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Titolo:
Upon prolonged allergen exposure IL-4 and IL-4R alpha knockout mice produce specific IgE leading to anaphylaxis
Autore:
Grunewald, SM; Teufel, M; Erb, K; Nelde, A; Mohrs, M; Brombacher, F; Brocker, EB; Sebald, W; Duschl, A;
Indirizzi:
Univ Wurzburg, Klin & Poliklin Haut & Gechlechskrankheiten, Wurzburg, Germany Univ Wurzburg Wurzburg Germany Gechlechskrankheiten, Wurzburg, Germany Univ Wurzburg, Zentrum Infekt Forsch, Wurzburg, Germany Univ Wurzburg Wurzburg Germany Zentrum Infekt Forsch, Wurzburg, Germany Univ Wurzburg, Biozentrum, Wurzburg, Germany Univ Wurzburg Wurzburg Germany Wurzburg, Biozentrum, Wurzburg, Germany Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Dept Med & Microbiol Immunol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Cape Town, Dept Immunol, Cape Town, South Africa Univ Cape Town CapeTown South Africa Immunol, Cape Town, South Africa
Titolo Testata:
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
fascicolo: 4, volume: 125, anno: 2001,
pagine: 322 - 328
SICI:
1018-2438(200108)125:4<322:UPAEIA>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEFICIENT MICE; INTERLEUKIN-4-DEFICIENT MICE; IMMUNOGLOBULIN (IG)E; IMMUNE-RESPONSE; IN-VIVO; RECEPTOR; STAT6; INTERLEUKIN-13; INFECTION; REVEAL;
Keywords:
IgE; IL-4; IL-4 receptor; in vivo animal models; allergy; anaphylaxis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Grunewald, SM Univ Wurzburg, Dept Dermatol, Josef Schneider Str 2, D-97080Wurzburg, Germany Univ Wurzburg Josef Schneider Str 2 Wurzburg Germany D-97080
Citazione:
S.M. Grunewald et al., "Upon prolonged allergen exposure IL-4 and IL-4R alpha knockout mice produce specific IgE leading to anaphylaxis", INT A AL IM, 125(4), 2001, pp. 322-328

Abstract

Background: IL-4 and IL-13 are key regulators in atopic disorders and bothsignal through the receptor chain IL4R alpha. IL-4 and IL-13 are also the only cytokines known to induce class switching to IgE. We sought to compareallergen-specific IgE responses and allergic reactivity of wild-type (wt) mice with IL-4(-/-) and IL-4R alpha (-/-) mice, which lack both IL-4 and IL-13 functions. Methods: BALB/c wt, IL-4(-/-) and IL-4R alpha (-/-) mice were immunized with ovalbumin intranasally or intraperitoneally and specific antibody titers were measured by ELISA. Bronchoalveolar lavage fluids and lung tissue were analyzed cytologically and histologically. Allergic reactivity was determined by active cutaneous anaphylaxis and anaphylactic shock. Results: wt mice immunized intranasally or intraperitoneally showed high titers of specific IgE 3 and 6 weeks after primary sensitization, resulting incutaneous anaphylaxis and anaphylactic shock upon challenge. Intranasal sensitization resulted in airway eosinophilia and goblet cell metaplasia. In contrast, IL-4(-/-) and IL-4R alpha (-/-) mice showed no specific IgE after3 weeks, but produced high titers after 6 weeks. At this time cutaneous anaphylaxis and anaphylactic shock could be induced as in wt mice, but lung pathology was absent. Conclusions: We conclude that upon long-term allergen exposure, alternative switch mechanisms independent of IL-4 and IL4R alpha may induce IgE but not asthma-like lung pathology. This may be relevant forthe development of allergic disease, since long-term allergen exposure is a frequent condition during allergic sensitization. Copyright (C) 2001 S. Karger AG, Basel.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 14:29:37