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16 results on '"DE RE, VALLI"'

10. Epstein-Barr Virus Strains With Latent Membrane Protein-1 Deletions: Prevalence in the Italian Population and High Association With Human Immunodeficiency Virus–Related Hodgkin's Disease

Author

Dolcetti, Riccardo, primary, Zancai, Paola, additional, De Re, Valli, additional, Gloghini, Annunziata, additional, Bigoni, Beatrice, additional, Pivetta, Barbara, additional, De Vita, Salvatore, additional, Carbone, Antonino, additional, and Boiocchi, Mauro, additional

Published
1997
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11. Dendritic cells accumulate in the bone marrow of myeloma patients where they protect tumor plasma cells from CD8+T-cell killing

Author

Leone, Patrizia, Berardi, Simona, Frassanito, Maria Antonia, Ria, Roberto, De Re, Valli, Cicco, Sebastiano, Battaglia, Stefano, Ditonno, Paolo, Dammacco, Franco, Vacca, Angelo, and Racanelli, Vito

Abstract

Many researchers have speculated that the clinical progression from monoclonal gammopathy of undetermined significance (MGUS) to multiple myeloma (MM) is driven by defects in dendritic cell (DC) function. However, evidence supporting this assumption is controversial, and no mechanism for the putative DC dysfunction has been demonstrated thus far. We studied DC subsets from the bone marrow of MM patients compared with those of MGUS patients and control subjects. We found that myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) accumulate in the bone marrow during the MGUS-to-MM progression. After engulfment of apoptotic tumor plasma cells via CD91, bone marrow mDCs and pDCs mature and are able to activate tumor-specific CD8+T cells. However, by interacting directly with CD28 on live (nonapoptotic) tumor plasma cells, bone marrow mDCs downregulate the expression of proteasome subunits in these cells, thus enabling their evasion from human leukocyte antigen (HLA) class I–restricted CD8+T-cell killing. These results suggest that DCs play a dual, but opposing, role in MM: for one, DCs activate CD8+T cells against tumor plasma cells and, for the other, DCs protect tumor plasma cells from CD8+T-cell killing. This information should be taken into account in designing immunotherapy approaches to enhance immune surveillance in MGUS and to break down immune tolerance in MM.

Published
2015
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16. Dendritic cells accumulate in the bone marrow of myeloma patients where they protect tumor plasma cells from CD8+ T-cell killing.

Author

Leone, Patrizia, Berardi, Simona, Frassanito, Maria Antonia, Ria, Roberto, De Re, Valli, Cicco, Sebastiano, Battaglia, Stefano, Ditonno, Paolo, Dammacco, Franco, Vacca, Angelo, and Racanelli, Vito

Subjects
*DENDRITIC cells, *BONE marrow, *MULTIPLE myeloma, *T cells, *PROTEASOMES, *IMMUNOTHERAPY, *TUMOR proteins, *PLASMA cells, *PATIENTS
Abstract

Many researchers have speculated that the clinical progression from monoclonal gammopathy of undetermined significance (MGUS) to multiple myeloma (MM) is driven by defects in dendritic cell (DC) function. However, evidence supporting this assumption is controversial, and no mechanism for the putative DC dysfunction has been demonstrated thus far. We studied DC subsets from the bone marrow of MM patients compared with those of MGUS patients and control subjects. We found that myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) accumulate in the bone marrow during the MGUS-to-MM progression. After engulfment of apoptotic tumor plasma cells viaCD91,bonemarrowmDCs andpDCsmature and are able to activate tumor-specific CD8+ T cells. However, by interacting directly with CD28 onlive (nonapoptotic) tumor plasma cells, bone marrow mDCs downregulate the expression of proteasome subunits in these cells, thus enabling their evasion from human leukocyte antigen (HLA) class I-restricted CD8+ T-cell killing. These results suggest that DCs play a dual, but opposing, role in MM: for one, DCs activate CD8+ T cells against tumor plasmacells and, for the other, DCs protect tumor plasmacells from CD8+ T-cell killing. This information should be taken in to account in designing immunotherapy approaches to enhance immune surveillance in MGUS and to break down immune tolerance in MM. [ABSTRACT FROM AUTHOR]

Published
2015
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