LILRB1 (Leukocyte Immunoglobulin Like Receptor B1)

Differences in MCLIR/RCLIR magnitude and persistence are explained by differences in implied sojourn time and detectable reservoir size. These findings motivate evaluation of risk-targeted and repeated early-detection strategies and highlight key empirical priorities for improving inference on bladder cancer natural history.

Overall, LILRB1 serves as a key immune checkpoint driving cytotoxic dysfunction, marking exhausted CD8+ T cells and CD16+ NK cells. The nine-gene signature links CD8+ T-cell impairment to poor prognosis, while NK-cell involvement positions LILRB1 as a promising therapeutic target for restoring anti-leukemic immunity.

In LILRB2, the deletion of exon 9 is the most prominent event, next to deletion of exon 10 and the use of alternative 3' splice sites near exons 10 and 15. The exons that encode the extracellular domains remain largely intact, suggesting that alternative splicing predominantly affects the stem region and the signaling capacity of the LILRB1 and LILRB2 receptors.

Together, these results highlight distinct tumorigenic mechanisms in HIV+ DLBCL and underscore the need for mutational profiling of HIV+ DLBCL cohorts worldwide to identify biomarkers and therapeutic targets.

Senescent TAMs influence NB immunosuppression and progression. EIF5 is a key regulator of TAM senescence and a potential therapeutic target. Our risk model may guide clinical stratification and targeted interventions.

These detailed studies demonstrate that most of Tmod regulation is ligand dependent. Expression levels of the CAR affect activation/proliferation in a LIR-1 NOT gate, but the ITIM signaling module plays only a minor role in ligand-independent activity.

The knockdown of LILRB1 promoted apoptosis in MM cells, enhanced sensitivity to bortezomib and diminished tumourigenicity in a subcutaneous mouse model. Mechanistically, LILRB1 triggers downstream GATA Binding Protein 2 (GATA2) and sustains MM cell proliferation via the GATA2-Sarcoma Antigen 1 (SAGE1) signalling pathway. Consequently, the targeting of LILRB1 may represent a promising therapeutic approach for MM.

In this work, we revealed that LILRB1 was highly expressed in DLBCL cells and was negatively correlated with patient survival. Furthermore, we found that the LILRB1-CREB-SORBS3 pathway played a role in maintaining the proliferation of DLBCL cells. These data suggest that LILRB1 might be a potential target for the treatment of DLBCL.

By synthesizing current knowledge on macrophage polarization in ovarian cancer, this study underscores the potential of targeting TAMs to improve clinical outcomes and personalize treatment strategies for OC patients. Continued research in this domain is essential to develop robust therapeutic frameworks that can mitigate the immunosuppressive TME and enhance the efficacy of existing and novel cancer therapies.

Additionally, we identified LILRB1 in monocytic acute myeloid leukemia (AML) and demonstrated LILRB1 CAR-T cell cytotoxicity against AML cell lines in vitro and in vivo. These findings establish LILRB1 as a novel target for cancer immunotherapy and show evidence for the preclinical efficacy of LILRB1 CAR-T cells against haematological malignancies, including cases resistant to previous lines of immunotherapy, thus holding promise for further clinical development.

Our study demonstrated that tumor-infiltrating CD4+GzmB+ T cells fail to eliminate tumors. Dual blockade of PD-1 and CD85j alongside IL-15 restores the effector function of CD4+GzmB+ T cells and drives CD4+GzmB+ T-cell transformation in the tumor microenvironment to combat MHC-II-expressing tumors.

In vitro tumor conditioning did not reduce the phagocytic response to CD47 blockade, suggesting that induction of a macrophage phenotype with increased expression of CD163 does not directly limit the capacity for phagocytosis of tumor cells. In conclusion, these findings suggest that CD163+ macrophages remain responsive to CD47 blockade, highlighting their potential as targets for immunotherapy in ovarian cancer.