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1.

001-es BibID:BIBFORM076382
Első szerző:Balogh Emese (reumatológus)
Cím:Autoimmune and angiogenic biomarkers in autoimmune atherosclerosis / Emese Balogh, Anita Pusztai, Attila Hamar, Edit Végh, Szilvia Szamosi, György Kerekes, Jennifer McCormick, Monika Biniecka, Sándor Szántó, Gabriella Szűcs, Zoltán Nagy, Ursula Fearon, Douglas J. Veale, Zoltán Szekanecz
Dátum:2019
ISSN:1521-6616
Megjegyzések:Several inflammatory, proteolytic, angiogenic and bone-associated factors play a role in the development of autoimmune, accelerated atherosclerosis in rheumatic diseases. Some of these may serve as biomarkers of vascular pathology and may be useful in the follow-up of vascular damage and outcome. Multi-biomarker profiles rather than a single markers would likely be optimal in this respect.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Autoimmune atherosclerosis
Cardiovascular disease
Autoimmunity
Angiogenesis
Biomarkers
Megjelenés:Clinical Immunology. - 199 (2019), p. 47-51. -
További szerzők:Karancsiné Pusztai Anita (1989-) (tudományos segédmunkatárs) Hamar Attila Béla (1990-) (általános orvos) Végh Edit (1978-) (reumatológus, belgyógyász) Szamosi Szilvia (1975-) (belgyógyász, reumatológus) Kerekes György (1973-) (belgyógyász, kardiológus, angiológus) McCormick, Jennifer Biniecka, Monika Szántó Sándor (1968-) (belgyógyász, reumatológus) Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Nagy Zoltán (orvos) Fearon, Ursula Veale, Douglas J. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
Pályázati támogatás:TÁMOP-4.2.4.A/2-11/1-2012-0001
TÁMOP
GINOP-2.3.2-15-2016-00015
GINOP
GINOP-2.3.2-15-2016-00050
GINOP
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2.

001-es BibID:BIBFORM044036
Első szerző:Besenyei Tímea (reumatológus, belgyógyász)
Cím:Non-MHC Risk Alleles in Rheumatoid Arthritis and in the Syntenic Chromosome Regions of Corresponding Animal Models / Besenyei Timea, Kadar Andras, Tryniszewska Beata, Kurko Julia, Rauch Tibor A., Glant Tibor T., Mikecz Katalin, Szekanecz Zoltan
Dátum:2012
ISSN:1740-2522
Megjegyzések:Rheumatoid arthritis (RA) is a polygenic autoimmune disease primarily affecting the synovial joints. Numerous animal models show similarities to RA in humans; some of them not only mimic the clinical phenotypes but also demonstrate the involvement of homologous genomic regions in RA. This paper compares corresponding non-MHC genomic regions identified in rodent and human genome-wide association studies (GWAS). To date, over 30 non-MHC RA-associated loci have been identified in humans, and over 100 arthritis-associated loci have been identified in rodent models of RA. The genomic regions associated with the disease are designated by the name(s) of the gene having the most frequent and consistent RA-associated SNPs or a function suggesting their involvement in inflammatory or autoimmune processes. Animal studies on rats and mice preferentially have used single sequence length polymorphism (SSLP) markers to identify disease-associated qualitative and quantitative trait loci (QTLs) in the genome of F2 hybrids of arthritis-susceptible and arthritis-resistant rodent strains. Mouse GWAS appear to be far ahead of rat studies, and significantly more mouse QTLs correspond to human RA risk alleles
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Rheumatoid arthritis
polygenic autoimmune disease
Megjelenés:Clinical And Development Immunology. - 2012 (2012), p. 1-14. -
További szerzők:Kádár András (1977-) (belgyógyász) Tryniszewska Beáta Kurkó Júlia Emese (1979-) (reumatológus) Rauch Tibor A. Glant Tibor T. Mikecz Katalin Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
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3.

