A 38-year-old male was admitted to Renji Hospital (Shanghai, China) with the major complaint of back pain due to left hydronephrosis. Imaging analysis revealed an area of nodular soft-tissue density in the left ureteral wall. The patient’s left kidney was non-functional. Thus, a left nephroureterectomy was performed for the purpose of pathological diagnosis, and histopathological examination revealed follicular lymphoma. The patient received R-CHOP chemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone) every three weeks. Following six courses of chemotherapy, positron emission tomography-computed tomography revealed that the patient was in complete remission. From this case we showed that in cases where a partial ureteral stenosis with ureteral wall thickening was observed by imaging analysis, further histological examination of tissue samples should be assigned as soon as possible.

Neutrophils fight infections by generating reactive oxygen species (ROS) and extracellular traps (NETs). However, how neutrophils modulate ROS/NET generation is mechanistically unclear. Kindlin-3, an essential integrin activator expressed in hematopoietic cells, is required to support integrin-mediated neutrophil recruitment during inflammation. Here, we report a novel role of kindlin-3 in regulating ROS/NET generation in neutrophils. When overexpressing kindlin-3 in neutrophil-like differentiated HL-60 cells (HL-60N), ROS/NET generation from these cells were significantly suppressed. Interestingly, overexpression of a kindlin-3 mutant that is defective for interacting with integrins in HL-60N cells still inhibited ROS/NET generation, suggesting that the role of kindlin-3 in inhibiting ROS/NET signaling may be independent of its binding to integrins. Consistently, knockdown of kindlin-3 in HL-60N cells led to enhanced ROS/NET generation. In addition, bone marrow neutrophils isolated from kindlin-3-deficient mice showed elevated ROS/NET generation when compared with WT counterparts. As expected, overexpression of exogenous kindlin-3 in mouse neutrophils could suppress NET release ex vivo and in vivo. Collectively, these results demonstrate that kindlin-3 in neutrophils is involved in modulating the ROS/NET signaling, providing a novel mechanism for fine-tuning neutrophil behaviors during inflammation.

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