The nasal mucosa functions as a highly specialized barrier that integrates epithelial, stromal, neuronal, and immune signals to maintain homeostasis and mount rapid responses to environmental challenges. Among its resident immune populations, innate lymphoid cells—particularly type 2 ILCs (ILC2s)—play a pivotal role in orchestrating type 2 inflammation driven by epithelial-derived alarmins such as IL-25, IL-33, and TSLP. Upon activation, ILC2s release IL-5 and IL-13, promoting eosinophilic inflammation, goblet cell hyperplasia, mucus hypersecretion, and tissue remodeling, all central features of chronic rhinosinusitis with nasal polyps (CRSwNP) and severe allergic rhinitis. Recent advances have revealed substantial ILC plasticity, the presence of nasal-resident ILC progenitors, and the influence of metabolic and neuroimmune cues in shaping ILC activation and persistence. Dupilumab, a monoclonal antibody targeting IL-4Rα, has emerged as a highly effective therapy, providing unique mechanistic insight into the epithelial–ILC axis. By blocking IL-4/IL-13 signaling, dupilumab dampens ILC2 effector functions, reduces IL-5/IL-13 output, restores epithelial barrier integrity, interrupts alarmin-driven amplification loops, and rebalances innate and adaptive immune networks. Clinical and translational studies indicate that baseline ILC2 phenotypes—particularly inflammatory ILC2 subsets—may predict treatment responsiveness, positioning ILC profiling as a promising biomarker strategy. This review synthesizes current knowledge of ILC classification, plasticity, progenitor biology, and epithelial–ILC communication in the nasal mucosa, while integrating emerging evidence on dupilumab-mediated immunomodulation. Collectively, these insights highlight ILCs as central drivers of type 2 inflammation and key targets for precision immunomodulation, offering a framework for personalized treatment approaches in CRSwNP and allergic rhinitis.

In recent years, the development of new immunotherapy strategies has been a significant breakthrough in cancer treatment. Among these, engineered T cell therapy with chimeric antigen receptors (CAR-T) has produced notable clinical results, especially in hematological malignancies. This success has sparked growing interest in extending the application of CAR-Ts to solid tumors, including gliomas. Gliomas—in particular, glioblastoma multiforme (GBM)—are among the most aggressive primary brain tumors, associated with a poor prognosis and a median survival of approximately one year after diagnosis. However, the translation of CAR-T therapy to gliomas presents significant challenges, related to factors such as tumor heterogeneity, presence of the blood–brain barrier (BBB), and a strongly immunosuppressive tumor environment. Despite this, in recent years, there has been an intensification of research efforts aimed at the identification of new antigenic targets and the development of preclinical models—both in vitro and in vivo—to evaluate the efficacy and safety of CAR-Ts in the treatment of gliomas. Despite promising results, currently available models still have essential limitations in faithfully reproducing the complexity of human gliomas. This review aims to offer an exhaustive overview of the most recent preclinical studies on CAR-T therapy in gliomas, with a focus on the identification of molecular targets, experimental strategies aimed at overcoming immunological barriers, and translational challenges that need to be addressed for future successful clinical implementation.

Periodontitis (PD) and atrial fibrillation (AF) are two prevalent chronic conditions with substantial public health burdens worldwide. While traditionally studied separately, increasing evidence reveals a complex interplay between PD and AF, mediated primarily by shared inflammatory and immune mechanisms. Chronic periodontal inflammation can trigger systemic immune activation, leading to atrial structural remodeling, fibrosis, and electrical disturbances that predispose individuals to AF. Observational and longitudinal studies consistently demonstrate a higher incidence and recurrence of AF in patients with moderate to severe PD, independent of established cardiovascular risk factors. Key periodontal pathogens, especially Porphyromonas gingivalis, and altered immune cell profiles are implicated in this association, further supported by genetic analyses revealing common molecular pathways. Mechanistic insights from experimental models highlight the role of inflammation-related atrial fibrosis and immune dysregulation as critical drivers linking oral disease to arrhythmogenesis. Additionally, better oral hygiene practices and periodontal treatment have been associated with a reduced risk of AF, suggesting modifiable intervention potential. This review synthesizes current clinical, epidemiological, molecular, and experimental evidence to elucidate the PD–AF relationship, emphasizing periodontal health as a promising target in cardiovascular disease prevention strategies.

