Objectives To explore the relationship between the levels of new inflammatory markers (MLR, PLR, NLR, SII and SIRI) and the disease activity in patients with antineutrophil cytoplasmic antibody-associated vasculitis. Patients and methods In this study, 974 patients with AAV were included. On the basis of the Birmingham vasculitis activity score (BVAS), the patients were divided into high-disease-activity (BVAS ≥ 12) and low-disease-activity (BVAS < 12) groups. The new inflammatory markers in the two groups were compared. Multivariate linear regression analysis was performed to assess the influencing factors of disease activity in patients with AAV. Results The levels of MLR, NLR, PLR, SII, and SIRI in the high-disease-activity group significantly increased (P < 0.05) compared with those in the low-disease-activity group, and some indictors (SII and SIRI) recovered after AAV disease-inducing remission. Furthermore, the MLR, NLR, SII, SIRI, and BVAS of the patients with AAV with renal involvement significantly increased (P < 0.05). Spearman correlation analysis showed that these new inflammation markers were positively correlated with BVAS and traditional inflammatory markers, such as C-reactive protein and erythrocyte sedimentation rate (all P < 0.001). Multivariate linear regression analysis revealed that MLR, NLR and SIRI were independent risk factors for high disease activity (P < 0.05). Conclusion These nonspecific inflammatory indicators, derived from routine blood tests, may serve as potential supportive markers for assessing disease activity in patients with AAV.

Tumor cells possess nucleic-acid sensing systems that detect aberrant DNA and RNA arising from genomic and transcriptomic dysregulation. Cytosolic DNA and RNA sensors, together with endosomal nucleic acid sensors, can induce type I interferons, inflammatory chemokines, antigen presentation programs, and immune cell recruitment. Yet many tumors remain immunologically silent despite harboring potentially immunostimulatory nucleic acids, indicating that malignant cells can restrain these pathways at multiple levels. Nucleic acid clearance, selective RNA editing and remodeling, extracellular second messenger degradation, and epigenetic silencing can suppress these responses. These regulatory layers may favor immune-poor tumor states and limit responsiveness to immune checkpoint blockade. Therapeutic reactivation must be spatially and temporally controlled, because persistent signaling can undergo maladaptive rewiring. We review these molecular brakes, therapeutic strategies to restore innate sensing, and a proposed biomarker framework integrating sensor competence, suppressor activity, and functional immune output. We distinguish the effects arising within tumor cells from those mediated by sensing mechanisms in neighboring host cells and discuss cellular and spatial context, signaling dynamics, and safety. The proposed framework for matching treatments to patients remains investigational and requires prospective clinical validation.