Osteoarthritis (OA) is a chronic, degenerative joint disease presenting a significant global health threat. While current therapeutic approaches primarily target symptom relief, their efficacy in repairing joint damage remains limited. Recent research has highlighted mesenchymal stem cells (MSCs) as potential contributors to cartilage repair, anti-inflammatory modulation, and immune regulation in OA patients. Notably, MSCs from different sources and their derivatives exhibit variations in their effectiveness in treating OA. Moreover, pretreatment and gene editing techniques of MSCs can enhance their therapeutic outcomes in OA. Additionally, the combination of novel biomaterials with MSCs has shown promise in facilitating the repair of damaged cartilage. This review summarizes recent studies on the role of MSCs in the treatment of OA, delving into their advantages and exploring potential directions for development, with the aim of providing fresh insights for future research in this critical field.

Summary: Neutrophils are important in the context of innate immunity and actively contribute to the progression of diverse autoimmune disorders. Distinct death mechanisms of neutrophils may exhibit specific and pivotal roles in autoimmune diseases and disease pathogenesis through the orchestration of immune homeostasis, the facilitation of autoantibody production, the induction of tissue and organ damage, and the incitement of pathological alterations. In recent years, more studies have provided in‐depth examination of various neutrophil death modes, revealing nuances that challenge conventional understanding and underscoring their potential clinical utility in diagnosis and treatment. This review explores the multifaceted processes and characteristics of neutrophil death, with a focus on tailored investigations within various autoimmune diseases. It also highlights the potential interplay between neutrophil death and the landscape of autoimmune disorders. The review encapsulates the pertinent pathways implicated in various neutrophil death mechanisms across diverse autoimmune diseases while also charts possible avenues for future research.

In this study, the available data from published randomized, controlled trials (RCTs) of the use of intestinal microecological regulators as adjuvant therapies to relieve the disease activity of rheumatoid arthritis (RA) are systematically compared. An English literature search was performed using PubMed, Embase, Scopus, Web of Science and the Cochrane Central Registry of Controlled Trials and supplemented by hand searching reference lists. Three independent reviewers screened and assessed the quality of the studies. Among the 2355 citations identified, 12 RCTs were included. All data were pooled using a mean difference (MD) with a 95% CI. The disease activity score (DAS) showed a significant improvement following microecological regulators treatment (MD (95% CI) of −1.01 (−1.81, −0.2)). A borderline significant reduction in the health assessment questionnaire (HAQ) scores was observed (MD (95% CI) of −0.11 (−0.21, −0.02)). We also confirmed the known effects of probiotics on inflammatory parameters such as the C-reactive protein (CRP) (MD −1.78 (95% CI −2.90, −0.66)) and L-1β (MD −7.26 (95% CI −13.03, −1.50)). No significant impact on visual analogue scale (VAS) of pain and erythrocyte sedimentation rate (ESR) reduction was observed. Intestinal microecological regulators supplementation could decrease RA activity with a significant effect on DAS28, HAQ and inflammatory cytokines. Nevertheless, these findings need further confirmation in large clinical studies with greater consideration of the confounding variables of age, disease duration, and individual medication regimens.

MDA5+ dermatomyositis (MDA5+DM) frequently complicates interstitial lung disease (ILD), especially rapidly progressive ILD (RP-ILD), which worsens prognosi