CCL

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001-es BibID:BIBFORM005805
Első szerző:Glant Tibor T.
Cím:Two loci on chromosome 15 control experimentally induced arthritis through the differential regulation of IL-6 and lymphocyte proliferation / Tibor T. Glant, Sandor Szanto, Aniko Vegvari, Zoltan Szabo, Katalin Kis-Toth, Katalin Mikecz, Vyacheslav A. Adarichev
Dátum:2008
Megjegyzések:Using genetic linkage analysis of proteoglycan-induced arthritis (PGIA), a murine model for rheumatoid arthritis, we identified two loci, Pgia8 and Pgia9, on chromosome 15 (chr15) that appear to be implicated in disease susceptibility. Immunization of congenic strains carrying the entire chr15 and separately each of the two loci of DBA/2 arthritis-resistant origin in susceptible BALB/c background confirmed locations of two loci on chr15: the major Pgia9 and lesser Pgia8 locus. Distal part of chr15 (Pgia9) showed a major suppressive effect on PGIA susceptibility in females (40%, p < 0.001), whereas the effect of this locus in congenic males was still significant but weaker. Proximal part of chr15 (Pgia8) demonstrated mild and transient effect upon arthritis; this effect was PGIA-promoting in males and suppressive in females. Pgia8 and Pgia9 loci demonstrated an additive mode of inheritance, since when they were both incorporated in consomic chr15 strain, the total effect was a sum of the two loci. Using F-2 population of the intercross of wild-type and chr15 consomic strain, we confirmed and refined quantitative trait locus positions and identified a strong correlation between disease susceptibility and lymphocyte-producing cytokines of TNF-alpha and IL-6. Both Pgia8 and Pgia9 loci on chr15 appear to control IL-6 production in spleen cultures of arthritic mice, providing an important link to the mechanism of autoimmune inflammation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Collagen-induced arthritis
Quantitative trait loci
Proteoglycan-induced arthritis
Rheumatoid-arthritis
Susceptibility loci
Genome scan
Genetic dissection
Autoimmune-disease
Murine model
Identification
Megjelenés:The Journal of Immunology. - 181 : 2 (2008), p. 1307-1314. -
További szerzők:Szántó Sándor (1968-) (belgyógyász, reumatológus) Végvári Anikó (belgyógyász, III. sz. Belgyógyászati Klinika) Szabó Zoltán (1970-) (belgyógyász, reumatológus) Kis-Tóth Katalin (1975-) (immunológus) Mikecz Katalin Adarichev, Vyacheslav A.
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2.

001-es BibID:BIBFORM046534
Első szerző:Szántó Sándor (belgyógyász, reumatológus)
Cím:Expression of L-selectin, but not CD44, is required for early neutrophil extravasation in antigen-induced arthritis / Sándor Szántó, István Gál, Andrea Gonda, Tibor T. Glant, Katalin Mikecz
Dátum:2004
Megjegyzések:L (leukocyte)-selectin (CD62L) and CD44 are major adhesion receptors that support the rolling of leukocytes on endothelium, the first step of leukocyte entry into inflamed tissue. The specific contribution of L-selectin or CD44 to the regulation of cell traffic to joints in arthritis has not been investigated. We used CD44-deficient, L-selectin-deficient, and CD44/L-selectin double knockout mice to determine the requirement for these receptors for inflammatory cell recruitment during Ag-induced arthritis. Intraperitoneal immunization resulted in similar activation status and Ag-specific responses in wild-type and gene-targeted mice. However, extravasation of neutrophil granulocytes, but not the emigration of T cells, into the knee joints after intra-articular Ag injection was significantly delayed in L-selectin-deficient and double knockout mice. Intravital videomicroscopy on the synovial microcirculation revealed enhanced leukocyte rolling and diminished adherence in mice lacking either CD44 or L-selectin, but CD44 deficiency had no significant effect on the recruitment of L-selectin-null cells. Compared with wild-type leukocytes, expression of L-selectin was down-regulated in CD44-deficient cells in the spleen, peripheral blood, and inflamed joints, suggesting that reduced expression of L-selectin, rather than the lack of CD44, could be responsible for the delayed influx of granulocytes into the joints of CD44-deficient mice. In conclusion, there is a greater requirement for L-selectin than for CD44 for neutrophil extravasation during the early phase of Ag-induced arthritis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Immunology. - 172 : 11 (2004), p. 6723-6734. -
További szerzők:Gál István (1957-) (belgyógyász) Gonda Andrea (1970-) (onkológus szakorvos) Glant Tibor T. Mikecz Katalin
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3.

001-es BibID:BIBFORM046535
Első szerző:Végvári Anikó (belgyógyász, III. sz. Belgyógyászati Klinika)
Cím:Two major interacting chromosome loci control disease susceptibility in murine model of spondyloarthropathy / Vegvari A., Szabo Z., Szanto S., Nesterovitch A. B., Mikecz K., Glant T. T., Adarichev V. A.
Dátum:2005
Megjegyzések:Autoimmune spondylitis was induced in BALB/c mice and their MHC-matched (BALB/c x DBA/2)F1 and F2 hybrids by systemic immunization with cartilage/intervertebral disk proteoglycan (PG). As in human ankylosing spondylitis, the MHC was the major permissive genetic locus in murine PG-induced spondylitis (PGIS). Two major non-MHC chromosome loci with highly significant linkage were found on chromosomes 2 (Pgis2) and 18 (Pgis1) accounting for 40% of the entire F2 trait variance. The dominant spondylitis-susceptibility allele for Pgis2 locus is derived from the BALB/c strain, whereas the Pgis1 recessive allele was present in the disease-resistant DBA/2 strain. The Pgis1 locus significantly affected the disease-controlling Pgis2 locus, inducing as high incidence of spondylitis in F2 hybrids as was found in the spondylitis-susceptible parent BALB/c strain. Additional disease-controlling loci with suggestive linkage were mapped to the chromosomes 12, 15, and 19. Severity of spondylitis in F2 mice positively correlated with serum levels of amyloid A, IL-6, and Pg-specific Abs, and showed negative correlation with Ag-induced T cell proliferation, IFN-gamma, IL-4, and TNF-alpha production. A major locus controlling serum IL-6 was found on chromosome 14 near osteoclast differentiation factor Tnfsf11. Locus on chromosome 11 near the Stat3 and Stat5 genes controlled serum level of the Ig IgG2a isotype. The two major genetic loci Pgis1 and Pgis2 of murine spondylitis were homologous to chromosome regions in human genome, which control ankylosing spondylitis in human patients. Thus, this animal model of experimentally induced spondylitis might facilitate the identification of spondylitis-susceptibility genes in humans.újratöltve - BIBFORM015971
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Immunology. - 175 : 4 (2005), p. 2475-2483. -
További szerzők:Szabó Zoltán (1970-) (belgyógyász, reumatológus) Szántó Sándor (1968-) (belgyógyász, reumatológus) Nesterovitch, Andrew B. Mikecz Katalin Glant Tibor T. Adarichev, Vyacheslav A.
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