Figure 2
Figure 2. Impaired cytokine production in NK cells from Bcl10- and Malt1-deficient NK cells upon NK-cell receptor stimulation. (A) Total splenocytes from control or Bcl10-deficient mice were stimulated with plate-bound anti-NK1.1, anti-Ly49D, or anti-NKG2D, stained for CD49b (DX5) and CD3 and intracellular cytokine production, and analyzed by flow cytometry. Cells were gated for DX5+CD3− cells. The percentages of IFN-γ– or TNF-α–positive cells with respect to total NK cells are indicated. (B) IL-15–expanded splenic NK cells from Bcl10- and Malt1-deficient mice were stimulated with plate-bound antibodies directed against various activating NK- cell receptors or PMA and ionomycin (PMA/Iono) as indicated for 24 hours. (C) NK cells from 2 wild-type and 2 Bcl10-deficient mice were prepared as in panel B and stimulated with 10 ng/mL IL-12 and/or 25 ng/mL IL-18 for 24 hours. Cytokine release was measured by ELISA. Data are means plus or minus SD of triplicate samples and representative of 3 independent experiments.

Impaired cytokine production in NK cells from Bcl10- and Malt1-deficient NK cells upon NK-cell receptor stimulation. (A) Total splenocytes from control or Bcl10-deficient mice were stimulated with plate-bound anti-NK1.1, anti-Ly49D, or anti-NKG2D, stained for CD49b (DX5) and CD3 and intracellular cytokine production, and analyzed by flow cytometry. Cells were gated for DX5+CD3 cells. The percentages of IFN-γ– or TNF-α–positive cells with respect to total NK cells are indicated. (B) IL-15–expanded splenic NK cells from Bcl10- and Malt1-deficient mice were stimulated with plate-bound antibodies directed against various activating NK- cell receptors or PMA and ionomycin (PMA/Iono) as indicated for 24 hours. (C) NK cells from 2 wild-type and 2 Bcl10-deficient mice were prepared as in panel B and stimulated with 10 ng/mL IL-12 and/or 25 ng/mL IL-18 for 24 hours. Cytokine release was measured by ELISA. Data are means plus or minus SD of triplicate samples and representative of 3 independent experiments.

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