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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)
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2.

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)
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3.

001-es BibID:BIBFORM005613
Első szerző:Réthi Bence (biológus, immunológus)
Cím:Priming of T cells to Fas-mediated proliferative signals by interleukin-7 / Bence Rethi, Nancy Vivar, Stefano Sammicheli, Caroline Fluur, Nicolas Ruffin, Ann Atlas, Eva Rajnavolgyi, Francesca Chiodi
Dátum:2008
Megjegyzések:T-cell depletion associated with HIV infection or cytoreductive therapies triggers potential T-cell regenerative mechanisms such as peripheral T-lymphocyte expansion to weak antigenic stimuli and the increased availability of interleukin-7 (IL-7), a cytokine with potent antiapoptotic and proliferative activities. Deleterious mechanisms also associated with lymphopenia, such as increased Fas expression and apoptosis of T cell, however, may result in opposing effects. In this study, we show that Fas molecules, primarily associated with T-cell depletion in lymphopenic settings, may also contribute to compensatory T-cell expansion through transmitting costimulatory signals to suboptimally activated T cells. Proliferation of T lymphocytes in response to concomitant Fas and T-cell receptor (TCR) triggering was shown to be increased in HIV-infected individuals compared with noninfected controls. As IL-7 levels are often elevated in lymphopenic individuals in association with increased Fas expression, we analyzed whether IL-7 Would influence Fas-mediated proliferative signals in T cells. We show that IL-7 is able to increase the efficacy of Fas to induce proliferation of suboptimally activated T cells. Thus, high IL-7 levels associated with lymphopenic conditions may simultaneously induce sensitivity to Fas-mediated apoptosis in nonactivated T cells and increase Fas-induced costimulatory signals in T cells recognizing low-affinity antigens.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Virus TYPE-1 Infection
HIV-1 Infection
Homeostatic Proliferation
Receptro Expression
Sooty Mangabeys
Down-regulation
Up-regulation
Activation
Apoptosis
Megjelenés:Blood. - 112 : 4 (2008), p. 1195-1204. -
További szerzők:Vivar, Nancy Sammicheli, Stefano Fluur, Caroline Ruffin, Nicolas Atlas, Ann Rajnavölgyi Éva (1950-) (immunológus) Chiodi, Francesca
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