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. 2022 May 23;7(10):e158889. doi: 10.1172/jci.insight.158889

Figure 4. OMCPmutIL-2 facilitates NFAT signaling but does not signal through canonical JAK/STAT pathway like IL-2 family cytokines.

Figure 4

(A) STAT5 localization by confocal microscopy after in vitro activation with anti-CD3/28 stimulation in the presence of IL-2, IL-15, OMCPmutIL-2, or saline control. Original magnification, 20× (top) and 63× (bottom). (B) Gene enrichment analysis for STAT5-dependent genes in memory T cells generated from naive cells in vitro in the presence of IL-2 or IL-15 versus OMCPmutIL-2. (C) Principal component analysis between IL-2 (blue), IL-15 (green), and OMCPmutIL-2 (red) and differential gene expression in murine splenic CD8+ T cells expanded in IL-2, IL-15, or OMCPmutIL-2 as expressed via Venn diagram and Kyoto Encyclopedia of Genes and Genomes pathway analysis comparing top differential pathways. OMCPmutIL-2 versus IL-2 and OMCPmutIL-2 versus IL-15 are presented in separate graphs (purple for OMCPmutIL-2 vs. IL-2 and orange for OMCPmutIL-2 vs. IL-15). (D) Phosphorylated (inactive) NFAT quantification in CD8+ T cells after expansion in various cytokines. (E) Change in CD8+ T cell expansion and cytotoxicity in the presence or absence of NFAT inhibitor FK506. (F) Change in CD8+ T cell proliferation and cytokine production in the presence or absence of NFAT inhibitor FK506. *P < 0.05; **P < 0.01; ***P < 0.001; t test.