Journal Information
ISSN / EISSN : 25729241 / 25729241
Current Publisher: Ovid Technologies (Wolters Kluwer Health) (10.1097)
Total articles ≅ 2,737
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Latest articles in this journal

Adrián Alegre, Javier De La Rubia, Anna Sureda Balari, Cristina Encinas Rodríguez, Alexia Suárez, María Jesús Blanchard, Joan Bargay Lleonart, Paula Rodríguez-Otero, Andrés Insunza, Luis Palomera, et al.
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000380

Paolo Corradini, Giorgia Gobbi, Filippo De Braud, Jessica Rosa, Chiara Rusconi, Giovanni Apolone, Cristiana Carniti
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000408

Alexandre Guy, Anicee Danaee, Koralia Paschalaki, Lisa Boureau, Etienne Rivière, Gabriel Etienne, Olivier Mansier, Michael Laffan, Mallika Sekhar, Chloe James
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000364

David G. Kent
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000416

Nikolaos Sousos, Gemma Buck, Alba Rodriguez-Meira, Ruggiero Norfo, Angela Hamblin, Francesco Pezzella, Jennifer Davies, Philip Hublitz, Bethan Psaila, Adam J. Mead
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000356

Simone Oerlemans, M. Christine Bennink, Mark David Levin, Annemiek Broijl, Marjolein Van Der Klift, Judith Van Deursen, Daphne Vogels, Lonneke V. Van De Poll-Franse, Pieter Sonneveld, Jan A. Hazelzet, et al.
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000366

Tom Hofland, Iris De Weerdt, Sanne Endstra, Aldo Jongejan, Laura Platenkamp, Ester B.M. Remmerswaal, Perry D. Moerland, Ineke J.M. Ten Berge, Mark-David Levin, Arnon P. Kater, et al.
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000337

Acquired T cell dysfunction is a hallmark of chronic lymphocytic leukemia (CLL), and is linked to an increased risk of infections, but also reduced immune surveillance and disappointing responses to autologous T cell-based immunotherapy. The mechanisms of T cell dysfunction in CLL are not well understood. Studying immunity against chronic viruses allows for detailed analysis of the effect of CLL on T cells chronically exposed to a specific antigen. Cytomegalovirus (CMV) reactivations are rare in CLL, which corroborates with preserved CMV-specific T cell function. Epstein-Barr virus (EBV) is another herpesvirus that results in chronic infection, but unlike CMV, is characterized by subclinical reactivations in CLL patients. Since both herpesviruses induce strong CD8+ T cell responses, but have different clinical outcomes, studying these specific T cells may shed light on the mechanisms of CLL-induced T cell dysfunction. We first analyzed the phenotype of EBV-specific CD8+ T cells in CLL and healthy controls, and found that in CLL EBV-specific CD8+ T cells are in an advanced differentiation state with higher expression of inhibitory receptors. Secondly, CLL-derived EBV-specific CD8+ T cells show reduced cytotoxic potential, in contrast to CMV-specific T cells. Finally, we performed transcriptome analysis to visualize differential modulation by CLL of these T cell subsets. While T cell activation and differentiation genes are unaffected, in EBV-specific T cells expression of genes involved in synapse formation and T cell exhaustion is altered. Our findings on the heterogeneity of antigen specific T cell function in CLL aids in understanding immune-dysregulation in this disease.
Jacques Zimmer
HemaSphere, Volume 4; doi:10.1097/hs9.0000000000000348

Juerg Schwaller
HemaSphere, Volume 4; doi:10.1097/HS9.0000000000000343

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