CCL

Összesen 4 találat.
#/oldal:
Részletezés:
Rendezés:

1.

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.
Internet cím:elektronikus változat
DOI
elektronikus változat
Borító:

2.

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.
Internet cím:elektronikus változat
elektronikus változat
Borító:

3.

001-es BibID:BIBFORM015783
Első szerző:Nesterovitch, Andrew B.
Cím:Spontaneous insertion of a B2 element in the ptpn6 gene drives a systemic autoinflammatory disease in mice resembling neutrophilic dermatosis in humans / Andrew B. Nesterovitch, Sandor Szanto, Andrea Gonda, Tamas Bardos, Katalin Kis-Toth, Vyacheslav A. Adarichev, Katalin Olasz, Sheida Ghassemi-Nejad, Mark D. Hoffman, Michael D. Tharp, Katalin Mikecz, Tibor T. Glant
Dátum:2011
ISSN:0002-9440
Megjegyzések:We found a spontaneous autosomal mutation in a mouse leading to neutrophil infiltration with ulceration in the upper dermis of homozygous offspring. These animals had increased neutrophil numbers, associated with normal lymphocyte count, in peripheral blood and bone marrow, suggesting a myeloproliferative disorder; however, granulocyte precursor proliferation in bone marrow was actually reduced (because circulating neutrophils were less susceptible to apoptosis). Neutrophil infiltration of the skin and other organs and high serum levels of immunoglobulins and autoantibodies, cytokines, and acute-phase proteins were additional abnormalities, all of which could be reduced by high-dose corticosteroid treatment or neutrophil depletion by antibodies. Use of genome-wide screening localized the mutation within an 0.4-Mbp region on mouse chromosome 6. We identified insertion of a B2 element in exon 6 of the Ptpn6 gene (protein tyrosine phosphatase, non-receptor type 6; also known as Shp-1). This insertion involves amino acid substitutions that significantly reduced the enzyme activity in mice homozygous for the mutation. Disease onset was delayed, and the clinical phenotype was milder than the phenotypes of other Ptpn6-mutants described in motheaten (me, mev) mice; we designated this new genotype as Ptpn6(meB2/meB2) and the phenotype as meB2. This new phenotype encompasses an autoinflammatory disease showing similarities to many aspects of the so-called neutrophilic dermatoses, a heterogeneous group of skin diseases with unknown etiology in humans.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Pathology 178 : 4 (2011), p. 1701-1714. -
További szerzők:Szántó Sándor (1968-) (belgyógyász, reumatológus) Gonda Andrea (1970-) (onkológus szakorvos) Bárdos Tamás Kis-Tóth Katalin (1975-) (immunológus) Adarichev, Vyacheslav A. Olasz Katalin Ghassemi-Nejad, Sheida (1980-) (fogorvos) Hoffman, Mark D. Tharp, Michael D. Mikecz Katalin Glant Tibor T.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
elektronikus elérés
Borító:

4.

001-es BibID:BIBFORM005804
Első szerző:Tunyogi-Csapó Miklós
Cím:Cytokine-controlled RANKL and osteoprotegerin expression by human and mouse synovial fibroblasts : fibroblast-mediated pathologic bone resorption / Miklos Tunyogi-Csapo, Katalin Kis-Toth, Marianna Radacs, Balint Farkas, Joshua J. Jacobs, Alison Finnegan, Katalin Mikecz, Tibor T. Glant
Dátum:2008
Megjegyzések:To determine whether proinflammatory cytokine treatment or the complete absence of select cytokines modulates the expression of RANKL and osteoprotegerin (OPG) in synovial fibroblasts. Methods. Fibroblasts were isolated from normal and rheumatoid human synovium and from normal or arthritic joints of wild-type and cytokine gene-deficient (interleukin-4-knockout [IL-4(-/-)] and interferon-gamma-knockout [IFN-gamma(-/-)]) mice. Fibroblasts were stimulated with proinflammatory cytokines (tumor necrosis factor alpha [TNF alpha], IL-1 beta, and IL-17) or antiosteoclastogenic cytokines (IL-4 and IFN-gamma), alone or in combination, and the expression of RANKL and OPG was measured. Results. Proinflammatory cytokine-stimulated fibroblasts from rheumatoid and arthritic mouse joints expressed higher levels of RANKL and OPG than those from normal joints. IL-4 suppressed RANK-L expression and increased OPG expression, IFN gamma reduced the production of both RANKL and OPG, and IL-17 had only a modest effect on the expression of RANKL or OPG. Additive effects of combination treatment (TNF alpha/IL-17 or IL-1 beta/1L-17) were observed only in the human system. Extensive destruction was observed in the arthritic joints of IL-4(-/-) mice, with a corresponding upward shift of the RANKL:OPG ratios. However, an IL-17 deficiency did not attenuate arthritis or reduce bone resorption. Conclusion. Proinflammatory cytokines induce the expression of RANKL and OPG in both human and murine synovial fibroblasts. The RANKL: OPG ratios are shifted in favor of bone protection by IL-4 treatment, and, to a lesser extent, by IFN gamma treatment. Unexpectedly, an IL-17 deficiency alone does not induce reduced inflammatory bone destruction. Our results suggest that synovial fibroblasts may significantly contribute to bone resorption through modulation of RANKL and OPG production in a cytokine-rich milieu of inflamed joints.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Kappa-B Ligand
Soluble receptor activator
Rheumatoid-arthritis
T-cells
Osteoclast formation
Mediated Osteoclastogenesis
Bone destruction
Interferon-gamma
Ifn-Gamma
TNF-Alpha
Megjelenés:Arthritis and Rheumatism. - 58 : 8 (2008), p. 2397-2408. -
További szerzők:Kis-Tóth Katalin (1975-) (immunológus) Radács Marianna Farkas Bálint Jacobs, Joshua J. Finnegan, Alison Mikecz Katalin Glant Tibor T.
Internet cím:elektronikus változat
DOI
elektronikus változat
Borító:
Rekordok letöltése1