CCL

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1.

001-es BibID:BIBFORM010321
Első szerző:Dammeyer, Pascal
Cím:Vaccination with beta(2)-microglobulin-deficient dendritic cells protects against growth of beta(2)-microglobulin-deficient tumours / Pascal Dammeyer, Amos R. Mwakigonja, Réthi Bence, Francesca Chiodi, Elisabeth Wolpert
Dátum:2009
ISSN:0300-9475 (Print)
Megjegyzések:Defects in cell surface expression of major histocompatibility complex class I antigen molecules are common in tumour cells. We have previously described the generation of adaptive immunity to tumour cells deficient in the transporter associated with antigen processing molecule. In this study, we demonstrate enhanced in vivo protection against growth of beta(2)-microglobulin-deficient tumour cells in syngeneic C57Bl/6 mice, following vaccination with beta(2)-microglobulin-deficient dendritic cells. In vitro analysis suggested that vaccinated mice produced CD3+ cells, which could induce apoptosis in syngeneic beta(2)-microglobulin-deficient tumour and non-malignant cells. Further investigation of target cell recognition suggested that also tumour cells lacking expression of classical major histocompatibility complex class I heavy chains and functional transporter associated with antigen processing molecules were recognized by CD3+ effector cells from vaccinated mice. Histopathological examination of organs from vaccinated mice showed no significant vaccination-induced pathology. The present findings point to a new possible strategy to counteract the growth of major histocompatibility complex class I-deficient tumour cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
MHC Class-I
Natural Cytotoxicity Receptors
Antigen Processing Machinery
HIV-1 Nef Protein
Melanoma Cells
NKG2D Ligands
Heavy-Chains
T-Cells
Killer Lymphocytes
Immune-Responses
Megjelenés:Scandinavian Journal of Immunology. - 70 : 1 (2009), p. 44-52. -
További szerzők:Mwakigonja, Amos R. Réthi Bence (1973-) (biológus, immunológus) Chiodi, Francesca Wolpert, Elisabeth
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DOI
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2.

001-es BibID:BIBFORM001996
Első szerző:Eidsmo, Liv
Cím:FasL and TRAIL induce epidermal apoptosis and skin ulceration upon exposure to Leishmania major / Liv Eidsmo, Caroline Fluur, Bence Rethi, Sofia Eriksson Ygberg, Nicolas Ruffin, Angelo De Milito, Hannah Akuffo, Francesca Chiodi
Dátum:2007
Megjegyzések:Receptor-mediated apoptosis is proposed as an important regulator of keratinocyte homeostasis in human epidermis. We have previously reported that Fas/FasL interactions in epidermis are altered during cutaneous leishmaniasis (CL) and that keratinocyte death through apoptosis may play a pathogenic role for skin ulceration. To further investigate the alterations of apoptosis during CL, a keratinocyte cell line (HaCaT) and primary human epidermal keratinocytes were incubated with supernatants from Leishmania major-infected peripheral blood mononuclear cells. An apoptosis-specific microarray was used to assess mRNA expression in HaCaT cells exposed to supernatants derived from L. major-infected cultures. Fas and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA and protein expression were significantly up-regulated, and apoptosis was detected in both HaCaT and human epidermal keratinocyte cells. The keratinocyte apoptosis was partly inhibited through blocking of Fas or FasL and even more efficiently through TRAIL neutralization. Up-regulation of Fas on keratinocytes in epidermis and the presence of FasL-expressing macrophages and T cells in dermis were previously reported by us. In this study, keratinocytes expressing TRAIL, as well as the proapoptotic receptor TRAIL-R2, were detected in skin biopsies from CL cases. We propose that activation of Fas and TRAIL apoptosis pathways, in the presence of inflammatory mediators at the site of infection, leads to tissue destruction and ulceration during CL.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
apoptosis
skin
leishmania
Megjelenés:The American Journal of Pathology. - 170 : 1 (2007), p. 227-239. -
További szerzők:Fluur, Caroline Réthi Bence (1973-) (biológus, immunológus) Ygberg, Sofia Eriksson Ruffin, Nicolas De Milito, Angelo Akuffo, Hannah Chiodi, Francesca
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DOI
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3.

