Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
CXCR3 and CCR5 ligands in rheumatoid arthritis synovium
Autore:
Patel, DD; Zachariah, JP; Whichard, LP;
Indirizzi:
Duke Univ, Med Ctr, Dept Med, Div Rheumatol Allergy & Clin Immunol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 llergy & Clin Immunol, Durham, NC 27710 USA Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 Med Ctr, Dept Immunol, Durham, NC 27710 USA Duke Univ, Med Ctr, Arthrit Ctr, Durham, NC 27710 USA Duke Univ Durham NCUSA 27710 Med Ctr, Arthrit Ctr, Durham, NC 27710 USA
Titolo Testata:
CLINICAL IMMUNOLOGY
fascicolo: 1, volume: 98, anno: 2001,
pagine: 39 - 45
SICI:
1521-6616(200101)98:1<39:CACLIR>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHEMOKINE RECEPTORS; T-CELLS; MULTIPLE-SCLEROSIS; HIV-1 INFECTION; EXPRESSION; LYMPHOCYTES; ADHESION; CYTOKINE; MACROPHAGES; CHEMOTAXIS;
Keywords:
chemokine; rheumatoid arthritis; CCR5; CXCR3; IP-10; Mig; Mip-1 beta;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Patel, DD Duke Univ, Med Ctr, Dept Med, Div Rheumatol Allergy & Clin Immunol, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 lin Immunol, Durham, NC 27710 USA
Citazione:
D.D. Patel et al., "CXCR3 and CCR5 ligands in rheumatoid arthritis synovium", CLIN IMMUNO, 98(1), 2001, pp. 39-45

Abstract

The pathogenesis of rheumatoid arthritis (RA) may be mediated by Th1-type T cells. Since chemokine receptors CXCR3 and CCR5 are preferentially expressed on Th1 cells, we tested the expression and regulation of several chemokines, including those that signal through CXCR3 (interferon-gamma -inducible protein of 10 kDa, IP-10, CXCL10; and monokine induced by interferon-gammay, Mig, CXCL9) and CCR5 (macrophage inflammatory protein (Mip)-1 alpha, CCL3; and Mip-1 beta, CCL4) in RA synovial fluids, synovial tissues, and blood. Synovial fluid (SF) protein levels of IP-10 (32.1 +/- 10.5 ng/ml), Mig (15.0 +/- 6.4 ng/ml), Mip-1 beta (0.7 +/- 0.3 ng/ml), and Mip-1 alpha (0.8 +/- 0.1 ng/ml) were 100-, 50-, 25-, and 2-fold elevated in RASF compared to control SF (P < 0.001, P < 0.001, P < 0.001, and P < 0.02, respectively). Tissue levels of IP-10, Mig, and Mip-1 beta were significantly higher in RA than in OA (P < 0.01). Serum levels of IP-10 (3.1 +/- 1.2 ng/ml) were higher in patients with seropositive RA compared to controls (1.2 +/- 0.2 ng/ml)(P < 0.02). There was a gradient of IP-10, Mig, Mip-1 alpha, and Mip-1 beta from the blood into the synovial fluid in RA. Infiltrating T cells aroundhigh endothelial venules in RA synovium and 90 +/- 3% of SF CD3(+)CD4(+) Tcells expressed CXCR3, and 85 +/- 2% of SF CD3(+)CD4(+) T cells expressed CCR5. Chemokines, including IP-10, Mig, Mip-1 alpha, and Mip-1 beta, may participate in the selective recruitment of CCR5(+)CXCR3(+) T cells to the inflamed synovium. (C) 2000 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 13:40:51