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Functional profile of cytomegalovirus (CMV)‐specific CD8 + T cells and kinetics of NKG2C + NK Cells associated with the resolution of CMV DNAemia in allogeneic stem cell transplant recipients
Author(s) -
MuñozCobo Beatriz,
Solano Carlos,
Benet Isabel,
Costa Elisa,
Remigia María José,
de la Cámara Rafael,
Nieto José,
López Javier,
Amat Paula,
GarciaNoblejas Ana,
Bravo Dayana,
Clari María Ángeles,
Navarro David
Publication year - 2012
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.22254
Subject(s) - cd8 , cytomegalovirus , cytotoxic t cell , virology , biology , transplantation , immunology , cd16 , t cell , population , human cytomegalovirus , antigen , immune system , virus , medicine , viral disease , herpesviridae , cd3 , in vitro , biochemistry , environmental health
Immune mechanisms involved in control of cytomegalovirus (CMV) infection in the allogeneic stem cell transplantation setting have not been fully disclosed. CMV pp65 and IE‐1‐specific CD8 + T cells expressing IFN‐γ, TNF‐α, and CD107a, alone or in combination, and NKG2C + NK cells were prospectively enumerated during 13 episodes of CMV DNAemia. The expansion of monofunctional and polyfunctional CD8 + T cells was associated with CMV DNAemia clearance. The size and functional diversity of the expanding CD8 + T‐cell population was greater in self‐resolved episodes than in episodes treated with antivirals. These differences were related to the magnitude of expansion of cognate antigen IFN‐γ CD4 + T cells. The resolution of CMV DNAemia was associated frequently with a marked expansion of both CD56 dim /CD16 + NK cells and NKG2C + CD56 bright /CD16 − NK cells. The data lend support to the role of polyfunctional CD8 + T cells in controlling CMV replication in the allogeneic stem cell transplantation setting, and suggest that NKG2C + NK cells may be involved critically in the resolution of CMV DNAemia episodes. J. Med. Virol. 84:259–267, 2012. © 2011 Wiley Periodicals, Inc.