Figure 4
Figure 4. Activation of Vδ2neg γδ T cells through CD16 stimulates their production of IFNγ. (A) The long-term CD16pos Vδ2neg γδ T-cell line was incubated for 24 hours with coated anti-CD16 agonist mAb or control mAb, and recombinant cytokines (IL12 and/or IFNα). The amount of IFNγ released in the supernatant was quantified by ELISA (mean ± SD). Data are representative of 3 different experiments. (B) Seven CD16pos primary Vδ2neg γδ T-cell lines were generated from 7 different HCMV-infected KTRs and incubated for 24 hours with coated anti-CD16 agonist mAb or control mAb and/or recombinant cytokines (IL12 and IFNα). The amount of IFNγ released in the supernatant was quantified by ELISA (mean ± SD) and compared between control and anti-CD16 activation without and with cytokines (P = .02 and P = .01, respectively).

Activation of Vδ2neg γδ T cells through CD16 stimulates their production of IFNγ. (A) The long-term CD16pos Vδ2neg γδ T-cell line was incubated for 24 hours with coated anti-CD16 agonist mAb or control mAb, and recombinant cytokines (IL12 and/or IFNα). The amount of IFNγ released in the supernatant was quantified by ELISA (mean ± SD). Data are representative of 3 different experiments. (B) Seven CD16pos primary Vδ2neg γδ T-cell lines were generated from 7 different HCMV-infected KTRs and incubated for 24 hours with coated anti-CD16 agonist mAb or control mAb and/or recombinant cytokines (IL12 and IFNα). The amount of IFNγ released in the supernatant was quantified by ELISA (mean ± SD) and compared between control and anti-CD16 activation without and with cytokines (P = .02 and P = .01, respectively).

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