## 2 Figure Legend  
In the original article, there were mistakes in the legends for Figures 1-4. The figure legends were not described comprehensively. The correct legends appear below. The editors and authors apologize for any inconvenience caused and state that the scientific conclusions are unaffected. The original article has been updated.  
Figure 1. Historical progression of CNT-induced toxicity. Timeline summarizing the discoveries on CNT toxicity obtained by LTAP teams (UCLouvain, Brussels, Belgium) and their scientific collaborators from around the world. For this collective work, we used diverse and relevant in vivo and in vitro models and CNT possessing diverse morphological and physico-chemical properties.  
Figure 2. A new pathological pathway governs carcinogenesis induced by mesothelioma are modelled CNT-N. Persistent inflammation and immunosuppression orchestrate carcinogenesis and mesothelioma. Toxic CNT-N induce an inflammatory cascade (in blue) resulting in the influx of inflammatory macrophages and neutrophils. Sustained production of free radicals by these activated immune cells induces irreversible DNA damage. Pro-inflammatory cytokines are also considered as potent polypeptide growth factors for transformed mesothelial cells and angiogenesis. An unexpected conjoint immunosuppression (in red) is induced by mesothelioma CNT. These early responses to CNT-N are characterized by persistent accumulation of immunosuppressive macrophages and monocytes and a sustained production of regulatory cytokines (i.e., IL-10 and TGF-\(\beta\)). These immunoregulatory components are incriminated in carcinogenesis by preventing host immune responses directed against transformed cells and favoring tumor growth.  
Figure 3. Mesothelioma CNT-N and non-mesotheliomagenic CNT-T induce early comparable peritoneal lesions and macrophage accumulation in rats. Wistar rats untreated or injected (i.p) with CNT-N or CNT-T (2 mg) were sacrificed (day 15) and peritoneal tissues (diaphrag) were harvested, fixed in paraformaldehyde and embedded in paraffin. 5 um sections were stained with classical H&E coloration (A-D-G for controls, B-E-H for CNT-N and C-F-I for CNT-T, magnification \(\times\)4 first line, \(\times\)40 other lines). The red arrows indicate granulomas containing CNT crystalline structures within the connective tissue (selected from the frame of A-B-C panels). Granulomas mainly comprise macrophages around nanotube aggregates (G-H-I). For macrophage identification, 5 um sections were incubated  
with mouse anti-rat CD68 antibody (Abcam monoclonal) and secondary antibody donkey anti-mouse (Jackson ImmunoReserch) coupled with HRP. After incubation with AlexaFluor Tyramide 488, a counterstaining with Hoechst44432 dye was performed. Stained slides were digitalized using a Panoramic 250 FlashIII scanner (3 DHistech) at \(\times\)20 magnification.  
Figure 4. New opportunities to use CNT for delineating specific macrophage immune pathways specifically associated with malignant mesothelioma. Cellular and molecular characterization of macrophage subpopulations by using next-generation sequencing (NGS) technologies. Peritoneal macrophages from CNT-N or CNT-T-treated rats (day 15) were isolated from peritoneal cell suspensions using flow cytometry cell sorting (FACSAria III, BD Biosciences) and APC-antibodies specific for CD68 (mouse anti-rat CD68 antibody, Abcam monoclonal). Cytocentrifuge preparations of purified macrophages were stained with Diff-Quick. RNA was isolated using Qiagen kits and libraries were prepared and sequenced using the Illumina platform. The gene count matrix was transformed in fold-change-related tables or barcode plots.