001-es BibID:BIBFORM001994
Első szerző:Fluur, Caroline
Cím:Relationship between serum IL-7 concentrations and lymphopenia upon different levels of HIV immune control / Caroline Fluur, Bence Rethi, Pham Hong Thang, Nancy Vivar, Frida Mowafi, Lucia Lopalco, Caterina, Uberti Foppa, Anders Karlsson, Giuseppe Tambussi, Francesca Chiodi
Dátum:2007
Megjegyzések:Serum IL-7 levels correlate with T-cell depletion in HIV-infected individuals. In some patients, we observed that serum IL-7 decreases upon progression to AIDS, suggesting a role for IL-7 in T-cell maintenance in sporadic cases. Interestingly, IL-7 levels were significantly lower in stable long-term non-progressors (LTNP) than in patients who lost the LTNP status in a 3-year follow-up (P < 0.001), indicating that the serum IL-7 concentration might be a valuable marker for maintenance of the LTNP state.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
IL-7
HIV
T cell depletion
Megjelenés:AIDS. - 21 : 8 (2007), p. 1048-1050. -
További szerzők:Chiodi, Francesca Réthi Bence (1973-) (biológus, immunológus) Thang, Pham Hong Vivar, Nancy Mowafi, Frida Lopalco, Lucia Karlsson, Anders Uberti Foppa, Caterina Tambussi, Giuseppe
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DOI
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4.

001-es BibID:BIBFORM002005
Első szerző:Fluur, Caroline
Cím:Potential role for IL-7 in Fas-mediated T cell apoptosis during HIV infection / Caroline Fluur, Angelo De Milito, Terry J. Fry, Nancy Vivar, Liv Eidsmo, Ann Atlas, Cristina Federici, Paola Matarrese, Mariantonia Logozzi, Éva Rajnavölgyi, Crystal L. Mackall, Stefano Fais, Francesca Chiodi, and Bence Réthi
Dátum:2007
Megjegyzések:IL-7 promotes survival of resting T lymphocytes and induces T cell proliferation in lymphopenic conditions. As elevated IL-7 levels occur in HIV-infected individuals in addition to high Fas expression on T cells and increased sensitivity to Fas-induced apoptosis, we analyzed whether IL-7 has a regulatory role in Fas-mediated T cell apoptosis. We show that IL-7 up-regulates Fas expression on naive and memory T cells through a mechanism that involves translocation of Fas molecules from intracellular compartments to the cell membrane. IL-7 induced the association of Fas with the cytoskeletal component ezrin and a polarized Fas expression on the cell surface. The potential role of IL-7 in Fas up-regulation in vivo was verified in IL-7-treated macaques and in HIV-infected or chemotherapy treated patients by the correlation between serum IL-7 levels and Fas expression on T cells. IL-7 treatment primed T cells for Fas-induced apoptosis in vitro and serum IL-7 levels correlated with the sensitivity of T cells to Fas-induced apoptosis in HIV-infected individuals. Our data suggest an important role for IL-7 in Fas-mediated regulation of T cell homeostasis. Elevated IL-7 levels associated with lymphopenic conditions, including HIV-infection, might participate in the increased sensitivity of T cells for activation-induced apoptosis
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
IL-7
Fas
HIV
Megjelenés:Journal of Immunology. - 178 : 8 (2007), p. 5340-5350. -
További szerzők:De Milito, Angelo Eidsmo, Liv Atlas, Ann Federici, Cristina Matarrese, Paola Logozzi, Mariantonia Mackall, Crystal L. Fais, Stefano Chiodi, Francesca Rajnavölgyi Éva (1950-) (immunológus) Réthi Bence (1973-) (biológus, immunológus) Vivar, Nancy Fry, Terry J.
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5.

001-es BibID:BIBFORM091323
Első szerző:Réthi Bence (biológus, immunológus)
Cím:Loss of IL-7Rα is associated with CD4 T-cell depletion, high interleukin-7 levels and CD28 down-regulation in HIV infected patients / Rethi Bence, Fluur Caroline, Atlas Ann, Krzyzowska Malgorzata, Mowafi Frida, Grützmeier Sven, De Milito Angelo, Bellocco Rino, Falk Kerstin I., Rajnavölgyi Éva, Chiodi Francesca
Dátum:2005
ISSN:0269-9370 1473-5571
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Aids. - 19 : 18 (2005), p. 2077-2086. -
További szerzők:Fluur, Caroline Atlas, Ann Krzyzowska, Malgorzata Mowafi, Frida Grützmeier, Sven De Milito, Angelo Bellocco, Rino Falk, Kerstin I. Rajnavölgyi Éva (1950-) (immunológus) Chiodi, Francesca
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6.

