Although immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment, primary resistance and acquired resistance continue to limit their efficacy for many patients. To address resistance and enhance the anti-tumor activity within the tumor immune microenvironment (TIME), numerous therapeutic strategies targeting both innate and adaptive immune cells have emerged. These include combination therapies with ICIs, chimeric antigen receptor T-cell (CAR-T), chimeric antigen receptor macrophages (CAR-Ms) or chimeric antigen receptor natural killer cell (CAR-NK) therapy, colony stimulating factor 1 receptor (CSF1R) inhibitors, dendritic cell (DC) vaccines, toll-like receptor (TLR) agonists, cytokine therapies, and chemokine inhibition. These approaches underscore the significant potential of the TIME in cancer treatment. This article provides a comprehensive and up-to-date review of the mechanisms of action of various innate and adaptive immune cells within the TIME, as well as the therapeutic strategies targeting each immune cell type, aiming to deepen the understanding of their therapeutic potential.

The monolithic catalyst of CeO₂-loaded ceramic foam for the catalytic ozonation of organic pollutants operated in a continuous-flow mode was developed, achieving effective TOC removal of organic pollutants and high utilization efficiency of ozone.

MZB1 (Marginal Zone B and B1 Cell-Specific Protein), an endoplasmic reticulum-resident protein, has recently garnered significant attention for its role in immune regulation. As a critical modulator within various immune cells, MZB1 influences key processes such as cell differentiation, antibody production, and immune microenvironment dynamics. Despite advances in understanding, the precise mechanisms by which MZB1 contributes to immune homeostasis and dysregulation in pathological conditions remain incompletely defined. Emerging evidence highlights its involvement in tumor biology, inflammatory responses, and autoimmune diseases, positioning MZB1 as a potential therapeutic target. This review aims to synthesize current research findings on MZB1’s functions across different immune cell types, elucidate its interactions with other immune regulatory factors, and explore its impact on the tumor microenvironment and immune-mediated disorders.

Background IL2RA has been shown to play an important function in tumorigenesis. However, the exact mechanism by which it functions in KIRC is poorly understood. Methods Initially, we performed a pan-cancer study using the TIMER database to identify the expression variation of IL2RA in KIRC. Then, Kaplan-Meier, clinicopathological, and COX regression analyses using the TCGA database were performed to show the association of the IL2RA expression level with overall survival and clinicopathology of KIRC patients. Next, we used GO and KEGG enrichment analysis to reveal the association of IL2RA level with immunity. Finally, in order to explore the association of IL2RA expression levels with immunity, our group adopted an immunotherapeutic research approach to determine the mechanism of its influence. Results IL2RA was found to have high expression levels in KIRC and to be correlated with clinicopathology. Based on GSEA analysis, it was discovered that IL2RA is associated with immune pathways in KIRC. Immunotherapy analysis provided further clarification on the correlation between IL2RA and immunotherapy. Conclusions The expression level of IL2RA has an important role in the development and escape of KIRC. IL2RA has a complex immunoregulatory mechanism in this tumor. Our study suggests that it contributes to the poor prognosis for KIRC patients mainly by affecting the early stages of lymphocyte response.

B cell activating factor (BAFF), originally characterized as a canonical survival factor for B cells, is now recognized as a pleiotropic immunoregulator that bridges innate and adaptive immunity. Its biological effects are highly context-dependent, manifesting as promotion of malignant B-cell survival in hematological malignancies, conflicting activities in solid tumors, and disruption of B-cell tolerance in autoimmune diseases. Current literature has largely examined BAFF within disease-specific frameworks, leaving cross-disease mechanistic relationships inadequately resolved. In this review, we propose a multi-factorial framework for integrating evidence across cancer and autoimmunity through four proposed variables: ligand concentration, oligomeric form, cellular source, and receptor availability. By dissecting receptor signaling via BAFF receptor (BAFF-R), transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), and B cell maturation antigen (BCMA), we evaluate the therapeutic landscape, safety profiles, and combination strategies of BAFF-targeted agents. The framework is a working hypothesis, not a validated causal model. We propose three integrated perspectives: (i) a proposed multi-factorial framework for interpreting BAFF’s divergent functions; (ii) a conceptual, testable inverted U-shaped working hypothesis for solid tumors, without validated concentration thresholds; and (iii) the translational utility of BAFF system molecules as stratification biomarkers and precision therapeutic targets. Autoimmune disease data provide conceptual support for this concentration-form-context framework, which was initially developed to reconcile contradictory observations in tumors. The framework requires direct experimental titration and oligomer-specific validation. Finally, we identify critical knowledge gaps, including distinct signaling pathways elicited by BAFF oligomers and crosstalk with inflammatory networks, to inform next-generation personalized immunotherapy.

B cells play a variety of complex roles in cancer, both promoting cancer progression and enhancing anti-tumor immune responses, but their mechanism of action in kidney cancer has not been elucidated. We collected kidney cancer sample data from the GEO database and TCGA database, mapped the single-cell landscape inside kidney cancer tissue, identified 25 B-cell-related genes, and based on this, identified related molecular subtypes of kidney cancer patients, and explored their internal microenvironment characteristics. Finally, we constructed a 6-gene biological prognostic model that can be used to predict survival in patients with renal cancer, and we further validated the predictive performance of the model based on imaging omics. It is worth mentioning that the structural patterns and functional sites of 6 model gene transcription proteins were also mined. Overall, we explored for the first time the profound role of B cells in kidney cancer and developed a bio-predictive model based on B cell-related genes, providing scientific guidance for personalized treatment of kidney cancer patients.