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Titolo:
Modulation of immunoglobulin (Ig)E-mediated systemic anaphylaxis by low-affinity Fc receptors for IgG
Autore:
Ujike, A; Ishikawa, Y; Ono, M; Yuasa, T; Yoshino, T; Fukumoto, M; Ravetch, JV; Takai, T;
Indirizzi:
Tohoku75,iv, Dept Expt Immunol, Inst Dev Aging & Canc, Sendai, Miyagi 98085 Tohoku Univ Sendai Miyagi Japan 9808575 ging & Canc, Sendai, Miyagi 98085 Tohokupaniv, Dept Pathol, Inst Dev Aging & Canc, Sendai, Miyagi 9808575, Ja Tohoku Univ Sendai Miyagi Japan 9808575 Canc, Sendai, Miyagi 9808575, Ja JST, CREST, Tokyo 1010062, Japan JST Tokyo Japan 1010062JST, CREST, Tokyo 1010062, Japan Okayama Univ, Sch Med, Dept Pathol 2, Okayama 7008558, Japan Okayama UnivOkayama Japan 7008558 Dept Pathol 2, Okayama 7008558, Japan Rockefeller Univ, Lab Mol Genet & Immunol, New York, NY 10021 USA Rockefeller Univ New York NY USA 10021 & Immunol, New York, NY 10021 USA
Titolo Testata:
JOURNAL OF EXPERIMENTAL MEDICINE
fascicolo: 10, volume: 189, anno: 1999,
pagine: 1573 - 1579
SICI:
0022-1007(19990517)189:10<1573:MOI(SA>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
MAST-CELL DEGRANULATION; INOSITOL PHOSPHATASE SHIP; GAMMA-RIIB; TARGETED DISRUPTION; CYTOPLASMIC DOMAIN; DEFICIENT MICE; MOUSE; RESPONSES; LYMPHOCYTES; ACTIVATION;
Keywords:
systemic anaphylaxis; Fc receptor; immunoglobulin E; mast cell; gene targeting;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Takai, T TohokuMiyagi Dept Expt Immunol, Inst Dev Aging & Canc, 4-1 Seiryo, Sendai, Tohoku Univ 4-1 Seiryo Sendai Miyagi Japan 9808575 eiryo, Sendai,
Citazione:
A. Ujike et al., "Modulation of immunoglobulin (Ig)E-mediated systemic anaphylaxis by low-affinity Fc receptors for IgG", J EXP MED, 189(10), 1999, pp. 1573-1579

Abstract

It is widely accepted that immunoglobulin (Ig)E triggers immediate hypersensitivity responses by activating a cognate high-affinity receptor, Fc epsilon RI, leading to mast cell degranulation with release of vasoactive and proinflammatory mediators. This apparent specificity, however, is complicated by the ability of IgE to bind with low affinity to Fc receptors for IgG, Fc gamma RII and III. We have addressed the in vivo significance of this interaction by studying IgE-mediated passive systemic anaphylaxis in Fc gammaR-deficient mice. Mice deficient in the inhibitory receptor for IgG, Fc gamma RIIB, display enhanced IgE-mediated anaphylactic responses, whereas mice deficient in an IgG activation receptor, Fc gamma RIII, display a corresponding attenuation of IgE-mediated responses. Thus, in addition to modulating IgG-triggered hypersensitivity responses, Fc gamma RII and III on mast cells are potent regulators of IgE-mediated responses and reveal the existence of a regulatory pathway for IgE triggering of effector cells through IgGFc receptors that could contribute to the etiology of the atopic response.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/21 alle ore 01:52:06