FIGURE 2. Characterization of Rab11Fip5-associated transcriptional signatures in B cell and NK cells.

(A and B) CCR1L1 expression in immunized RAB11FIP5^−/− (KO) mice or RAB11FIP5^fl/fl control mice shown as fragments per kb of transcript per million mapped reads in different cell types (A) and relative expression as determined by qPCR in B cells (B). (C and D) Effect of RAB11FIP5 deficiency on IL-4 and IL-5 production in mouse NK cells following stimulation with PMA + ionomycin. Mouse spleen cells were stimulated with 500 ng/ml PMA and 5 mg/ml ionomycin for 4 h in the presence of the protein transport inhibitor monensin. Intracellular staining was performed after stimulation. Representative example of the IL-4 and IL-5 intracellular staining (C) and percentages of IL-4 and IL-5 positive subsets (D) were shown. Each dot indicates one animal. The statistical significance of differences between groups in (B) and (C) was determined by Mann–Whitney U test. *p < 0.05; ns, not significant. (E) Comparison of Rab11Fip5-associated transcriptional changes in human NK cells and mouse NK cells. In humans, we studied NK cells from HIV-infected individuals expressing different levels of RAB11FIP5 in PBMC, and transcriptional expression fold change indicates comparison between NK cells from subjects expressing low levels of RAB11FIP5 (RAB11FIP5^low) versus high levels of RAB11FIP5 (RAB11FIP5^high) in NK cells (n = 4/group) (11), whereas for mice, we studied NK cells isolated from HIV-1 Env-immunized animals and compared RAB11FIP5 KO cells with control cells (n = 6/group). Significantly (p < 0.05) upregulated or downregulated genes are shown as a heat map.