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. 2010 Mar 1;107(11):5100–5105. doi: 10.1073/pnas.0913108107

Fig. 4.

Fig. 4.

NKp65 triggers cytolytic activity and stimulates cytokine secretion. (A) NK92 and NK92MI, but not YT or NKL, express NKp65. Real-time PCR analysis of NKp65 transcripts (n.d., not detectable). (B) NKp65 expression on NK92MI. NK92MI transduced with tagged NKp65 or untransduced cells were stained for NKp65 with anti-FLAG mAb (solid) or KACL tetramers (shaded) or isotype control (dotted). (C) NKp65 triggers redirected cytolysis. Redirected lysis assay using P815 as targets and NK92MI-NKp65 or mock transductants as effectors either in the presence of anti-FLAG mAb M2 or isotype control. (D) Tyrosine 7 of NKp65 is critically involved in NKp65-mediated cytotoxicity. Redirected lysis assay using P815 as targets and NK92MI-NKp65 (WT) or NK92MI-NKp65Y7F (Mut) as effectors in the presence of anti-NKp44 mAb, anti–histidine-tag mAb or isotype control. (E) P815-KACL, but not P815-neo, are lysed by NK92MI-NKp65. Lysis of P815-KACL was inhibited to background levels in the presence of OMA1, but not in presence of an isotype control. (F) KACL stimulates IFN-γ secretion by NK92MI-NKp65. NK92MI-NKp65 were cocultured with P815-neo or P815-KACL in presence or absence of OMA1, IL-12, or IL-18, and subsequently, IFN-γ secretion was measured by ELISA. (G) KACL-dependent lysis of U937. Cytolysis of U937 in presence of OMA1 or isotype control by NK92MI-NKp65.