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1.

001-es BibID:BIBFORM110227
035-os BibID:(cikkazonosító)6216 (Scopus)85152336402 (WoS)000969756600001
Első szerző:Cozzolino, Marco (biológus)
Cím:The Voltage-Gated Hv1 H⁺ Channel Is Expressed in Tumor-Infiltrating Myeloid-Derived Suppressor Cells / Cozzolino Marco, Gyöngyösi Adrienn, Korpos Eva, Gogolak Peter, Naseem Muhammad Umair, Kállai Judit, Lanyi Arpad, Panyi Gyorgy
Dátum:2023
ISSN:1422-0067
Megjegyzések:Myeloid-derived suppressor cells (MDSCs) are key determinants of the immunosuppressive microenvironment in tumors. As ion channels play key roles in the physiology/pathophysiology of immune cells, we aimed at studying the ion channel repertoire in tumor-derived polymorphonuclear (PMN-MDSC) and monocytic (Mo-MDSC) MDSCs. Subcutaneous tumors in mice were induced by the Lewis lung carcinoma cell line (LLC). The presence of PMN-MDSC (CD11b+/Ly6G+) and Mo-MDSCs (CD11b+/Ly6C+) in the tumor tissue was confirmed using immunofluorescence microscopy and cells were identified as CD11b+/Ly6G+ PMN-MDSCs and CD11b+/Ly6C+/F4/80?/MHCII? Mo-MDSCs using flow cytometry and sorting. The majority of the myeloid cells infiltrating the LLC tumors were PMN-MDSC (~60%) as compared to ~10% being Mo-MDSCs. We showed that PMN- and Mo-MDSCs express the Hv1 H+ channel both at the mRNA and at the protein level and that the biophysical and pharmacological properties of the whole-cell currents recapitulate the hallmarks of Hv1 currents: ~40 mV shift in the activation threshold of the current per unit change in the extracellular pH, high H+ selectivity, and sensitivity to the Hv1 inhibitor ClGBI. As MDSCs exert immunosuppression mainly by producing reactive oxygen species which is coupled to Hv1-mediated H+ currents, Hv1 might be an attractive target for inhibition of MDSCs in tumors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Myeloid-derived suppressor cell
Hv1 proton channel
tumor microenvironment
Megjelenés:International Journal Of Molecular Sciences. - 24 : 7 (2023), p. 1-24. -
További szerzők:Gyöngyösi Adrienn (1982-) (biológus) Korpos Éva (1974-) Gogolák Péter (1968-) (biológus, immunológus) Naseem, Muhammad Umair (1993-) (biofizikus, molekuláris biológus) Kállai Judit (1983-) (molekuláris biológus) Lányi Árpád (1962-) (biológus, immunológus) Panyi György (1966-) (biofizikus)
Pályázati támogatás:K119417
OTKA
K131708
OTKA
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2.

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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3.

001-es BibID:BIBFORM065574
Első szerző:Nagy Noémi, M. (vegyész, angol szakfordító)
Cím:SH2D1A and SLAM protein expression in human lymphocytes and derived cell lines / Noémi Nagy, Cristina Cerboni, Karin Mattsson, Akihiko Maeda, Péter Gogolák, János Sümegi, Árpád Lányi, LáSzló Székely, Ennio Carbone, George Klein, Eva Klein
Dátum:2000
ISSN:0020-7136
Megjegyzések:he gene defect responsible for the X-linked lymphoproliferative disease (XLP) is associated with an impaired control of Epstein-Barr virus (EBV) infection. The gene has been recently identified and the encoded protein (designated SH2D1A, DSHP or SAP) was characterized. It is a 128 amino acid (aa) protein, containing a single Src homology 2 (SH2) domain. It interacts with signaling lymphocytic activation molecule (SLAM) expressed on the surface of activated T and B cells. We show that activated T, but not activated B, cells express the SH2D1A protein. NK cells express the protein as well. Tumor lines originating from B, T or NK cells exhibited similar SH2D1A protein expression as the corresponding normal cells, with some notable exceptions. EBV-carrying, tumor phenotype representative (type I), but not EBV-carrying lymphoblastoid cell line (LCL)-like (type III) or EBV-negative Burkitt lymphoma (BL) lines expressed SH2D1A. The phenotypic switch from type I to type III in the EBV-carrying BL line Mutu was associated with a down-regulation of SH2D1A and up-regulation of SLAM. In contrast to normal ex vivo and long-term activated NK cells, 2 of 3 NK leukemia lines expressed SLAM. All 3 lines expressed SH2D1A, like their normal counterparts.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Journal Of Cancer 88 : 3 (2000), p. 439-447. -
További szerzők:Cerboni, Cristina Mattsson, Karin Maeda, Akihiko Gogolák Péter (1968-) (biológus, immunológus) Sümegi János Lányi Árpád (1962-) (biológus, immunológus) Székely László Carbone Ennio Klein, George Klein Éva
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM086897
Első szerző:Réthi Bence (biológus, immunológus)
Cím:CD150 (SLAM) modulates TLR and CD40 pathways in monocyte-derived dendritic cells / Réthi Bence, Gogolák Péter, Rajnavölgyi Éva, Terhorst C., Lányi Árpád
Dátum:2005
ISSN:1521-6616
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Clinical Immunology. - 115 : Suppl1 (2005), p. S26-S26. -
További szerzők:Gogolák Péter (1968-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Terhorst, Cox Lányi Árpád (1962-) (biológus, immunológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

