il-25 impact on malignant b cells survival and t cells activation in chronic lymphocytic leukemia

T cell dysregulation and shift to t helper 2 responses, boosting tumor microenvironment support, contributes to the survival of leukemic b cells in chronic lymphocytic leukemia. interleukin (il)-25 is involved in the initiation of t helper 2 cell responses. signal transduction of il-25 begins with the heterodimer receptor (il-17ra/il-17rb). the presence of il-25 in the tumor microenvironment may affect the supportive effects of t cells in the surrounding tumor cell environment. the purpose of this study was to evaluate the role of il-25 in the biology of cll. il-17rb expression in cd3^+ and cd19^+ cells was assessed in isolated peripheral blood mononuclear cells (pbmcs) of nine cll patients and nine healthy subjects by real-time polymerase chain reaction and flow cytometry. b cells were positively enriched from pbmcs using magnetic-activated cell sorting (macs). pbmcs and purified leukemic b cells were cultured with recombinant human il-25 (20ng/ml) for 72 hours, then the viability and apoptosis of cultured cells were measured by mtt assay and annexinv/7aad. furthermore, the levels of cd69 expression on t lymphocytes and il-17rb in t and b cells were determined by flow cytometry. the basal level of il-17rb expression in cll patients was significantly higher than that in control individuals. in addition, the percentage of il-17rb^+/cd3^+, il-17rb^+/cd19^+ cells and cd69^+/cd3^+ cells increased after 72 hours of culture with il-25 in cll patients compared to healthy subjects. il-25 also reduces the apoptosis rate of tumor cells. we found that il-25 could stimulate t cells in cll patients and lower b cell death. this suggests that il-25 might have a role in enhancing the survival of tumor cell by expressing receptors for inflammation, such as il-17rb, and might be involved in the development of cll.