Effects of JAK inhibition in HLH mouse models. The figure illustrates the impact of JAK inhibition in both primary and secondary HLH mouse models compared with controls. The primary model uses perforin-deficient−/− mice challenged by lymphocytic choriomeningitis virus, whereas the secondary model is induced by CpG+ IL-10 receptor-blocking antibody. Key observations include changes in various immune cell populations and cytokine levels. G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; IL, interleukin; MnPs, mononuclear phagocytes (Ly6C+ of CD11b+ cells); Neut, CD80+ neutrophils; sCD25, soluble CD25. ∗Difference between itacitinib and fedratinib treatments. ∗∗Difference between itacitinib and ruxolitinib treatments.

Effects of JAK inhibition in HLH mouse models. The figure illustrates the impact of JAK inhibition in both primary and secondary HLH mouse models compared with controls. The primary model uses perforin-deficient−/− mice challenged by lymphocytic choriomeningitis virus, whereas the secondary model is induced by CpG+ IL-10 receptor-blocking antibody. Key observations include changes in various immune cell populations and cytokine levels. G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; IL, interleukin; MnPs, mononuclear phagocytes (Ly6C+ of CD11b+ cells); Neut, CD80+ neutrophils; sCD25, soluble CD25. ∗Difference between itacitinib and fedratinib treatments. ∗∗Difference between itacitinib and ruxolitinib treatments.

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