001-es BibID:BIBFORM015807
Első szerző:Centola, Michael
Cím:Gene expression profiles of systemic lupus erythematosus and rheumatoid arthritis / Centola, M., Szekanecz, Z., Kiss, E., Zeher, M., Szegedi, G., Nakken, B., Szodoray, P.
Dátum:2007
ISSN:1744-666X
Megjegyzések:Gene expression profiling using microarray technology is being employed to define specific molecular mediators and pathways involved in immunobiology, to understand the intricate interplay of genes participating in the pathogenesis, and to develop biomarkers of disease activity in both systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). This review summarizes the latest information on the pathogenesis of SLE and RA and describes the utilization of microarray technology in these systemic autoimmune diseases.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
gene expression profile
microarray
rheumatoid arthritis
systemic lupus erythematosus
Megjelenés:Expert Review of Clinical Immunology. - 3 : 5 (2007), p. 797-806. -
További szerzők:Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Kiss Emese (1960-) (belgyógyász, immunológus) Zeher Margit (1957-2018) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Szegedi Gyula (1936-2013) (belgyógyász, immunológus) Nakken, Britt Szodoray Péter (1973-) (belgyógyász, orvos)
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4.

001-es BibID:BIBFORM007073
Első szerző:Koch, Alisa E.
Cím:Effects of thrombospondin-1 on disease course and angiogenesis in rat adjuvant-induced arthritis / Koch, A. E., Szekanecz, Z., Friedman, J., Haines, G. K., Langman, C. B., Bouck, N. P.
Dátum:1998
ISSN:0090-1229 (Print)
Megjegyzések:Leukocyte extravasation into the synovium is important in rheumatoid arthritis (RA). Thrombospondin (TSP)-1 mediates cell adhesion and migration and inhibits angiogenesis, and it has been implicated in RA. However, little information is available on the role of TSP-1 in arthritis-associated inflammation and neovascularization. Therefore, we analyzed the effects of TSP-1 in adjuvant-induced arthritis (AIA), a rat model for RA. Hydron pellets containing TSP-1 were implanted in one ankle of AIA rats post-adjuvant injection, while the contralateral ankle received sham implants. Body weight loss and joint swelling were determined in comparison to nonimplanted AIA controls. In addition, synovial vessel counts were obtained in TSP-1-versus sham-implanted ankles of the same rat. The implantation of TSP-1 pellets into one ankle resulted in an enhancement of swelling in both ankles. Furthermore, TSP-1 exhibited a biphasic modulatory effect on synovial vessel counts (P < 0.05). In conclusion, TSP-1 implanted into one ankle of AIA rats may augment the severity of the disease. One possible explanation, among others, for the modulating effect of TSP-1 on inflammation may be its effect on arthritis-related angiogenesis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Animals
Arthritis, Experimental
Arthritis, Rheumatoid
Body Weight
Disease Models, Animal
Dose-Response Relationship, Drug
Joints
Neovascularization, Pathologic
Rats
Rats, Inbred Lew
Tarsus, Animal
Thrombospondin 1
Megjelenés:Clinical Immunology and Immunopathology. - 86 : 2 (1998), p. 199-208. -
További szerzők:Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Friedman, J. Haines, G. Kenneth Langman, C. B. Bouck, N. P.
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5.

