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Titolo:
Intercellular adhesion molecule-1 (ICAM-1, CD54) deficiency segregates theunique pathophysiological requirements for generating idiopathic pneumoniasyndrome (IPS) versus graft-versus-host disease following allogeneic murine bone marrow transplantation
Autore:
Panoskaltsis-Mortari, A; Hermanson, JR; Haddad, IY; Wangensteen, OD; Blazar, BR;
Indirizzi:
Univ Minnesota, Dept Pediat, Div Hematol Oncol, Blood & Marrow Transplant Program,Canc Ctr, Minneapolis, MN 55455 USA Univ Minnesota Minneapolis MN USA 55455 nc Ctr, Minneapolis, MN 55455 USA Univ Minnesota, Dept Physiol, Minneapolis, MN 55455 USA Univ Minnesota Minneapolis MN USA 55455 hysiol, Minneapolis, MN 55455 USA Univ Minnesota, Dept Pulm Crit Care Med, Minneapolis, MN 55455 USA Univ Minnesota Minneapolis MN USA 55455 re Med, Minneapolis, MN 55455 USA
Titolo Testata:
BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
fascicolo: 7, volume: 7, anno: 2001,
pagine: 368 - 377
SICI:
1083-8791(2001)7:7<368:IAM(CD>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; FUNCTION-ASSOCIATED ANTIGEN-1; CD8(+) T-CELLS; LUNG INFLAMMATION; LEUKOCYTE RECRUITMENT; MONOCYTE MIGRATION; CROSS-LINKING; P-SELECTIN; MICE; INJURY;
Keywords:
ICAM-1; allogeneic BMT; idiopathic pneumonia syndrome;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Panoskaltsis-Mortari, A Univ Minnesota, Dept Pediat, Div Hematol Oncol, Blood & Marrow Transplant Program,Canc Ctr, Mayo Mail Code 366,420 Delaware St SE, Minneapolis, MN 55455 USA Univ Minnesota Mayo Mail Code 366,420 Delaware St SE Minneapolis MN USA 55455
Citazione:
A. Panoskaltsis-Mortari et al., "Intercellular adhesion molecule-1 (ICAM-1, CD54) deficiency segregates theunique pathophysiological requirements for generating idiopathic pneumoniasyndrome (IPS) versus graft-versus-host disease following allogeneic murine bone marrow transplantation", BIOL BLOOD, 7(7), 2001, pp. 368-377

Abstract

Following allogeneic bone marrow transplantation (alloBMT), idiopathic pneumonia syndrome (TPS) and graft-versus-host disease (GVHD) caused by donor cell alloreactivity remain major obstacles to a successful outcome. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that is involved in regulating lymphohematopoietic cell migration and facilitating T-cell responses. To determine whether ICAM-1 expression in the host would affect IPS or GVHD tissue injury responses, ICAM-1(-/-) mice were compared with ICAM-1(+/+) controls. ICAM-1(-/-) recipients did not exhibit the manifestations of IPS injury such as an increase in lung weights nor decreased lung function. The influx of T cells, macrophages, and neutrophils was dramaticallydampened as was the production of the inflammatory cytokines interferon-gamma and tumor necrosis factor a and the chemokines monocyte chemotactic protein 1, macrophage inflammatory protein 1 alpha (MIP-1 alpha), MIP-1 beta, and lymphotactin, normally upregulated in the lung during IPS. In contrast,systemic levels of these mediators were unaffected and GVHD-induced lesions in the liver and colon did not differ in severity regardless of ICAM-1 expression. GVHD-mediated mortality was accelerated in ICAM-1(-/-) recipientsat doses of allogeneic spleen cells that are otherwise not uniformally lethal. These data implicate ICAM-1 as playing a critical role in the generation of IPS; therefore, ICAM-1 may be a discerning element, segregating IPS from GVHD injury post-alloBMT.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 22:07:46