SELL (Selectin L)

Our data identify ADAM17 as an easily quantifiable, longitudinal biomarker that concurrently reflects tumor development stage and renal function damage in MM patients. Incorporation of ADAM17 into existing risk algorithms may enhance prognostic precision and enable earlier, patient-tailored intervention.

Our research indicates that apheresis-derived granulocytes and pooled GCs do not differ enough to not consider more frequent use of the latter in daily clinical practice. Moreover, we concluded that gamma irradiation does not worsen the quality of granulocyte components, and freshly collected GCs should be preferred.

Our findings suggest that elevated levels of miR-19a-3p in the serum of patients with HER2 + metastatic breast cancer may result from effective NK cell-mediated ADCC and activation of CD4 + Th1 cells, which could be responsible for the anti-tumor immune response associated with a favorable prognosis. Blood levels of miR-19a-3p might help identify breast cancer patients who have effective trastuzumab-induced anti-tumor immune responses.

In XIAP deficiency, MDP-flow CD62L enabled faster functional analysis than MDP-flow TNF-α. These analyses are also useful for post-HCT functional assessment.

Bioinformatics predictions and dual-luciferase reporter assays indicated that the transcription factor LEF1 may regulate Itgae transcription by binding to its promoter sequence. Collectively, our findings demonstrate that splenic CD103+CD8+ T cells express fewer activation and function-associated molecules, which may contribute to their limited role in the course of P. yoelii NSM infection in C57BL/6 mice, and implicates LEF1 in the regulation of CD103 expression.

The antitumor effect induced by the combinational therapy was abolished by administration of an anti-VCAM-1 neutralizing antibody. Our findings demonstrate that combining metformin with fasting exerts a synergistic antitumor effect by recruiting CD8+ T cells-relocated to the BM during fasting-back to the tumor during refeeding, facilitated by enhanced VCAM-1 expression on normalized tumor vasculature.

Notably, during the chronic phase of the infection, pop1 cannot retain its functionality, irrespective of its origin, which may hamper its ability to control reactivation. Our observations emphasize that the differentiation of exhausted CD8 T cells in non-viral infections, like chronic toxoplasmosis, follows a different pattern than established models and highlights the need to develop new immune strategies better tailored for a broad range of pathogens.

Furthermore, a DMBT1 neutralizing antibody was developed with the promise to inhibit tumor-KC interaction and treat metastatic cancer. In conclusion, our work reveals a KC subset that accounts for the liver tropism of breast cancer cells and NETs, and provides potential strategies in metastasis treatment.

Together, these findings highlight that simultaneous modulation of PD-L1 and CD226 pathways can restore CMV-specific T cell function, offering a promising strategy to boost TCR-T efficacy in cytokine-deprived environments. [BMB Reports 2025; 58(7): 307-312].

Our integrated multi-omics analysis identified genetic variants influencing spontaneous abortion risk and their downstream molecular mechanisms, providing insights into potential therapeutic targets. The implicated pathways and cell types may guide future investigations into the pathogenesis of spontaneous abortion.

In conclusion, consistent CD4+ phenotype, superior expansion capacity, and enhanced CD62L expression of CB-CAR-iNK T cells suggest that they may provide an alternative off-the-shelf source for effective CAR-iNK T cell therapy, while reducing the risk of severe cytokine release syndrome through their immunomodulatory properties. Thus, our results support the potential use of CB-iNK T cells as an allogeneic CAR-T cell therapy platform as they maintain a potent cytotoxicity with potentially better safety profile given a Th2-biased cytokine production upon activation.

Further prediction of the binding residue sites revealed that seven residues of the GoAstV-P2 protein (THR124, ILE22, VAL24, TRP51, PRO66, GLN100, and VAL125) and twelve residues of the HSPA5 protein (ARG2, HIS3, LEU4, LEU6, ALA7, LEU8, LEU9, LEU10, LEU11, ASP411, VAL413, and LEU415) may be involved in the interaction between these two proteins. Our research results have preliminarily elucidated the interaction mechanisms between viral proteins and receptors, facilitating exploration from multiple angles of the roles of candidate protein in the process of GoAstV infecting host cells. This provides a theoretical basis for further identification of GoAstV receptors and clarification of its infection mechanisms.