Objective: Chronic stress affects the immune system via the hypothalamic–pituitary–adrenal (HPA) axis and autonomic system. Chronic inflammation is a risk factor for cardiovascular diseases, cancer onset and progression, susceptibility to infection, and cognitive impairment. Mind–body interventions (MBIs) could affect the immune and neuroendocrine systems, and we aimed to assess the correlations among these systems through a meta-analysis. Methods: RCTs were identified by searching three databases: PubMed, Embase, and Scopus. Of the 1697 studies identified, 89 were included in this study. Risk of bias was examined using the Cochrane risk-of-bias assessment tool. Data were pooled using a random-effects model, and SMDs were calculated. I² statistics and Egger’s test were used to assess the significance of the asymmetry. Influence diagnostics were used to assess whether pooled effects were disproportionately dependent on any single study. The trim-and-fill method was applied to all identified asymmetric instances. Meta-regression was used to examine the moderating effect of MBI efficacy on biomarkers. Results: MBIs generally decreased the levels of inflammatory factors, such as the CRP, IL-6, TNF-α, IL-1, IL-8, IL-17, ESR, and cortisol, and increased IL-10, IFN-γ, IL-1ra, BDNF, and secretory IgA. In a subgroup analysis of the CNS and cancer, qigong and yoga showed increased BDNF and IL-6, respectively. Notably, IL-10 was increased in inflammatory diseases, and IFN-γ was increased in viral infections. Conclusions: This study revealed MBIs decrease inflammatory cytokine and increase anti-inflammatory, antiviral, and immune-activating factors. These results suggest the MBIs including gentle physical exercise may be beneficial for neuropsychiatric disorders or tumors. Prospero registration number: CRD42024507646.

Background: The body maintains homeostasis by inflammation, and arthritis is related to autoimmunity or inflammation. Angiogenesis contributes to synovitis through angiogenic factors and proteolytic enzymes, while different inflammatory arthritis conditions, such as osteoarthritis and rheumatoid arthritis, share similar cytokine networks and immune cell populations. Notably, progressive joint damage can occur despite effective systemic immunosuppression, suggesting that local stromal–immune interactions within the joint microenvironment may sustain inflammation and tissue destruction. Methods: We conducted an exploratory single-cell RNA-sequencing analysis using publicly available datasets from the NCBI GEO database, including synovial tissue and synovial fluid samples. Cell–cell communication and transcriptional regulatory networks were inferred using CellChat and SCENIC. Results: Computational analyses suggested that, in RA, macrophage-associated signaling shifts from TNF-related pathways toward SPP1-associated patterns, coinciding with transcriptional features of MMP3⁺ fibroblast-like synoviocytes (FLS). FLS–FLS interactions were associated with FGF-related signaling across disease contexts. ANGPTL-related signaling patterns differed among arthritis subtypes, with ANGPTL4 more prominent in OA and PsA and ANGPTL2 more frequently in RA-related transcriptional programs. Conclusions: These findings provide an exploratory framework for stromal–immune interactions and ANGPTL-associated signaling across inflammatory arthritis. The therapies for PsA may focus on systemic immune modulation and preservation of joint structural integrity. For OA and RA, the highlight may target ANGPTL4 and ANGPTL2 in the early and late stages of disease progression. Given the reliance on computational inference, the results warrant further experimental validation.