Fig. 1

Characterization of autophagy-marker protein levels at baseline and following BCR engagement. a Protein was extracted from snap-frozen PBMCs isolated from CLL patients or HDB purified by negative selection. The level of LC3B-II (n = 43), GABARAPL2 (n = 19), ATG3 (n = 42), and ATG7 (n = 40) was quantified by immunoblotting and normalized protein levels relative to the Hsc70 loading control are shown. Mean values are indicated. A Mann–Whitney test was used for statistical analysis. b Basal LC3B-II protein levels in CLL samples (n = 43) divided by IGHV mutational status into mutated (M-CLL) and unmutated (U-CLL) cases, and (c) BCR signaling capacity defined by U-CLL, M-CLL signallers (M-CLL-S) (>5% iCa²⁺ flux), and M-CLL low signallers (M-CLL-LS) (≤5% iCa²⁺ flux). Mean values are indicated. A Mann–Whitney test was used for statistical analysis. d CLL samples were treated with bead-bound isotype control antibody (IC), anti-IgM, or anti-IgD for 2, 4, or 24 h, and the level of LC3B-II (n = 21) assessed by immunoblotting. Blots were quantified and the mean fold change (±SEM) in the level of LC3B-II with anti-IgM normalized to the IC at 2 h is shown. A Wilcoxon’s matched-pairs signed-rank test was  used for statistical analysis. e A larger cohort of patient samples (n = 45) were treated with bead-bound anti-IgM for 24 h and LC3B-II levels divided according to IGHV status into M-CLL and U-CLL as previously described. Mean values are indicated. A Mann–Whitney test was used for statistical analysis