Figure 6.
Figure 6. IRS+ T cells from patients with PNH kill more efficiently GPI+ than GPI- cells. Cytolytic activity of IRS+ T cells from 3 different patients with PNH (A: PNH6; B: PNH7; C: PNH11) against GPI+ K562 cell line or its GPI- counterpart (KCRN) was analyzed in a 4-hour 51Cr release assay at the indicated effector-target (E/T) ratios. Anti-LFA-1 mAb (5 μg/mL) was added to the cytotoxic assay in order to block the contribution of LFA-1/ICAM-1 interaction to the activation of T cells. As the 2 K562 cell lines differ from each other for the expression of GPI-linked molecules, this shows the relative contribution of GPI molecules to target-cell lysis. Results are expressed as % of 51Cr release, mean of triplicate samples plus or minus SD.♦ indicates KCRN (K562 GPI-); •, KCRN (K562 GPI-) plus anti-LFA-1 mAb; ▴, K562 (GPI+); ▪, K562 (GPI+) plus anti-LFA-1 mAb.

IRS+ T cells from patients with PNH kill more efficiently GPI+ than GPI- cells. Cytolytic activity of IRS+ T cells from 3 different patients with PNH (A: PNH6; B: PNH7; C: PNH11) against GPI+ K562 cell line or its GPI- counterpart (KCRN) was analyzed in a 4-hour 51 Cr release assay at the indicated effector-target (E/T) ratios. Anti-LFA-1 mAb (5 μg/mL) was added to the cytotoxic assay in order to block the contribution of LFA-1/ICAM-1 interaction to the activation of T cells. As the 2 K562 cell lines differ from each other for the expression of GPI-linked molecules, this shows the relative contribution of GPI molecules to target-cell lysis. Results are expressed as % of 51 Cr release, mean of triplicate samples plus or minus SD.♦ indicates KCRN (K562 GPI-); •, KCRN (K562 GPI-) plus anti-LFA-1 mAb; ▴, K562 (GPI+); ▪, K562 (GPI+) plus anti-LFA-1 mAb.

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