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Titolo:
PROTECTION FROM COLLAGEN-INDUCED ARTHRITIS IN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR-DEFICIENT MICE
Autore:
CAMPBELL IK; RICH MJ; BISCHOF RJ; DUNN AR; GRAIL D; HAMILTON JA;
Indirizzi:
WALTER & ELIZA HALL INST MED RES,AUTOIMMUN & TRANSPLANTAT DIV,PO ROYAL MELBOURNE HOSP MELBOURNE VIC 3050 AUSTRALIA ROYAL MELBOURNE HOSP,LUDWIG INST CANC RES PARKVILLE VIC 3050 AUSTRALIA UNIV MELBOURNE,DEPT MED,INFLAMMAT RES CTR PARKVILLE VIC 3052 AUSTRALIA
Titolo Testata:
The Journal of immunology (1950)
fascicolo: 7, volume: 161, anno: 1998,
pagine: 3639 - 3644
SICI:
0022-1767(1998)161:7<3639:PFCAIG>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC INFLAMMATORY ARTHRITIS; TUMOR-NECROSIS-FACTOR; RHEUMATOID-ARTHRITIS; IFN-GAMMA; GM-CSF; DENDRITIC CELLS; HUMAN-MONOCYTES; FACTOR AUGMENTS; SUSCEPTIBILITY; NEUTROPHILS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
I.K. Campbell et al., "PROTECTION FROM COLLAGEN-INDUCED ARTHRITIS IN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR-DEFICIENT MICE", The Journal of immunology (1950), 161(7), 1998, pp. 3639-3644

Abstract

The involvement of granulocyte-macrophage CSP (GM-CSF) in collagen-induced arthritis (CIA) was examined using GM-CSF-deficient mice. Although CIA is generally considered to be restricted to mice of the H-2(q) or H-2(r) haplotypes, we examined the role of GM-CSF in the CIA model using GM-CSF-deficient (-/-) and wild-type (+/+) mice on a C57BL/6 (H-2(b)) background. Mice were immunized by intradermal injection at the base of the tail with chick;type II collagen followed by a repeat injection 21 days later. We found, based on both clinical and histologic assessments, that wild-type mice on this background developed severe CIA, while the GM-CSF-deficient mice had virtually no disease. Mice thatwere heterozygous for the GM-CSF gene (+/-) collectively displayed anintermediate response between those of the GM-CSF+/+ and GM-CSF-/- groups, suggesting a gene dosage effect, GM-CSF+/+ and GM-CSF+/- mice exhibited CIA responses ranging from mild (single digits) to severe swelling of ail four paws, while in the few GM-CSF-/- mice that developed CIA the disease was confined to single digits. Despite the putative role of GM-CSF in dendritic cell development, GM-CSF-deficient mice exhibited both humoral and cellular (delayed-type hypersensitivity) responses to type II collagen; however, the cellular response was significantly reduced in the GM-CSF-deficient mice compared with the wild-type controls. These findings suggest that GM-CSF is required for CIA development in mice and support the idea that GM-CSF is a key cytokine in inflammatory joint disease.

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Documento generato il 29/11/20 alle ore 06:19:02