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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Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM037289
Első szerző:Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:Temporally designed treatment of melanoma cells by ATRA and polyI:C results in enhanced chemokine and IFNb secretion controlled differently by TLR3 and MDA5 / Szabo Attila, Osman Rolah M., Bacskai Ildiko, Kumar Brahma V., Agod Zsofia, Lanyi Arpad, Gogolak Peter, Rajnavolgyi Eva
Dátum:2012
ISSN:0960-8931
Megjegyzések:In the last three decades, the incidence of melanoma has increased worldwide and no effective treatment modalities have been developed yet. All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. We addressed the question of whether ATRA pretreatment could enhance the efficacy of polyI:C and, if so, would ATRA have any additional effects on this process. We found that the combined treatment of human melanoma cells with ATRA and polyI:C strongly increased the expression of TLR3 and MDA5 in both WM35 and WM983A cells associated with significantly higher mRNA and secreted levels of interferon b (IFNb), CXCL1, CXCL8/IL-8, CXCL9, and CXCL10 than cells treated with either ATRA or polyI:C. Silencing of MDA5 by siRNA moderately affected IFNb secretion, whereas TLR3 knockdown interfered with both CXCL chemokine and IFNb production. Furthermore, the supernatants of ATRA + polyI:C-activated cultures increased the migration of both human monocyte-derived macrophages and CD1a + dendritic cells significantly as compared with the supernatants of cells treated with either ATRA or polyI:C, and this effect occurred in a TLR3-dependent manner. In conclusion, consecutive treatment with ATRA and polyI:C results in strong, TLR3/MDA5-mediated chemokine and IFN responses in cultured human melanoma cells, which triggers a functional migratory response in professional antigen-presenting cells. This novel mode of concomitant activation may represent a more efficient treatment option for future melanoma therapy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Melanoma Research 22 : 5 (2012), p. 351-361. -
További szerzők:Osman, Rolah M. Bacskai Ildikó (1985-) (immunológus) Kumar, Brahma V. Agod Zsófia Lányi Árpád (1962-) (biológus, immunológus) Gogolák Péter (1968-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
NK101538
OTKA
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM034344
Első szerző:Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:RLR-mediated production of interferon-beta by a human dendritic cell subset and its role in virus-specific immunity / Szabo, A., Bene, K., Gogolak, P., Rethi, B., Lanyi, A., Jankovich, I., Dezso, B., Rajnavolgyi, E.
Dátum:2012
ISSN:0741-5400
Megjegyzések:Cytosolic RIG-I-like helicases (RLR) are PRRs involved in type I IFN production and antiviral immunity. This study focuses to the comparison of the expression, function, and signaling cascades associated to RLR in the previously identified CD14(-)DC-SIGN(+)PPARγ(low)CD1a(+) and CD14(low)DC-SIGN(+)PPARγ(high)CD1a(-) human moDC subsets. Our results revealed that the expression of RLR genes and proteins as well as the activity of the coupled signaling pathways are significantly higher in the CD1a(+) subset than in its phenotypically and functionally distinct counterpart. Specific activation of RLR in moDCs by poly(I:C) or influenza virus was shown to induce the secretion of IFN-beta via IRF3, whereas induction of proinflammatory cytokine responses were predominantly controlled by TLR3. The requirement of RLR-mediated signaling in CD1a(+) moDCs for priming naïve CD8(+) T lymphocytes and inducing influenza virus-specific cellular immune responses was confirmed by RIG-I/MDA5 silencing, which abrogated these functions. Our results demonstrate the subset-specific activation of RLR and the underlying mechanisms behind its cytokine secretion profile and identify CD1a(+) moDCs as an inflammatory subset with specialized functional activities. We also provide evidence that this migratory DC subset can be detected in human tonsil and reactive LNs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Journal of Leukocyte Biology. - 92 : 1 (2012), p. 159-169. -
További szerzők:Bene Krisztián (1986-) (Biológus) Gogolák Péter (1968-) (biológus, immunológus) Réthi Bence (1973-) (biológus, immunológus) Lányi Árpád (1962-) (biológus, immunológus) Jankovics István Dezső Balázs (1951-) (pathológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
Collaboration of signalling pathways in stem- and dendritic cell subsets
NK 101538
OTKA
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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