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. Author manuscript; available in PMC: 2016 Jan 7.
Published in final edited form as: Cell. 2015 May 7;161(4):750–761. doi: 10.1016/j.cell.2015.03.021

Figure 2. AQP9 Deficiency Impairs Formation of LCMV-Specific Memory CD8+ T Cells.

Figure 2

(A and B) Bone marrow chimeric mice containing a 1:1 ratio of Aqp9+/+ (open circles, Ly5.2+Thy1.1+) and Aqp9−/− (black squares, Ly5.2+Thy1.2+) bone marrow cells were infected with LCMV-Armstrong and the frequency of the two populations within the DbGP33–41-specific CD8+ T cells were analyzed longitudinally by flow cytometry.

(C) Aqp9−/− or littermate Aqp9+/+ P14 CD8+ T cells (104 cells) were adoptively transferred into B6 mice that were subsequently infected with LCMV-Armstrong. The numbers of donor P14 CD8+ T cells were determined at the indicated dpi.

(D) P14 chimeric mice described in (C) were given BrdU drinking water (1 mg/ml) from 30–51 dpi to measure the rates of homeostatic proliferation in the memory CD8+ T cells. Amounts of nuclear BrdU were measured by flow cytometry.

(E) Aqp9−/− or littermate Aqp9+/+ P14 CD8+ T cells were purified at 25 dpi, labeled with CTV, adoptively transferred to naive B6 mice, and analyzed by flow cytometry for CTV dilution. The bar graph shows the percentages of divided cells.

Data are representative (A, C–E) or cumulative (B) of three and four (C) independent experiments (n = 5–15 mice/group): **p < 0.01 (see also Figure S2).