{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T23:09:42Z","timestamp":1777504182246,"version":"3.51.4"},"reference-count":43,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2009,2,27]],"date-time":"2009-02-27T00:00:00Z","timestamp":1235692800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2009,9]]},"abstract":"<jats:p><jats:bold>Background:\u2002<\/jats:bold> Exposure to antigens of the fish parasite <jats:italic>Anisakis<\/jats:italic> is associated with the development of protein contact dermatitis in seafood\u2010processing workers. Understanding the basic mechanisms controlling allergic sensitization through the skin is critical for designing therapies that will prevent the progression of allergic disease.<\/jats:p><jats:p><jats:bold>Objective:\u2002<\/jats:bold> To investigate the roles of interleukin (IL)\u20104, IL\u201013 and the IL\u20104R\u03b1 in both local skin pathology and systemic sensitization following epicutaneous exposure to <jats:italic>Anisakis<\/jats:italic> proteins.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> BALB\/c wild\u2010type (WT) mice and mice deficient in IL\u20104, IL\u201013 or IL\u20104 and IL\u201013, as well as mice with cell\u2010specific impairment of IL\u20104R\u03b1 expression, were sensitized to <jats:italic>Anisakis<\/jats:italic> antigen by repeated epicutaneous application of <jats:italic>Anisakis<\/jats:italic> extract. Following this sensitization, skin pathology was recorded and systemic responses were investigated. Intravenous challenge with <jats:italic>Anisakis<\/jats:italic> extract was performed to test for the development of biologically relevant systemic sensitization.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> In WT mice, epicutaneous sensitization with <jats:italic>Anisakis<\/jats:italic> larval antigens induced localized inflammation, epidermal hyperplasia, production of T<jats:sub>H<\/jats:sub>2 cytokines, antigen\u2010specific IgE and IgG1. Intravenous challenge of sensitized mice resulted in anaphylactic shock. Interestingly, IL\u201013 deficient mice failed to develop epidermal hyperplasia and inflammation, whilst anaphylaxis was reduced only in strains deficient either in IL\u20104 only, or deficient in IL\u20104 and IL\u201013 concurrently, as well as in mice deficient in IL\u20104R\u03b1 or with impaired IL\u20104R\u03b1 expression on CD4<jats:sup>+<\/jats:sup> T cells.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold> Interleukin\u201013 plays a central role in protein contact dermatitis associated with repeated epicutaneous exposure to <jats:italic>Anisakis<\/jats:italic> extract, whereas IL\u20104 drives systemic sensitization and resultant anaphylactic shock.<\/jats:p>","DOI":"10.1111\/j.1398-9995.2009.02002.x","type":"journal-article","created":{"date-parts":[[2009,2,27]],"date-time":"2009-02-27T10:08:00Z","timestamp":1235729280000},"page":"1309-1318","source":"Crossref","is-referenced-by-count":21,"title":["Differential requirements for interleukin (IL)\u20104 and IL\u201013 in protein contact dermatitis induced by <i>Anisakis<\/i>"],"prefix":"10.1111","volume":"64","author":[{"given":"N.","family":"Nieuwenhuizen","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. R.","family":"Herbert","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F.","family":"Brombacher","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. 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