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001-es BibID:	BIBFORM046369
Első szerző:	Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:	Differential distribution of intercellular adhesion molecules (ICAM-1, ICAM-2, and ICAM-3) and the MS-1 antigen in normal and diseased human synovia : their possible pathogenetic and clinical significance in rheumatoid arthritis / Szekanecz Z., Haines G. K., Lin T. R., Harlow L. A., Goerdt S., Rayan G., Koch A. E.
Dátum:	1994
ISSN:	0004-3591
Megjegyzések:	Cellular adhesion and differentiation molecules (CAMs) may play a role in the recruitment and retention of inflammatory cells into rheumatoid arthritis synovial tissue (RA ST). In order to determine if certain CAMs are up-regulated in RA ST compared with normal ST, we studied the distribution of intercellular adhesion molecules (ICAMs) 1, 2, and 3 in ST. We also studied the MS-1 antigen since it is preferentially expressed on discontinuous endothelia, such as those found in RA ST; MS-1 is also expressed differentially upon cytokine activation of cells in vitro or in pathologic conditions in situ. Thus, we postulated a possible similarity between MS-1 and ICAM-1 expression in inflamed ST. METHODS. Immunohistochemical analysis was used to determine the distribution of ICAMs and MS-1 in ST from 10 patients with RA, 10 with osteoarthritis (OA), and 4 normal individuals. RESULTS. ICAM-1 expression was found on significantly more RA ST endothelial cells compared with normal cells, as well as on RA ST macrophages and lining cells. ICAM-2, also found on endothelial cells, showed no differential staining pattern. ICAM-3 was present on RA ST macrophages and lining cells as well as on some RA and OA endothelial cells. The MS-1 antigen was present on most RA and OA ST endothelia, lining cells, and macrophages. ICAM-1 expression and MS-1 expression in the lining layer were positively correlated in both RA and OA. CONCLUSION. ICAM-1, while found mainly on endothelial cells, is up-regulated on RA ST macrophages and lining cells, suggesting a role for these cells in the infiltration and tissue damage seen in the RA ST. ICAM-3, which is present mainly on normal resting leukocytes but not on normal endothelium, is expressed by some diseased ST leukocytes and endothelial cells. MS-1 is also found on the RA ST specialized, fenestrated endothelium, on macrophages, and in the lining layer. These results suggest that the differential expression of ICAMs and MS-1 in RA ST compared with normal ST might play a special role in the pathogenesis of RA.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Arthritis and Rheumatism. - 37 : 2 (1994), p. 221-231. -
További szerzők:	Haines, G. Kenneth Lin, Theodore R. Harlow, Lisa A. Goerdt, Sergij Rayan, Ghazi Koch, Alisa E.
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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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.
Internet cím:	elektronikus változat DOI Intézményi repozitóriumban (DEA) tárolt változat
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