001-es BibID:BIBFORM018161
Első szerző:Réthi Bence (biológus, immunológus)
Cím:Loss of IL-7Ra is Associated With CD4+ T Cell Depletion, High IL-7 Levels and CD28 Down-regulation in HIV Infected Patients / Rethi Bence, Fluur Caroline, Atlas Ann, Grützmeier Sven, De Milito Angelo, Rajnavölgyi Éva, Chiodi Francesca
Dátum:2005
ISSN:1742-4690
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:Retrovirology. - 2 : Suppl.1. (2005), p. P84. -
További szerzők:Fluur, Caroline Atlas, Ann Grützmeier, Sven De Milito, Angelo Rajnavölgyi Éva (1950-) (immunológus) Chiodi, Francesca
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7.

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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8.

001-es BibID:BIBFORM005817
Első szerző:Titanji, Kehmia
Cím:Altered distribution of natural killer cell subsets identified by CD56, CD27 and CD70 in primary and chronic human immunodeficiency virus-1 infection / Kehmia Titanji, Stefano Sammicheli, Angelo De Milito, Paola Mantegani, Claudio Fortis, Louise Berg, Klas Karre, Giovanna Travi, Chiara Tassandin, Lucia Lopalco, Bence Rethi, Giuseppe Tambussi, Francesca Chiodi
Dátum:2008
Megjegyzések:Human natural killer (NK) (CD3(-) CD56(+)) cells can be divided into two functionally distinct subsets, CD3(-) CD56(dim) and CD3(-) CD56(bright). We analysed the distribution of NK cell subsets in primary and chronic human immunodeficiency virus-1 (HIV-1) infection, to determine if HIV infection stage may influence the subset distribution. In primary infection, contrary to chronic infection, the CD3(-) CD56(dim) subset was expanded compared to healthy controls. We also studied the effect of antiretroviral therapy administered early in infection and found that NK cell subset distribution was partially restored after 6 months of antiretroviral therapy in primary infection, but not normalized. Recently, NK cells have been divided into CD27(-) and CD27(+) subsets with different migratory and functional capacity and CD27-mediated NK cell activation has been described in mice. We therefore investigated whether CD27 and/or CD70 (CD27 ligand) expression on NK cells, and thus the distribution of these novel NK subsets, was altered in HIV-1-infected patients. We found up-regulated expression of both CD27 and CD70 on NK cells of patients, resulting in higher proportions of CD27(high) and CD70(high) NK cells, and this phenomenon was more pronounced in chronic infection. Experiments conducted in vitro suggest that the high interleukin-7 levels found during HIV-1 infection may participate in up-regulation of CD70 on NK cell subsets. Imbalance of NK cell subsets and up-regulated expression of CD27 and CD70 initiated early in HIV-1 infection may indicate NK cell activation and intrinsic defects initiated by HIV-1 to disarm the innate immune response to the virus.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
HIV-1
CD27
CD70
NK cells
immune activation
antiretroviral therapy
Megjelenés:Immunology. - 123 : 2 (2008), p. 164-170. -
További szerzők:Sammicheli, Stefano De Milito, Angelo Mantegani, Paola Fortis, Claudio Berg, Louise Karre, Klas Travi, Giovanna Tassandin, Chiara Lopalco, Lucia Réthi Bence (1973-) (biológus, immunológus) Tambussi, Giuseppe Chiodi, Francesca
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9.

001-es BibID:BIBFORM005809
Első szerző:Vivar, Nancy
Cím:Potential role of CD8+CD28- T lymphocytes in immune activation during HIV-1 infection / Nancy Vivar, Pham Hong Thang, Ann Atlas, Francesca Chiodi, Bence Rethi
Dátum:2008
Megjegyzések:As CD8+CD28- T cells have been associated with dendritic and T cell suppression, we analyzed whether an increase in CD8+CD28- T cell numbers during HIV-1 infection could lead to impaired T cell responses. In contrast to the in-vitro generated CD8+CD28- suppressors, peripheral blood CD8+CD28- T cells of both HIV-infected and noninfected individuals promoted dendritic cell activation. The CD8+CD28- T cell accumulation during HIV-1 infection may thus contribute to accelerated inflammatory reactions and immune activation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Regulatory T-Cells
Suppressor
CD28
Expression
Molecules
Responses
Markers
Megjelenés:AIDS. - 22 : 9 (2008), p. 1083-1086. -
További szerzők:Thang, Pham Hong Atlas, Ann Chiodi, Francesca Réthi Bence (1973-) (biológus, immunológus)
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