochemical Analysis Of Cd3
supporting
confidence: 93%
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“…T cell activation by Staphylococcal superantigens in AD is suggested by both in vitro and in vivo studies [12][13][14][15]19]. Our finding of enhanced proliferation to SEB of PBMC from children with AD supports a role for SEB in childhood AD.…”
Section: Discussion
supporting
confidence: 66%