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001-es BibID:	BIBFORM015938
Első szerző:	Glant Tibor T.
Cím:	Disease-associated qualitative and quantitative trait loci in proteoglycan-induced arthritis and collagen-induced arthritis / T. T. Glant, V. A. Adarichev, A. B. Nesterovitch, S. Szanto, J. P. Oswald, J. J. Jacobs, G. Firneisz, J. Zhang, A. Finnegan, K. Mikecz
Dátum:	2004
ISSN:	0002-9629 (Print)
Megjegyzések:	Two autoimmune murine models--proteoglycan (aggrecan)-induced arthritis (PGIA) and collagen-induced arthritis (CIA)--were developed in parent strains, F1 and F2 hybrids of major histocompatibility complex (MHC)-matched (H-2) BALB/c x DBA/2 and MHC-unmatched (H-2/H-2) BALB/c x DBA/1 intercrosses. The major goal of this comparative study was to identify disease (model)-specific (PGIA or CIA) and shared clinical and immunologic loci in 2 types of genetic intercrosses. Qualitative (binary/susceptibility) and quantitative (severity and onset) clinical trait loci were separated and analyzed independently or together with various pathophysiologic/immunologic traits, such as antigen-specific T- and B-cell responses and cytokine production. The major quantitative trait locus (QTL) was the MHC on chromosome 17, which was especially dominant in CIA. In addition, chromosomes 3, 5, 10, and X contained shared clinical loci in both models, and a total of 8 QTLs (clinical traits together with immunologic traits) were colocalized in PGIA and CIA.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Antibodies/immunology/metabolism Arthritis, Experimental/genetics/immunology Arthritis, Rheumatoid/chemically induced/genetics/immunology Cytokines/immunology/metabolism Disease Susceptibility Genetic Linkage Humans Major Histocompatibility Complex Mice Mice, Inbred BALB C Mice, Inbred DBA Proteoglycans/immunology/toxicity Quantitative Trait Loci T-Lymphocytes/immunology/metabolism
Megjelenés:	The American journal of the medical sciences. - 327 : 4 (2004), p. 188-95. -
További szerzők:	Adarichev, Vyacheslav A. Nesterovitch, Andrew B. Szántó Sándor (1968-) (belgyógyász, reumatológus) Oswald, J. P. Jacobs, Joshua J. Firneisz Gábor Zhang, J. Finnegan, Alison Mikecz Katalin
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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
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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.
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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