Figure 6.
Persistent TNF-α production and IL-10R signaling defects are found in an unaffected twin of a patient with MPN. (A) The monocytes of a patient with MPN, the unaffected twin of the patient, and normal donors (n = 2) were stimulated with 10 ng/mL LPS for 4, 9, 18, and 24 hours before supernatants were harvested for ELISA. The amount of TNF-α produced at 4 hours was normalized to 1. (B) The same supernatants harvested in A were taken for quantifying IL-10. (C) The monocytes of a patient with MPN, the unaffected twin of the patient, and normal donors (n = 2) were stimulated with 10 ng/mL LPS and various concentration of IL-10 simultaneously for 4 hours between harvesting of the supernatant for TNF-α ELISA. The percentage change in TNF-α is measured by the difference in TNF-α production between adding IL-10 and without IL-10.

Persistent TNF-α production and IL-10R signaling defects are found in an unaffected twin of a patient with MPN. (A) The monocytes of a patient with MPN, the unaffected twin of the patient, and normal donors (n = 2) were stimulated with 10 ng/mL LPS for 4, 9, 18, and 24 hours before supernatants were harvested for ELISA. The amount of TNF-α produced at 4 hours was normalized to 1. (B) The same supernatants harvested in A were taken for quantifying IL-10. (C) The monocytes of a patient with MPN, the unaffected twin of the patient, and normal donors (n = 2) were stimulated with 10 ng/mL LPS and various concentration of IL-10 simultaneously for 4 hours between harvesting of the supernatant for TNF-α ELISA. The percentage change in TNF-α is measured by the difference in TNF-α production between adding IL-10 and without IL-10.

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