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001-es BibID:	BIBFORM001482
Első szerző:	Gogolák Péter (biológus, immunológus)
Cím:	Differentiation of CD1a- and CD1a+ monocyte-derived dendritic cells is biased by lipid environment and PPARgamma / Gogolak P., Réthi B., Szatmári I., Nagy L., Lányi Á., Dezső B., Rajnavölgyi É.
Dátum:	2007
Megjegyzések:	Accumulating data have shown that the microenvironment of dendritic cells modulates subtype differentiation and CD1 expression, but the mechanisms by which exogenous factors confer these effects are poorly understood. Here we describe the dependence of CD1a- monocyte-derived dendritic cell (moDC) development on lipids associated with the expression of peroxisome proliferator-activated receptor-gamma (PPARgamma). We also show the consecutive differentiation of immature CD1a-PPARgamma+ moDCs to CD1a+PPARgamma- cells limited by serum lipoproteins and terminated by proinflammatory cytokines. Immature CD1a- moDCs possess higher internalizing capacity than CD1a+ cells, whereas both activated subtypes have similar migratory potential but differ in their cytokine and chemokine profiles, which translates to distinct T-lymphocyte-polarizing capacities. CD1a+ moDCs stand out by their capability to secrete high amounts of IL-12p70 and CCL1. As lipoproteins skew moDC differentiation toward the generation of CD1a-PPARgamma+ cells and inhibit the development of CD1a+PPARgamma- cells, we suggest that the uptake of lipids results in endogenous PPARgamma agonists that induce a cascade of gene transcription coordinating lipid metabolism, the expression of lipid-presenting CD1 molecules, subtype dichotomy, and function. The presence of CD1a-PPARgamma+ and CD1a+PPARgamma- DCs in lymph nodes and in pulmonary Langerhans cell histiocytosis confirms the functional relevance of these DC subsets in vivo.
Tárgyszavak:	Orvostudományok Természettudományok Elméleti orvostudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban dendritic cell differentiation CD1a PPARgamma lipid lipoprotein T cell polarization
Megjelenés:	Blood. - 109 : 2 (2007), p. 643-652. -
További szerzők:	Réthi Bence (1973-) (biológus, immunológus) Lányi Árpád (1962-) (biológus, immunológus) Dezső Balázs (1951-) (pathológus) Rajnavölgyi Éva (1950-) (immunológus) Szatmári István (1971-) (biológus) Nagy László (1966-) (molekuláris sejtbiológus, biokémikus)
Internet cím:	elektronikus változat elektronikus változat DOI
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001-es BibID:	BIBFORM019938
Első szerző:	Réthi Bence (biológus, immunológus)
Cím:	SLAM/SLAM interactions inhibit CD40-induced production of inflammatory cytokines in monocyte-derived dendritic cells / Bence Réthi, Péter Gogolák, Istvan Szatmari, Ágota Veres, Erika Erdős, Laszlo Nagy, Éva Rajnavölgyi, Cox Terhorst, Árpád Lányi
Dátum:	2006
ISSN:	0006-4971
Megjegyzések:	Signaling lymphocyte activation molecule (SLAM, CD150, or SLAMF1) is a self-ligand receptor on the surface of activated T- and B-lymphocytes, macrophages, and dendritic cells (DCs). Here we examine the effect of SLAM/SLAM interactions on CD40L-induced CD40 signaling pathways in human DCs. CD40L-expressing L929 cells induced DCs to produce interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and IL-12, which was strongly inhibited by coexpression of SLAM on the surface of the L929 cells. Similarly, transfection of DCs with SLAM strongly reduced CD40L-induced IL-12 production. Furthermore, the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide (LPS). LPS-Induced IL-12 secretion, however, was not inhibited by SLAM engagement. CD40L-activated DCs affected by exposure to SLAM/SLAM engagement were impaired in their ability to induce differentiation of naive T lymphocytes into interferon-gamma (IFN-gamma)-producing T-helper 1 (Th1) effector cells. These inhibitory effects were not the result of a general unresponsiveness of DCs to CD40L, as SLAM/SLAM interactions did not prevent CD40L-induced up-regulation of CD83, CD86, or human leukocyte antigen (HLA)-DQ on the surface of DCs. Taken together, the results indicate that SLAM/SLAM interactions inhibit CD40-induced signal transduction in monocyte-derived dendritic cells, an effect that was not detectable in earlier studies using anti-SLAM monoclonal antibodies.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban linked lymphoproliferative-disease lymphocytic activation molecule controls T-cell measles virus differential expression immune-responses encoding gene CD150 SLAM in-vitro SAP
Megjelenés:	Blood. - 107 : 7 (2006), p. 2821-2829. -
További szerzők:	Gogolák Péter (1968-) (biológus, immunológus) Szatmári István (1971-) (biológus) Veres Ágota (laboráns) Erdős Erika Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Rajnavölgyi Éva (1950-) (immunológus) Terhorst, Cox Lányi Árpád (1962-) (biológus, immunológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM065565
Első szerző:	Sümegi János
Cím:	Correlation of mutations of the SH2D1A gene and Epstein-Barr virus infection with clinical phenotype and outcome in X-linked lymphoproliferative disease / Janos Sumegi, Dali Huang, Arpad Lanyi, Jack D. Davis, Thomas A. Seemayer, Akihiko Maeda, George Klein, Marco Seri, Hiroshi Wakiguchi, David T. Purtilo, Thomas G. Gross
Dátum:	2000
ISSN:	0006-4971
Megjegyzések:	The purposes of this study were to determine the frequency of mutations in SH2D1A in X-linked lymphoproliferative disease (XLP) and the role of SH2D1A mutations and Epstein-Barr virus (EBV) infection in determining the phenotype and outcome of patients with XLP. Analysis of 35 families from the XLP Registry revealed 28 different mutations in 34 families-large genomic deletions (n = 3), small intragenic deletions (n = 10), splice-site (n = 3), nonsense (n = 3), and missense (n = 9) mutations. No mutations were found in 25 males, so-called sporadic XLP (males with an XLP phenotype after EBV infection but no family history of XLP) or in 9 patients with chronic active EBV syndrome. Of 304 symptomatic males in the XLP Registry, 38 had no evidence of EBV infection at first clinical manifestation. When fulminant infectious mononucleosis (FIM) was excluded, there was no statistical difference in the frequency of EBV infectivity in the other XLP phenotypes. Furthermore, there was no difference at age of first clinical manifestation between EBV(+) and EBV(-) males or in survival when patients with FIM were excluded. In conclusion, it was found that mutations in the SH2D1A gene are responsible for XLP but that there is no correlation between genotype and phenotype or outcome. It was also found that though EBV infection often results in FIM, it is unnecessary for the expression of other manifestations of XLP, and it correlates poorly with outcome. These results suggest that unidentified factors, either environmental or genetic (eg, modifier genes), contribute to the pathogenesis of XLP.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Blood 96 : 9 (2000), p. 3118-3125. -
További szerzők:	Huang, Dali Lányi Árpád (1962-) (biológus, immunológus) Davis, Jack Seemayer, Thomas A. Maeda, Akihiko Klein, George Seri, Marco Wakiguchi, Hiroshi Purtilo, David T. Gross, Thomas G.
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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