Figure 1
Figure 1. Identification of a p.Y640F STAT3 mutation in a patient with L-HES. (A) Clinical photographs of eosinophil-infiltrated papules and nodules on the patient’s trunk (upper) and elbow (lower). (B) Table of relevant laboratory findings, with reference values. (C) Intracellular cytokine staining of CD3−CD4+ T cells. Peripheral blood mononuclear cells were stimulated for 5 hours with phorbol 12-myristate 13-acetate (50 ng/mL) and ionomycin (1 μg/mL). Cells were subsequently fixed, permeabilized, and stained with a phycoerythrin/cyanin 7–labeled anti-human CD3 antibody (BD Pharmingen) and an antibody cocktail containing antibodies for CD4, IL-4, IL-17A, and interferon-γ (IFNγ) (BD Pharmingen). (D) Confirmation of the somatic STAT3 mutation in CD3−CD4+ T cells by Sanger sequencing. Matched normal CD3+CD19− B cells were used as a control.

Identification of a p.Y640F STAT3 mutation in a patient with L-HES. (A) Clinical photographs of eosinophil-infiltrated papules and nodules on the patient’s trunk (upper) and elbow (lower). (B) Table of relevant laboratory findings, with reference values. (C) Intracellular cytokine staining of CD3CD4+ T cells. Peripheral blood mononuclear cells were stimulated for 5 hours with phorbol 12-myristate 13-acetate (50 ng/mL) and ionomycin (1 μg/mL). Cells were subsequently fixed, permeabilized, and stained with a phycoerythrin/cyanin 7–labeled anti-human CD3 antibody (BD Pharmingen) and an antibody cocktail containing antibodies for CD4, IL-4, IL-17A, and interferon-γ (IFNγ) (BD Pharmingen). (D) Confirmation of the somatic STAT3 mutation in CD3CD4+ T cells by Sanger sequencing. Matched normal CD3+CD19 B cells were used as a control.

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