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001-es BibID:	BIBFORM005750
Első szerző:	Adarichev, Vyacheslav A.
Cím:	Congenic strains displaying similar clinical phenotype of arthritis represent different immunologic models of inflammation / Vyacheslav A. Adarichev, Akos Vegvari, Zoltan Szabo, Katalin Kis-Toth K, Katalin Mikecz, Tibor T. Glant
Dátum:	2008
Megjegyzések:	Proteoglycan (PG)-induced arthritis (PGIA) is an autoimmune inflammatory disease controlled by multiple genes in the murine genome. BALB/c x DBA/2 congenic strains carrying four major PGIA chromosome loci were immunized, and positions of loci on chromosomes 3, 7, 8 and 19 ( loci Pgia26, Pgia21, Pgia4 and Pgia12, respectively) were confirmed. Each congenic strain exhibited a different pattern of regulation of clinical and immunologic features of PGIA, and these features were significantly influenced by gender. Locus Pgia26 delayed PGIA onset in males and females, and the effect was associated with a lower rate of antigen-induced lymphocyte proliferation and lower production of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and interleukin-4 (IL-4). Pgia12 similarly delayed onset in males, but the effect was achieved by elevated proliferation of PG-specific lymphocytes and enhanced production of IFN-gamma and IL-4. The effect of the Pgia21 locus was arthritis-suppressive in females but PGIA-permissive in congenic males. These opposite effects are attributed to two-fold higher serum autoantibody and IL-6 levels in males than in females. Our study supports the idea that each congenic strain represents a different immunologic subtype of PGIA, providing an explanation for the complex etiology and various clinical phenotypes of rheumatoid arthritis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban proteoglycan-induced arthritis congenic strains inflammation cytokines autoimmunity sex effect
Megjelenés:	Genes and Immunity. - 9 : 7 (2008), p. 591-601. -
További szerzők:	Végvári Ákos Szabó Zoltán (1970-) (belgyógyász, reumatológus) Kis-Tóth Katalin (1975-) (immunológus) Mikecz Katalin Glant Tibor T.
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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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