001-es BibID:BIBFORM044038
Első szerző:Kurkó Júlia Emese (reumatológus)
Cím:Genetics of Rheumatoid Arthritis : a Comprehensive Review / Kurkó Júlia, Besenyei Timea, Laki Judit, Glant Tibor T., Mikecz Katalin, Szekanecz Zoltán
Dátum:2013
ISSN:1080-0549
Megjegyzések:The "Bermuda triangle" of genetics, environment and autoimmunity is involved in the pathogenesis of rheumatoid arthritis (RA). Various aspects of genetic contribution to the etiology, pathogenesis and outcome of RA are discussed in this review. The heritability of RA has been estimated to be about 60 %, while the contribution of HLA to heritability has been estimated to be 11-37 %. Apart from known shared epitope (SE) alleles, such as HLA-DRB1*01 and DRB1*04, other HLA alleles, such as HLA-DRB1*13 and DRB1*15 have been linked to RA susceptibility. A novel SE classification divides SE alleles into S1, S2, S3P and S3D groups, where primarily S2 and S3P groups have been associated with predisposition to seropositive RA. The most relevant non-HLA gene single nucleotide polymorphisms (SNPs) associated with RA include PTPN22, IL23R, TRAF1, CTLA4, IRF5, STAT4, CCR6, PADI4. Large genome-wide association studies (GWAS) have identified more than 30 loci involved in RA pathogenesis. HLA and some non-HLA genes may differentiate between anti-citrullinated protein antibody (ACPA) seropositive and seronegative RA. Genetic susceptibility has also been associated with environmental factors, primarily smoking. Some GWAS studies carried out in rodent models of arthritis have confirmed the role of human genes. For example, in the collagen-induced (CIA) and proteoglycan-induced arthritis (PgIA) models, two important loci - Pgia26/Cia5 and Pgia2/Cia2/Cia3, corresponding the human PTPN22/CD2 and TRAF1/C5 loci, respectively - have been identified. Finally, pharmacogenomics identified SNPs or multiple genetic signatures that may be associated with responses to traditional disease-modifying drugs and biologics
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Rheumatoid arthritis
Murine arthritis
Genetics
Single nucleotide polymorphisms
HLA-DR
GWAS
Megjelenés:Clinical Reviews In Allergy & Immunology 45 : 2 (2013), p. 170-179. -
További szerzők:Besenyei Tímea (1980-) (reumatológus, belgyógyász) Laki Judit Glant Tibor T. Mikecz Katalin Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
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6.

001-es BibID:BIBFORM035128
035-os BibID:(cikkazonosító)957151
Első szerző:Nakken, Britt
Cím:Immune-regulatory mechanisms in systemic autoimmune and rheumatic diseases / Britt Nakken, Philip Alex, Ludvig Munthe, Zoltan Szekanecz, Peter Szodoray
Dátum:2012
Megjegyzések:Systemic autoimmune and rheumatic diseases (SAIRDs) are thought to develop due to the failure of autoimmune regulation and tolerance. Current therapies, such as biologics, have improved the clinical results of SAIRDs; however, they are not curative treatments. Recently, new discoveries have been made in immune tolerance and inflammation, such as tolerogenic dendritic cells, regulatory T and B cells, Th 17 cells, inflammatory and tolerogenic cytokines, and intracellular signaling pathways. They lay the foundation for the next generation of the therapies beyond the currently used biologic therapies. New drugs should target the core processes involved in disease mechanisms with the aim to attain complete cure combined with safety and low costs compared to the biologic agents. Re-establishment of autoimmune regulation and tolerance in SAIRDs by the end of the current decade should be the final and realistic target.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical and Developmental Immunology. - 2012 (2012), p. 1-2. -
További szerzők:Philip, Alex Munthe, Ludvig A. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Szodoray Péter (1973-) (belgyógyász, orvos)
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7.

