Loss of pathogen-specific T cell memory is due to the absence of Runx2 in CD8+ T cells. Loss of pathogen-specific T cell memory is due to the absence of.

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Loss of pathogen-specific T cell memory is due to the absence of Runx2 in CD8+ T cells. Loss of pathogen-specific T cell memory is due to the absence of Runx2 in CD8+ T cells. WT P14 (CD90.1+/CD90.2+) and Runx2fl/fl P14 cells (CD90.1+) were mixed 1:1 and transferred into WT (CD90.2+) recipients. (A) Mixture of donor T cells prior to transfer. (B) One day after transfer, recipient mice were infected with LCMV–Armstrong, and splenocytes were analyzed on day 28 postinfection. WT P14 (CD90.1+/CD90.2+) and Runx2fl/fl P14 (CD90.1+) cells are shown (left), and the total numbers of WT P14 and Runx2fl/fl P14 splenocytes at day 28 postinfection were compiled (right). (C) Cells were stained for KLRG1 and CD127, and donor populations were gated (left); total numbers of WT P14 and Runx2fl/fl P14 TECs (middle) and MPCs (right) in host mice at day 28 postinfection are shown. (D) Normalized expression of Eomes, TCF-1, CD27, CD122, Bcl2, and Bcl6 at day 28 postinfection. Mean fluorescence intensity (MFI) values are normalized to the average of WT P14 cells analyzed in each sample. (E) Cells were restimulated with gp33–41 peptide for 4 h in vitro and stained for intracellular IFN-γ, TNF-α, and IL-2 as shown (left). Total numbers of H2-Db gp33–41–specific IFN-γ+, TNF-α+, and IL-2+ splenocytes (triple producers) in WT versus Runx2fl/fl P14 cells at day 28 after LCMV–Armstrong infection are shown (right). Data are from two independent experiments with a total of nine mice. ****p ≤ 0.0001. Elizabeth Olesin et al. ImmunoHorizons 2018;2:251-261 Copyright © 2018 The Authors