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. 2020 Oct 24;8:54. doi: 10.1186/s40364-020-00234-z

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Anti-CCR7 mAb mediates a strong CDC on T-PLL cells. a CDC on alemtuzumab-naïve patients. Leukemic cells from T-PLL patients (n = 8) were incubated with anti-CCR7, anti-CD52 (alemtuzumab), or an IC at the indicated concentrations and then exposed to rabbit complement for 1.5 h. The percentage of specific cell lysis was determined through quantification of 7-AAD incorporation by flow cytometry. b CDC on alemtuzumab-refractory patients. Specific lysis on T-PLL cells from 4 refractory patients was assayed as described in A. c Relative median fluorescence intensity (RMFI) of CCR7, CD52 and CCR4 in T-PLL cells from alemtuzumab-naïve or alemtuzumab-refractory patients (R/R). Cells obtained from PB samples of patients not treated with alemtuzumab (n = 8; black bars) or refractory to this mAb (n = 4; grey bars) were analyzed by flow cytometry to determine CCR7, CD52, and CCR4 surface density measured as MFI relative to a corresponding IC. d CCR7, CD52, and CCR4 surface expression in T-PLL cells from one representative alemtuzumab-naïve or -refractory patient. E) Proportion of CCR7⁺, CD52⁺ and CCR4⁺ in T-PLL cells from alemtuzumab-naïve or alemtuzumab–refractory patients. The percentage of positive cells was determined in naïve (n = 8; black bars) and refractory patients (n = 4; grey bars). f and g Anti-CCR7 antibody does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC). T-PLL cells were incubated with media alone or in the presence of an IC, anti-CD52 (alemtuzumab) or anti-CCR7 antibodies. f Isolated and IL-2-stimulated human NK cells from a healthy donor were used as effector cells at an effector to target (E:T) ratio of 6:1 (n = 1). g Isolated and IL-2-stimulated wild-type mouse NK cells from spleen (n = 2) were used as effector cells at an effector to target (E:T) ratio of 6:1. After 4 h, the percentage of T-PLL cells killed by ADCC was determined through 7-AAD staining by flow cytometry. In A, B, C, E, F, and G, bars (or symbols) represent mean ± SEM. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns, not significant