Fig. 5: AFM28 blocks IL-3R signaling inhibiting STAT5 phosphorylation in TF-1. | Nature Communications

Fig. 5: AFM28 blocks IL-3R signaling inhibiting STAT5 phosphorylation in TF-1.

From: The bispecific innate cell engager AFM28 eliminates CD123+ leukemic stem and progenitor cells in AML and MDS

Fig. 5: AFM28 blocks IL-3R signaling inhibiting STAT5 phosphorylation in TF-1.The alternative text for this image may have been generated using AI.

A, B TF-1 cell growth was stimulated with IL-3 (A) or GM-CSF (B) in the presence of titrated AFM28, a non-targeting control (RSV/CD16A), or without antibody addition and with IL-3/GM-CSF (gray dot) or without antibody addition and without IL-3/GM-CSF (cross), for 72 h at 37 °C. The relative number of metabolically active viable cells was determined using the CellTiter-Glo assay in three independent experiments. The results shown were normalized to the maximum cell viability signal, which represents 100%. Data shown as mean ± SD (n = 3). C, D Intracellular phosphorylated STAT5 or STAT6 was measured in TF-1 cells upon stimulation with IL-3 (C) or IL-4 (D) in the presence of titrated AFM28, a non-targeting control engager (RSV/CD16A) or without antibodies (cross). One representative experiment is shown out of three performed. SD standard deviation.

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