Persistence in Temporary Lung Niches: A Survival Strategy of Lung-Resident Memory CD8(+) T Cells

Takamura, Shiki

antigenic as well as inflammatory signals may be redundant at early phases of infection, which bias CD8 + T cell differentiation toward terminal effector cells, while weak signaling at later time points preferentially promotes memory differentiation (16) . Distinct microdistribution of CD8 + T cells also influences differential acquisition of the activation signals. For example, CXCR3 hi cells receive stronger stimulatory signals and preferentially become terminal effectors, while lack of this receptor puts cells away from the core of inflammatory microenvironment, and ultimately promotes memory differentiation (50, 66, 69) . All those factors must cooperatively regulate CD8 + T cell fate following late antigen recognition.