001-es BibID:BIBFORM015838
Első szerző:Orbach, Hedi
Cím:Prolactin and Autoimmunity : hyperprolactinemia Correlates with Serositis and Anemia in SLE Patients / Orbach, H., Zandman-Goddard, G., Boaz, M., Agmon-Levin, N., Amital, H., Szekanecz, Z., Szucs, G., Rovensky, J., Kiss, E., Doria, A., Ghirardello, A., Gomez-Arbesu, J., Stojanovich, L., Ingegnoli, F., Meroni, P. L., Rozman, B., Blank, M., Shoenfeld, Y.
Dátum:2012
ISSN:1559-0267 (Electronic)
Megjegyzések:Evidence points to an association of prolactin to autoimmune diseases. We examined the correlation between hyperprolactinemia and disease manifestations and activity in a large patient cohort. Age- and sex-adjusted prolactin concentration was assessed in 256 serum samples from lupus patients utilizing the LIASON prolactin automated immunoassay method (DiaSorin S.p.A, Saluggia, Italy). Disease activity was defined as present if European Consensus Lupus Activity Measurement (ECLAM) > 2 or Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) > 4. Lupus manifestations were grouped by organ involvement, laboratory data, and prescribed medications. Hyperprolactinemia was presented in 46/256 (18%) of the cohort. Hyperprolactinemic patients had significantly more serositis (40% vs. 32.4%, p = 0.03) specifically, pleuritis (33% vs. 17%, p = 0.02), pericarditis (30% vs. 12%, p = 0.002), and peritonitis (15% vs. 0.8%, p = 0.003). Hyperprolactinemic subjects exhibited significantly more anemia (42% vs. 26%, p = 0.02) and marginally more proteinuria (65.5% vs. 46%, p = 0.06). Elevated levels of prolactin were not significantly associated with other clinical manifestations, serology, or therapy. Disease activity scores were not associated with hyperprolactinemia. Hyperprolactinemia in lupus patients is associated with all types of serositis and anemia but not with other clinical, serological therapeutic measures or with disease activity. These results suggest that dopamine agonists may be an optional therapy for lupus patients with hyperprolactinemia.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical Reviews in Allergy and Immunology. - 42 : 2 (2012), p. 189-198. -
További szerzők:Zandman-Goddard, Gisele Boaz, Mona Agmon-Levin, Nancy Amital, Howard Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Rovensky, Josef Kiss Emese (1960-) (belgyógyász, immunológus) Doria, Andrea Ghirardello, A. Gomez-Arbesu, Jesus Stojanovich, Ljudmila Ingegnoli, Francesca Meroni, Pier Luigi Rozman, Blaz Blank, Marion Shoenfeld, Yehuda
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8.

001-es BibID:BIBFORM007089
Első szerző:Szamosi Szilvia (belgyógyász, reumatológus)
Cím:Plasma homocysteine levels, the prevalence of methylenetetrahydrofolate reductase gene C677T polymorphism and macrovascular disorders in systemic sclerosis : risk factors for accelerated macrovascular damage? / Szamosi, S., Csiki, Z., Szomjak, E., Szolnoki, E., Szoke, G., Szekanecz, Z., Szegedi, G., Shoenfeld, Y., Szucs, G.
Dátum:2009
ISSN:1080-0549 (Print)
Megjegyzések:The purpose of this study was to investigate plasma homocysteine (Hcy) levels in patients with systemic sclerosis (SSc) and to study the association between plasma Hcy, C677T polymorphism of 5,10-methylenetetrahydrofolate reductase (MTHFR), and the clinical manifestations in SSc. Associations of Hcy level, C677T MTHFR polymorphism, and macrovascular diseases were investigated in 152 patients with SSc and 58 controls. No significant differences in Hcy levels and MTHFR genotypes were found in SSc patients compared to controls or in SSc patients with limited cutaneous compared to diffuse disease. Significantly higher Hcy concentration was observed in patients with macroangiopathy/thromboembolic events compared to patients without such clinical manifestations (p < 0.05). There was significant correlation between age and macrovascular disorders, between Hcy level and the disease duration (r = 0.164; p < 0.05). Seventy-one percent of patients with macrovascular disorders had MTHFR polymorphism. In addition, 45% of patients with hyperhomocysteinemia had pulmonary hypertension. The presence of MTHFR C677T mutation influences the incidence of macrovascular abnormalities in SSc patients. Elevated Hcy levels may be associated with disease duration and the evolution of macrovascular disorders and pulmonary hypertension in SSc.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Female
egyetemen (Magyarországon) készült közlemény
Genetic Predisposition to Disease
Homocysteine
Humans
Hypertrophy, Right Ventricular
Male
Methylenetetrahydrofolate Reductase (NADPH2)
Middle Aged
Polymorphism, Single Nucleotide
Pulmonary Fibrosis
Risk Factors
Scleroderma, Systemic
Thromboembolism
Time Factors
Megjelenés:Clinical Reviews in Allergy and Immunology. - 36 : 2-3 (2009), p. 145-9. -
További szerzők:Csiki Zoltán (1962-) (belgyógyász, allergológus, klinikai immunológus, reumatológus) Szomják Edit (1961-) (belgyógyász) Szolnoki Erzsébet Szőke Gabriella Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Szegedi Gyula (1936-2013) (belgyógyász, immunológus) Shoenfeld, Yehuda Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus)
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DOI
elektronikus változat
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9.

