CBLB (Cbl Proto-Oncogene B)

MSC-derived exosomal CBLB has therapeutic potential in ameliorating the progression of IP probably by ubiquitinating MAPK14, which could lead to novel clinical interventions for treating this condition.

circ-CBLB and ETS-1 are downregulated in RA and correlate with inflammation and disease activity. They regulate each other bidirectionally. circ-CBLB reduces RA-FLS viability, promotes apoptosis, and inhibits migration by modulating cytokines. ETS-1 has similar effects, and interfering with its expression reverses the impact of circ-CBLB.

c.2213A > G mutation on the CBLB gene causes a new type of inherited thrombocytopenia, and the potential pathogenesis involves an imbalance in cellular immunity and excessive ferroptosis of megakaryocytes.

In vitro and in vivo studies showed that siRNA against cblb caused an effective inhibition of tumor progression in subcutaneous B16-F10 and LLC models, in which a significant increase of effector T cells in peripheral blood mononuclear cells and an increase of effector T cells and a significant decrease of Treg cells in the tumor were clearly observed. This polymersome-mediated down-regulation of the cblb gene in T cells provides a promising approach for activating T cells and enhancing their anti-tumor capacity.

In summary, we elucidate the mechanism by which the miR-23a/27a/24 - 2 cluster miRNAs maintain their own expression and the molecular mechanism by which the miR-23a/27a/24 - 2 cluster miRNAs promote tumor immune evasion and PD-1/PD-L1 blockade resistance. In addition, we provide a novel strategy for the treatment of NSCLC expressing high levels of the miR-23a/27a/24 - 2 cluster.

Additionally, the levels of IL-4 and IL-10 were higher, while the levels of IL-6 and TNF-α were lower. Conclusion XFC treatment upregulates the expression of circ-CBLB in RA-FLS, increases anti-inflammatory cytokines, decreases pro-inflammatory cytokines, inhibits the viability of RA-FLS, increases apoptosis rate, extends the cell cycle, suppresses the proliferation of RA-FLS, and promotes its apoptosis.

We also identified the distinct function of CD73 activity in adenocarcinoma and squamous cell carcinoma. Our findings indicated a role of CD73 in mediating NSCLC metastasis and propose it as a therapeutic target for NSCLC.

CBLB restricted the NTM growth and dissemination by promoting early granuloma formation in vivo. Our study shows that CBLB bolsters innate immune responses and helps prevent the dissemination of NTM during compromised T-cell immunity.

CD4 T cells from patients with ITP showed resistance to anergic induction, highly activated phosphoinositide 3-kinase (PI3K)-protein kinase B (AKT) signaling, decreased CBLB expression, and 5' UTR hypermethylation of CBLB. CBLB overexpression in T cells effectively attenuated the elevated p-AKT level and resistance to anergy. Low-dose decitabine treatment led to significantly elevated CBLB expression in CD4 T cells from seven patients showing a partial or complete response. These results indicate that the 5' UTR hypermethylation of CBLB in CD4 T cells induces resistance to T-cell anergy in ITP. Thus, the upregulation of CBLB expression by low-dose decitabine treatment may represent a potential therapeutic approach to ITP.

This study confirmed the utility and feasibility of ctDNA in the prognosis monitoring of gastric cancer.

In addition, we show that bbT369 T cells drive greater T cell expansion and durable tumor control compared with unedited controls in vivo using a xenograft NSG mouse model. Collectively, the data support the potential for bbT369 to provide deeper and more durable responses in NHL patients including those with more challenging disease characteristics.