Interleukin-7 (IL-7) is a multipotent cytokine that maintains the homeostasis of the immune system. IL-7 plays a vital role in T-cell development, proliferation, and differentiation, as well as in B cell maturation through the activation of the IL-7 receptor (IL-7R). IL-7 is closely associated with tumor development and has been used in cancer clinical research and therapy. In this review, we first summarize the roles of IL-7 and IL-7Rα and their downstream signaling pathways in immunity and cancer. Furthermore, we summarize and discuss the recent advances in the use of IL-7 and IL-7Rα as cancer immunotherapy tools and highlight their potential for therapeutic applications. This review will help in the development of cancer immunotherapy regimens based on IL-7 and IL-7Rα, and will also advance their exploitation as more effective and safe immunotherapy tools.

Tryptophanyl-tRNA synthetase (WRS) is an essential enzyme that catalyzes the ligation of tryptophan (Trp) to its cognate tRNAtrp during translation via aminoacylation. Interestingly, WRS also plays physiopathological roles in diseases including sepsis, cancer, and autoimmune and brain diseases and has potential as a pharmacological target and therapeutic. However, WRS is still generally regarded simply as an enzyme that produces Trp in polypeptides; therefore, studies of the pharmacological effects, therapeutic targets, and mechanisms of action of WRS are still at an emerging stage. This review summarizes the involvement of WRS in human diseases. We hope that this will encourage further investigation into WRS as a potential target for drug development in various pathological states including infection, tumorigenesis, and autoimmune and brain diseases.

The formation of immunological synapse (IS) is essential for natural killer (NK) cells to eliminate target cells. Although elucidation of the overall characteristics and formation processes of IS is ongoing, the mechanisms for regulating the stability of IS by cytoskeleton remain to be understood. The current study reports that Nogo receptor 1 (NgR1) plays a key role in modulating NK cell-mediated killing by destabilization of IS formation. NgR1 deficiency or blockade results in improved tumor control of NK cells by enhancing NK-totarget cell contact stability and regulating F-actin dynamics during IS formation. Clinically, patients with a tumor expressing abundant NgR1 ligand showed poor prognosis despite high levels of NK cell infiltration. Thus, our study identifies NgR1 as an immune checkpoint involved in IS formation and reveals a potential approach to improve the killing effect of NK cells in cancer immunotherapy.