001-es BibID:BIBFORM027494
Első szerző:Szegedi Gyula (belgyógyász, immunológus)
Cím:Polysystemic autoimmune diseases : clinical and basic research made in Hungary / Gyula Szegedi, Emese Kiss, Edit Bodolay, Margit Zeher, Katalin Dankó, László Czirják, Gabriella Szűcs, Zoltán Szekanecz, Sándor Sipka
Dátum:1996
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Allergy and Clinical Immunology International 8 : 3 (1996), p. 90-93. -
További szerzők:Kiss Emese (1960-) (belgyógyász, immunológus) Bodolay Edit (1950-) (belgyógyász, allergológus és klinikai immunológus) Zeher Margit (1957-2018) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Dankó Katalin (1952-2021) (belgyógyász, allergológus és klinikai immunológus) Czirják László Szűcs Gabriella (1963-) (belgyógyász, allergológus és klinikai immunológus, reumatológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Sipka Sándor (1945-) (laboratóriumi szakorvos)
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10.

001-es BibID:BIBFORM007104
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Increased synovial expression of transforming growth factor (TGF)-beta receptor endoglin and TGF-beta 1 in rheumatoid arthritis : possible interactions in the pathogenesis of the disease / Szekanecz, Z., Haines, G. K., Harlow, L. A., Shah, M. R., Fong, T. W., Fu, R., Lin, S. J., Rayan, G., Koch, A. E.
Dátum:1995
ISSN:0090-1229 (Print)
Megjegyzések:The ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST) plays a role in the pathogenesis of this disease. Transforming growth factor beta (TGF-beta) may play a role in this process. We have investigated the distribution of endoglin, a newly described receptor for TGF-beta 1 and -beta 3, in RA compared to osteoarthritis (OA) or normal ST. Immunohistochemical analysis was carried out using an anti-TGF-beta 1 monoclonal antibody (mAb) as well as 10 mAbs raised against various epitopes of endoglin. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. TGF-beta 1 expression was significantly up-regulated on RA compared to OA and normal ST lining cells, interstitial macrophages, and endothelial cells (P < 0.05). All anti-endoglin mAbs uniformly reacted with endothelial cells in RA, OA, and normal STs. However, 3 out of 10 anti-endoglin mAbs reacted with significantly more RA versus normal ST lining cells (P < 0.05), as well as RA compared to OA and normal macrophages (P < 0.05). There was a positive correlation between TGF-beta 1 and endoglin reactivity on the synovial lining layer and subsynovial macrophages (P < 0.05). These results indicate that TGF-beta 1 and certain epitopes of endoglin, a TGF-beta 1 and -beta 3 receptor, are up-regulated on myeloid elements in RA compared to normal ST. Endoglin is also present on ST endothelia, and its expression may also be increased on OA compared to normal ST lining cells. These findings implicate endoglin in the pathogenesis of RA.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Antibodies, Monoclonal
Antigens, CD
Arthritis, Rheumatoid
Humans
Membrane Glycoproteins
Osteoarthritis
Receptors, Cell Surface
Synovial Membrane
Transforming Growth Factor beta
Vascular Cell Adhesion Molecule-1
Megjelenés:Clinical Immunology and Immunopathology. - 76 : 2 (1995), p. 187-194. -
További szerzők:Haines, G. Kenneth Harlow, Lisa A. Shah, M. R. Fong, T. W. Fu, Rao Lin, S. J. Rayan, Ghazi Koch, Alisa E.
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DOI
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11.

