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Titolo:
Increased severity of local and systemic anaphylactic reactions in gp49B1-deficient mice
Autore:
Daheshia, M; Friend, DS; Grusby, MJ; Austen, KF; Katz, HR;
Indirizzi:
Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA Brigham & Womens Hosp Boston MA USA 02115 & Allergy, Boston, MA 02115 USA Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA Harvard Univ BostonMA USA 02115 Sch Med, Dept Med, Boston, MA 02115 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 munol & Infect Dis, Boston, MA 02115 USA
Titolo Testata:
JOURNAL OF EXPERIMENTAL MEDICINE
fascicolo: 2, volume: 194, anno: 2001,
pagine: 227 - 233
SICI:
0022-1007(20010716)194:2<227:ISOLAS>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
FC-GAMMA-RIIB; MAST-CELL ACTIVATION; NATURAL-KILLER-CELLS; IMMUNOGLOBULIN SUPERFAMILY; CARDIOPULMONARY ALTERATIONS; INHIBITORY RECEPTORS; DEFICIENT MICE; GP49B GENE; NK CELLS; MOUSE;
Keywords:
mast cells; immunoreceptor tyrosine-based inhibitory motif passive cutaneous anaphylaxis; active cutaneous anaphylaxis; active systemic anaphylaxis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Katz, HR Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, 1 Jimmy Fund Way,Rm 638A, Boston, MA 02115 USA Brigham & Womens Hosp 1 Jimmy Fund Way,Rm 638A Boston MA USA 02115
Citazione:
M. Daheshia et al., "Increased severity of local and systemic anaphylactic reactions in gp49B1-deficient mice", J EXP MED, 194(2), 2001, pp. 227-233

Abstract

gp49B1 is an immunoglobulin (Ig) superfamily member that inhibits Fc is anelement of RI-induced mast cell activation when the two receptors are coligated with antibodies in vitro. The critical question of in vivo function of gp49B1 is now addressed in gene-disrupted mice. gp49B1-deficient mice exhibited a significantly increased sensitivity to IgE-dependent passive cutaneous anaphylaxis as assessed by greater tissue swelling and mast cell degranulation in situ. Importantly, by the same criteria, the absence of gp49B1 also resulted in a lower threshold for antigen challenge in active cutaneous anaphylaxis, in which the antigen-specific antibody levels were comparable in gp49B1-deficient and sufficient mice. Moreover, the absence of gp49B1 resulted in a significantly: greater and faster death rate in active systemic anaphylaxis. These results indicate that gp49B1 innately dampens adaptive immediate hypersensitivity responses by suppressing mast cell activation in vivo. In addition, this study provides a new concept and target for regulation of allergic disease susceptibility and severity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/21 alle ore 16:09:34