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KIR3DL01 upregulation on gut natural killer cells in response to SIV infection of KIR- and MHC class I-defined rhesus macaques

Fig 4

NK cell proliferation and activation in response to SIV infection.

Longitudinal changes in the expression of Ki-67 (A & B), CD69 (C & D), HLA-DR (E & F), and α4β7 (G & H) were monitored for CD16+, CD56+ and CD16-CD56- NK cells (left panels: A, C, E & G) and for KIR3DL01+, KIR3DL05+ and KIR3DL01-05- NK cells (right panels: B, D, F & H). Absolute counts were calculated as a percentage of total NK cell counts by staining PBMCs with antibodies to CD3, CD8, NKG2A, CD16, CD56, KIR3DL01 and KIR3DL05 (tetramer), and to markers of proliferation (Ki-67), activation (CD69 & HLA-DR) and mucosal homing (α4β7). Representative gating for the proliferation and activation panel is shown in S4 Fig. The mean and standard error (error bars) are shown for each NK cell subset. Significance values for acute (weeks 1–4) and chronic (weeks 6–24) infection compared to pre-infection (week 0) are indicated with asterisks color-coded to the corresponding cell population (p<0.05*, p<0.01**, p< 0.005*** & p<0.001****, mixed effects models).

Fig 4