001-es BibID:BIBFORM007103
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Increased synovial expression of the adhesion molecules CD66a, CD66b, and CD31 in rheumatoid and osteoarthritis / Szekanecz, Z., Haines, G. K., Harlow, L. A., Shah, M. R., Fong, T. W., Fu, R., Lin, S. J., Koch, A. E.
Dátum:1995
ISSN:0090-1229 (Print)
Megjegyzések:Leukocyte-endothelial interaction mediated by adhesion molecules may play a role in the ingress of inflammatory cells into the rheumatoid (RA) synovial tissue (ST). A number of these molecules have been shown to be up-regulated in the inflamed compared to normal ST. We studied the distribution of two members of the CD66 carcinoembryonic antigen adhesion molecule family, as well as that of CD31, an antigen structurally related to CD66, on various cell types in the RA compared to osteoarthritic (OA) and normal ST. Immunoperoxidase histochemistry was carried out using monoclonal antibodies to CD66a, CD66b, and CD31. This study was performed on ST from 10 patients with RA, 10 with OA, and 4 normal individuals. CD66a, and CD66b were expressed on RA and OA ST myeloid cells but not on normal ST lining cells and interstitial macrophages, suggesting that these antigens may be specific markers of diseased compared to normal ST macrophages (P < 0.05). CD31 was present on more RA and OA than on normal ST macrophages. Also, CD31 was present on most RA, OA, and normal ST endothelial cells. Our results indicate that the expression of CD66a, CD66b, and CD31, members of the immunoglobulin superfamily of adhesion receptors, is up-regulated on cells of myeloid origin in the inflamed compared to normal ST. These results suggest that the CD66 antigens and CD31 may be involved in the adhesive events in the inflamed synovium.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Antigens, CD
Antigens, CD31
Antigens, Differentiation
Antigens, Differentiation, Myelomonocytic
Arthritis, Rheumatoid
Cell Adhesion Molecules
Humans
Osteoarthritis
Synovial Membrane
Megjelenés:Clinical Immunology and Immunopathology. - 76 : 2 (1995), p. 180-186. -
További szerzők:Haines, G. Kenneth Harlow, Lisa A. Shah, M. R. Fong, T. W. Fu, Rao Lin, S. J. Koch, Alisa E.
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12.

001-es BibID:BIBFORM007128
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Intercellular adhesion molecule-1 (ICAM-1) expression and soluble ICAM-1 (sICAM-1) production by cytokine-activated human aortic endothelial cells : a possible role for ICAM-1 and sICAM-1 in atherosclerotic aortic aneurysms / Szekanecz, Z., Shah, M. R., Pearce, W. H., Koch, A. E.
Dátum:1994
ISSN:0009-9104 (Print)
Megjegyzések:The interactions of inflammatory cells, cytokines, and cell adhesion molecules (CAM) may be important in the pathogenesis of vascular diseases such as abdominal aortic aneurysms (AAA), in which inflammation plays a role. The aim of this study was to investigate the pathogenic role of ICAM-1, a molecule involved in leucocyte-endothelial interactions, in vascular inflammation. ELISA of human explant culture supernatants revealed a four-fold increase in sICAM-1 production by AAA (n = 9) versus normal (n = 8) aortic explants. Human aortic endothelial cell (hAEC) culture was used for further studies as an in vitro model for aortic inflammatory conditions. Tumour necrosis factor-alpha (TNF-alpha) or IL-1 beta treatment of hAEC resulted in an up to 1.8-fold significant increase in sICAM-1 production compared with resting cells. In addition, the expression of ICAM-1 on cytokine-stimulated versus resting hAEC was measured by radioimmunoassay. TNF-alpha significantly induced ICAM-1 expression on these cells. These results suggest that different forms of ICAM-1, present on or released by the activated aortic endothelium, may be involved in leucocyte adhesion to and migration into the vessel wall.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Aorta, Abdominal
Aortic Aneurysm, Abdominal
Arteriosclerosis
Cells, Cultured
Culture Media, Conditioned
Cytokines
Endothelium, Vascular
Enzyme-Linked Immunosorbent Assay
HLA-DR Antigens
Humans
Intercellular Adhesion Molecule-1
Radioimmunoassay
Megjelenés:Clinical and Experimental Immunology. - 98 : 2 (1994), p. 337-343. -
További szerzők:Shah, M. R. Pearce, W. H. Koch, Alisa E.
Internet cím:elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
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