Contribution of pulmonary KLRG1(high) and KLRG1(low) CD8 T cells to effector and memory responses during influenza virus infection.

In response to pathogen insult, CD8 T cells undergo expansion and a dynamic differentiation process into functionally different subpopulations. In this study, we show that during the effector response to influenza virus infection lung CD8 T cell subsets expressing killer cell lectin-like receptor G1 (KLRG1)(high) or KLRG1(low) had similar effector functions and immediate recall efficacy. The KLRG1 expression profile of lung CD8 T cells was not permanent after adoptive transfer and recall. Airway CD8 T cells exhibited a unique phenotype expressing low levels of KLRG1 together with high levels of markers of cellular activation. We investigated the functional characteristics of these cells by analyzing their capacity to survive and to respond to a secondary challenge outside of the airway environment. KLRG1(high) CD8 T cells isolated from the lung during the peak of the effector T cell response could survive for more than a month in the absence of cognate viral Ags after systemic adoptive transfer, and these "rested" CD8 T cells proliferated and participated in a recall response to influenza virus infection. These data highlight the unique phenotype and plasticity of effector CD8 T cell responses in the lung.