Magyar
Toggle navigation
Tudóstér
Magyar
Tudóstér
Keresés
Egyszerű keresés
Összetett keresés
CCL keresés
Egyszerű keresés
Összetett keresés
CCL keresés
Böngészés
Saját polc tartalma
(
0
)
Korábbi keresések
CCL parancs
CCL
Összesen 2 találat.
#/oldal:
12
36
60
120
Rövid
Hosszú
MARC
Részletezés:
Rendezés:
Szerző növekvő
Szerző csökkenő
Cím növekvő
Cím csökkenő
Dátum növekvő
Dátum csökkenő
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:
Saját polcon:
2.
001-es BibID:
BIBFORM073044
Első szerző:
Miller, Frederick W.
Cím:
Genome-wide Association Study Identifies HLA 8.1 Ancestral Haplotype Alleles as Major Genetic Risk Factors for Myositis Phenotypes / Frederick W. Miller, Wei Chen, Terrance P. O'Hanlon, Robert G. Cooper, Jiri Vencovsky, Lisa G. Rider, Katalin Danko, Lucy R. Wedderburn, Ingrid E. Lundberg, Lauren M. Pachman, Ann M. Reed, Steven R. Ytterberg, Leonid Padyukov, Albert SelvaO'Callaghan, Timothy R. Radstake, David A. Isenberg, Hector Chinoy, William E. R. Ollier, Paul Scheet, Bo Peng, Annette Lee, Jinyoung Byun, Janine A. Lamb, Peter K. Gregersen, Christopher I. Amos, the Myositis Genetics Consortium
Dátum:
2015
ISSN:
1466-4879 1476-5470
Megjegyzések:
Autoimmune muscle diseases (myositis) comprise a group of complex phenotypes influenced by genetic and environmental factors. To identify genetic risk factors in patients of European ancestry, we conducted a genome-wide association study (GWAS) of the major myositis phenotypes in a total of 1710 cases, which included 705 adult dermatomyositis; 473 juvenile dermatomyositis; 532 polymyositis; and 202 adult dermatomyositis, juvenile dermatomyositis or polymyositis patients with anti-histidyl tRNA synthetase (anti-Jo-1) autoantibodies, and compared them with 4724 controls. Single-nucleotide polymorphisms showing strong associations (P < 5 ? 10?8) in GWAS were identified in the major histocompatibility complex (MHC) region for all myositis phenotypes together, as well as for the four clinical and autoantibody phenotypes studied separately. Imputation and regression analyses found that alleles comprising the human leukocyte antigen (HLA) 8.1 ancestral haplotype (AH8.1) defined essentially all the genetic risk in the phenotypes studied. Although the HLA DRB1*03:01 allele showed slightly stronger associations with adult and juvenile dermatomyositis, and HLA B*08:01 with polymyositis and anti-Jo-1 autoantibody-positive myositis, multiple alleles of AH8.1 were required for the full risk effects. Our findings establish that alleles of the AH8.1haplotype comprise the primary genetic risk factors associated with the major myositis phenotypes in geographically diverse Caucasian populations.
Tárgyszavak:
Orvostudományok
Klinikai orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
polymyositis
dermatomyositis
adult
juvenile
anti-Jo-1 autoantibodies
HLA 8.1 ancestral haplotype
Megjelenés:
Genes And Immunity 16 : 7 (2015), p. 470-480. -
További szerzők:
Chen, Wei
O'Hanlon, Terrance P.
Cooper, Robert G.
Vencovsky, Jiri
Rider, Lisa G.
Dankó Katalin (1952-2021) (belgyógyász, allergológus és klinikai immunológus)
Wedderburn, Lucy R.
Lundberg, Ingrid
Pachman, Lauren M.
Reed, Ann M.
Ytterberg, Steven R.
Padyukov, Leonid
Selva-O'Callaghan, Albert
Radstake, Timothy R. D. J.
Isenberg, David A.
Chinoy, Hector
Ollier, William E.
Scheet, Paul
Peng, Bo
Lee, Annette
Byun, Jinyoung
Lamb, Janine A.
Gregersen, Peter K.
Amos, Christopher I.
the Myositis Genetics Consortium
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
Rekordok letöltése
1
Corvina könyvtári katalógus v8.2.27
© 2023
Monguz kft.
Minden jog fenntartva.