KLRC1 (Killer Cell Lectin Like Receptor C1)

In particular, HLA-B leader matched patients had a higher CD57 expression of total NK and NKG2A+KIR- NK cells, with enhanced NKG2A+KIR- NK cell cytotoxicity (CD107a expression) and IFN-γ secretion at 1, 3, and 6 months post-transplantation (all false discovery rate-adjusted P <0.05). These findings identify HLA-B leader matching status as a disease-specific prognostic biomarker, suggesting its potential relevance for personalized donor selection considerations in haplo-HSCT settings.

We identified a feasible method to activate CD56+ cells and evaluate the safety of their infusion in patients. Despite the value of activating CD56+ cells with IL-15, further studies with larger sample sizes are needed to confirm and validate the current hypothesi (registration number: IRCT20230801058996N2).

In a human PBMC-engrafted NSG mouse xenograft lung cancer model, an anti-HER2 × anti-NKG2A BiNK markedly inhibited tumor growth as a monotherapy or in combination with pertuzumab. Cell depletion studies revealed that the BiNK enhanced antitumor activity of both NK and T cells. NKG2A blockade with potent and specific, fully human antibodies and BiNKs show promise for further development as cancer immunotherapeutics.

Co-editing the death receptor FAS increases the persistence of NKG2A-edited CAR NK cells both in vitro and in vivo. Together, our findings present a novel approach to enhance both cytotoxicity and persistence of CAR NK cell in cancer immunotherapy and reduce the risk of antigen-negative relapse.

These findings uncover a redox-independent role for PXDN in promoting immune evasion and tumor progression. Overall, our study highlights PXDN as a critical regulator of melanoma cell biology and a potential therapeutic target for NK-cell-based immunotherapy in melanoma and other solid cancers.

Overall, our study reveals major phenotypic and metabolic disturbances of circulating and tumor-infiltrating iNKT cells in melanoma, with clinical impacts. By unveiling new key features and skewing details on iNKT cells in melanoma, our study paves the way for innovative combination strategies exploiting metabolic pathways and/or disturbed ICP profiles to overcome immune subversion and better harness the potential of iNKT cells for cancer immunotherapy.

POSTN+ CAFs drive BCa progression by enhancing angiogenesis, migration, and immune suppression, mediated partly by the IL1B/IL1R1 axis.

These findings demonstrate that exercise-induced NK mobilization combined with cytokine pre-activation yields an adoptive cell therapy product with superior anti-leukemic activity. (NCT06643221).

First, the effectiveness of blocking the NKG2A-HLA-E interaction in vitro and in pre-clinical models as well as the presence of infiltrating NKG2A+ CD8+ T cells in some solid tumors has led to the generation of clinical grade NKG2A-specific monoclonal antibodies, pioneered by monalizumab, currently tested in clinical trials. Second, controlling NKG2A expression by genetic engineering constitutes a promising approach to improve advanced adoptive NK cell-based immunotherapies. Challenges include identifying predictive biomarkers of responsiveness, selecting appropriate clinical settings and optimizing combinatorial regimens.

Elevated immune cell infiltration and enhanced drug sensitivity characterized the high-risk group, exhibiting significant responsiveness to chemotherapy, targeted, and immunotherapy treatments (p < 0.05). The study developed an integrated LGCPN-WT model, significantly enhancing survival prediction accuracy and clinical utility for WT, thus supporting personalized treatment approaches.

Our findings suggest a potential causal association between MS and BC. KLRC1 is a robust and promising biomarker for predicting the prognosis of patients with MS and BC.

Our data suggest that human MAIT cell regulation is context-dependent. These findings have the potential to critically inform efforts targeting MAIT cells for cancer immunotherapy.