Cellular senescence represents a critical biological paradox in oncology. Although it evolved as a safety mechanism to halt tumorigenesis through stable cell cycle arrest, its persistence in tissues can alter the microenvironment, promoting tumor recurrence. In the context of glioblastoma (GBM), this phenomenon is critically important, as current standard therapies, such as radiotherapy and chemotherapy, inadvertently induce a state of senescence known as “therapy-induced senescence” (TIS). Senescent cells remain metabolically active and acquire a unique Senescence-Associated Secretory Phenotype (SASP), characterized by the release of pro-inflammatory cytokines, proteases, and growth factors. SASP reshapes the tumor microenvironment (TME) through paracrine signals, promoting immunosuppression, invasiveness, drug resistance and tumor recurrence. Different glial populations, including astrocytes, microglia, and oligodendrocyte precursor cells (OPCs), respond differently to senescence, specifically contributing to the creation of a permissive niche for tumor recurrence. To contrast the effects of this phenomenon, a promising therapeutic strategy has emerged, the “one-two punch,” which induces initial DNA damage followed by selective elimination of senescent cells with senolytic drugs. In this review, we analyze in detail the efficacy of targeted synthetic agents, such as the Bcl-2 family inhibitor Navitoclax, and natural bioactive compounds such as Quercetin and Fisetin. The analysis focuses on the molecular mechanisms through which these agents disrupt anti-apoptotic pathways (SCAPs) and inhibit the PI3K/AKT/mTOR axis, restoring sensitivity to apoptosis. We propose that the integration of senolytic adjuvants into standard clinical protocols may represent a crucial frontier for eliminating residual disease reservoirs and we also suggest the possibility of combining them with molecules with neuroprotective action to significantly improve the prognosis in GBM.

Background/Objectives: Acute myeloid leukemia (AML) comprises a heterogeneous group of diseases, with some subtypes displaying promyelocytic features and altered differentiation programs. Aberrant cytokine receptor signaling has been implicated in leukemogenesis, and IL-5Rα has recently emerged as a potential marker in selected AML subsets, including promyelocytic variants. Benralizumab is a monoclonal antibody directed against the alpha chain of the interleukin-5 receptor (CD125), which blocks IL-5Rα–mediated signaling. This proof-of-concept study aimed to explore the effects of the anti-IL-5Rα monoclonal antibody Benralizumab in an in vitro AML cell model with promyelocytic characteristics. Methods: Public transcriptomic datasets were analyzed to evaluate IL-5Rα expression in AML subtypes. HL-60 cells, an AML cell line expressing IL-5Rα, were treated with Benralizumab and analyzed for cell cycle distribution and modulation of key signaling and apoptotic pathways by flow cytometry and Western blotting. Results: IL-5Rα was highly expressed in AML, particularly in M2 and M3 subtypes. Benralizumab treatment reduced STAT3 expression, activated ERK and NF-κB signaling, induced p21 and p27 expression, altered cell cycle distribution, and induced caspase-8 cleavage, suggesting activation of extrinsic apoptotic signaling. Conclusions: These findings provide preliminary proof-of-concept evidence that IL-5Rα targeting by Benralizumab may directly affect cell survival and cell cycle regulation in AML cells with promyelocytic characteristics. When interpreted together with the in silico analyses performed on AML patient datasets, these results support the rationale for future validation in APL-oriented models carrying the PML::RARα fusion, the disease-defining oncogenic driver generated by the t(15;17) translocation that blocks myeloid differentiation. However, the in silico and in vitro datasets were not formally integrated at the patient level, and these functional results should be considered exploratory.