CD80 is mainly expressed on Ag-presenting cells (APCs) as a costimulatory molecule but is also detected on T cells. However, the origin and physiological role of CD80 on CD8+ T cells remain unclear. In the present study, we demonstrated that effector and memory CD8+ T cells, but not naïve CD8+ T cells, displayed CD80 molecules on their surfaces after acute lymphocytic choriomeningitis virus infection. Using adoptive transfer of CD80-knockout (KO) CD8+ T cells into a wild type or CD80-KO recipient, we demonstrated that the effector CD8+ T cells displayed CD80 by both intrinsic expression and extrinsic acquisition, while memory CD8+ T cells displayed CD80 only by extrinsic acquisition. Interestingly, the extrinsic acquisition of CD80 by CD8+ T cells was observed only in the lymphoid organs but not in the periphery, indicating the trogocytosis of CD80 molecules via interaction between CD8+ T cells and APCs. We compared the recall immune responses by memory CD8+ T cells that either extrinsically acquired CD80 or were deficient in CD80, and found that CD80, presented by memory CD8+ T cells, played a role in limiting their expansion and IL-2 production upon exposure to secondary challenge. Our study presents the in vivo dynamics of the extrinsic acquisition of CD80 by Ag-specific CD8+ T cells and its role in the regulation of recall immune responses in memory CD8+ T cells.
Keywords: B7-1 antigen; Extrinsic acquisition; Lymphocytic choriomeningitis virus; Recall immune response; Trogocytosis.