Author: Poccia, Fabrizio; Agrati, Chiara; Castilletti, Concetta; Bordi, Licia; Gioia, Cristiana; Horejsh, Douglas; Ippolito, Giuseppe; Chan, Paul K. S.; Hui, David S. C.; Sung, Joseph J. Y.; Capobianchi, Maria Rosaria; Malkovsky, Miroslav
Title: Anti–Severe Acute Respiratory Syndrome Coronavirus Immune Responses: The Role Played by Vγ9Vδ2 T Cells Cord-id: jh04b55m Document date: 2006_5_1
ID: jh04b55m
Snippet: Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus (SARS-CoV) strain. Analyses of T cell repertoires in health care workers who survived SARS-CoV infection during the 2003 outbreak revealed that their effector memory Vγ9Vδ2 T cell populations were selectively expanded ∼3 months after the onset of disease. No such expansion of their αβ T cell pools was detected. The expansion of the Vγ9Vδ2 T cell population was associated with higher anti–SARS-CoV immunoglobulin G
Document: Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus (SARS-CoV) strain. Analyses of T cell repertoires in health care workers who survived SARS-CoV infection during the 2003 outbreak revealed that their effector memory Vγ9Vδ2 T cell populations were selectively expanded ∼3 months after the onset of disease. No such expansion of their αβ T cell pools was detected. The expansion of the Vγ9Vδ2 T cell population was associated with higher anti–SARS-CoV immunoglobulin G titers. In addition, in vitro experiments demonstrated that stimulated Vγ9Vδ2 T cells display an interferon-γ–dependent anti–SARS-CoV activity and are able to directly kill SARS-CoV–infected target cells. These findings are compatible with the possibility that Vγ9Vδ2 T cells play a protective role during SARS
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