Abstract
Lung transplant recipients (LTRs) mismatched for CMV (D+R-) are at highest risk of primary CMV infection and have increased 1- and 5-yr mortality. We have previously shown the acquisition of highly functional CMV-specific CD8+ T cells during primary infection with contraction yet persistence during chronic infection in D+R- LTRs. The transcription factor, T-bet, has been shown in mouse models to be central for Type-1 effector responses. We have explored the role of T-bet in directing a highly functional CD8+ T cell response to CMV during human primary infection and its maintenance during chronic infection.
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