Figure 5. Opposite effects of pro-inflammatory cytokines on cells from JAK2^V617F or CALR mutated patients.

(A) When clonogenic activity was analyzed according to mutation status, the CFU-C growth of JAK2^V617F mutated patients was significantly up-regulated by IL-1β + TIMP-1 and IL-1β + TNF-α as compared with untreated control samples, the CALR mutated counterparts and the CB-derived cells (only IL-1β + TIMP-1). The results are expressed as growth fold change versus untreated CTR samples. All data are presented as mean ± SEM. (*p ≤ 0.05; **p ≤ 0.01 vs untreated cells) (^#p ≤ 0.05; ^##p ≤ 0.01; ^####p ≤ 0.0001 vs CB-derived cells) (B) When colony composition was analyzed according to mutation status, we found that the erythroid compartment of the untreated samples was reduced in both mutated groups as compared with the CB counterparts. However, no significant differences were observed between the two mutated groups. Interestingly, in the JAK2^V617F mutated group, the addition of IL-1β + TIMP-1 and IL-1β + TNF-α enhanced the erythroid compartment as compared with untreated samples. Conversely, some cytokines combinations significantly impaired BFU-E growth in CALR mutated patients. The results are expressed as mean percentage of CFU-GM/BFU-E as compared with the total CFU-C count.