Figure 2.
A albopictus SGE glands induce proinflammatory cytokine production by PBMCs from patients with CAEBV disease, which can be suppressed by STAT3. (A) Concentration of IFN-γ in the supernatant of PBMCs from the patient and her MZ twin after 16-hour stimulation with SGE from A aegypti (A. aeg) or A albopictus (A. albo) (25 μg/mL). (B) Percentage of each leukocyte population among IFN-γ+ PBMCs from the patient and her MZ twin stained after 4-hour stimulation with SGE from A aegypti or A albopictus. (C) Concentrations of IL-2 and IL-12 in the supernatant of PBMCs from the patient and her MZ twin after 16-hour stimulation with SGE from A aegypti or A albopictus. (D) Expression of CD25 in NK cells from the patient and her MZ twin after 16-hour stimulation with SGE from A aegypti or A albopictus. (E) Heat maps showing relative concentrations of IFN-γ, IL-12p70, IL-2, soluble IL-2R (sIL-2R), IL-6, IL-8, tumor necrosis factor α (TNFα), CCL3, CXCL10, granulocyte-monocyte colony-stimulating factor (GM-CSF), IL-5, and IL-13 after 16-hour stimulation with SGE from A aegypti or A albopictus, from the patient and her MZ twin at 6 months after referral (left), and patient and 2 unrelated healthy controls (URHCs) at 9 months after referral (right). Data are presented as a heat map scaled relative to the maximum concentration of each cytokine. Concentrations of IL-2 (F), IL-12 (G), and IFN-γ (H) in the supernatants of PBMCs from the patient and her MZ twin, preincubated with S3I-201 (200 μM), STAT5 inhibitor (200 μM), or ML-120B (10 μM), and then stimulated with Aedes SGEs for 16 hours. (I) Relative concentrations of cytokines in the supernatant of patient PBMCs preincubated with S3I-201, STAT5 inhibitor, or ML-120B; then stimulated with Aedes SGEs for 16 hours. Data are presented as a heat map, scaled relative to the maximum concentration of each cytokine. Data are shown from single replicates due to the limited amount of primary sample. DMSO, dimethyl sulfoxide.

A albopictus SGE glands induce proinflammatory cytokine production by PBMCs from patients with CAEBV disease, which can be suppressed by STAT3. (A) Concentration of IFN-γ in the supernatant of PBMCs from the patient and her MZ twin after 16-hour stimulation with SGE from A aegypti (A. aeg) or A albopictus (A. albo) (25 μg/mL). (B) Percentage of each leukocyte population among IFN-γ+ PBMCs from the patient and her MZ twin stained after 4-hour stimulation with SGE from A aegypti or A albopictus. (C) Concentrations of IL-2 and IL-12 in the supernatant of PBMCs from the patient and her MZ twin after 16-hour stimulation with SGE from A aegypti or A albopictus. (D) Expression of CD25 in NK cells from the patient and her MZ twin after 16-hour stimulation with SGE from A aegypti or A albopictus. (E) Heat maps showing relative concentrations of IFN-γ, IL-12p70, IL-2, soluble IL-2R (sIL-2R), IL-6, IL-8, tumor necrosis factor α (TNFα), CCL3, CXCL10, granulocyte-monocyte colony-stimulating factor (GM-CSF), IL-5, and IL-13 after 16-hour stimulation with SGE from A aegypti or A albopictus, from the patient and her MZ twin at 6 months after referral (left), and patient and 2 unrelated healthy controls (URHCs) at 9 months after referral (right). Data are presented as a heat map scaled relative to the maximum concentration of each cytokine. Concentrations of IL-2 (F), IL-12 (G), and IFN-γ (H) in the supernatants of PBMCs from the patient and her MZ twin, preincubated with S3I-201 (200 μM), STAT5 inhibitor (200 μM), or ML-120B (10 μM), and then stimulated with Aedes SGEs for 16 hours. (I) Relative concentrations of cytokines in the supernatant of patient PBMCs preincubated with S3I-201, STAT5 inhibitor, or ML-120B; then stimulated with Aedes SGEs for 16 hours. Data are presented as a heat map, scaled relative to the maximum concentration of each cytokine. Data are shown from single replicates due to the limited amount of primary sample. DMSO, dimethyl sulfoxide.

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