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Introduction: Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder affecting salivary and lacrimal glands, while endometriosis involves uterine‐like tissue growth outside the uterus, causing pelvic pain and infertility. Investigating their intricate relationship using real‐world data is crucial due to limited research on their connection. Material and Methods: This population‐based cohort study included patients with endometriosis and controls without endometriosis. Propensity score matching was used to balance baseline differences in demographic and clinic characteristics between the two groups. Cox proportional hazards model were used to estimate the effect of endometriosis on the risk of new‐onset pSS over time. A symmetrical cohort study, including patients with pSS and propensity score‐matched controls without pSS, was conducted to investigate the effect of pSS on the risk of endometriosis over time. To elaborate on the mechanisms linking endometriosis and pSS, Ingenuity Pathway Analysis was performed to identify activated pathways in eutopic endometrium from patients with endometriosis and parotid tissues from patients with pSS. Results: A total of 15 947 patients with endometriosis and 15 947 propensity score‐matched controls without endometriosis were included. Patients with endometriosis presented a significantly greater risk of pSS compared to non‐endometriosis controls (adjusted hazard ratio, aHR = 1.57, 95% CI = 1.29–1.91, p < 0.001). In the symmetrical cohort study, which included 4906 pSS patients and 4,906 propensity score‐matched controls without pSS, patients with pSS were found to be at a significantly higher risk of endometriosis compared to non‐pSS controls (aHR = 1.51, 95% CI = 1.12–2.04, p = 0.012). Ingenuity Pathway Analysis showed that the underlying cellular mechanisms involved autoimmune‐related pathways, including activation of dendritic cell maturation, and chronic inflammatory pathways, including the fibrosis signaling pathway. Conclusions: These findings support a bidirectional association between endometriosis and pSS, which may be driven by dendritic cell maturation and fibrosis signaling pathways. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Excess glucose alone depress young mesenchymal stromal/stem cell osteogenesis and mitochondria activity within hours/days via NAD+/ SIRT1 axis" published in the Journal of Biomedical Science. The correction addresses two figures in the original paper that still have revision red lettering on some legends. Additionally, the funding section of the article has been updated to reflect the correct year-based numbering of two grants. The original publication has been corrected. [Extracted from the article]

Objectives: The association of migraine with the risk of certain cancer has been reported. The aim of this pilot study was to examine the associations between migraine and the onset of head and neck cancers (HNC). Materials and Methods: A total of 1755 individuals were identified through a nationwide population‐based cohort registry in Taiwan between 2000 and 2013. The primary end point variable was new‐onset head and neck cancers in patients with migraine versus non‐migraine controls. Cox proportional hazard regression was used to derive the risk of HNC. Subgroup analyses were performed to determine subpopulations at risk of migraine‐associated HNC. Sub‐outcome analyses were carried out to provide the subtypes of migraine‐associated HNC. Propensity score matching was utilized to validate the findings. Results: A total of four patients out of 351 patients with migraine and seven out of 1404 non‐migraine controls developed HNC. The incidence of HNC was higher in patients with migraine than that in non‐migraine controls (108.93 vs. 48.77 per 100,000 person‐years) (adjusted hazard ratio, aHR = 2.908, 95% CI = 0.808–10.469; p = 0.102). The risk of HNC in patients with migraine with aura (aHR = 5.454, 95% CI = 0.948–26.875; p = 0.264) and without aura (aHR = 2.777, 95% CI = 0.755–8.473; p = 0.118) was revealed. The incidence of non‐nasopharyngeal HNC secondary to migraine (112.79 per 100,000 person‐years) was higher than that of nasopharyngeal cancer secondary to migraine (105.33 per 100,000 person‐years). Conclusion: A higher incidence of HNC was observed in a small sample of patients with migraine, especially in those with migraine with aura. Migraine‐associated HNC included non‐nasopharyngeal HNC. Studies with a larger sample are needed to confirm the finding of the high risk of HNC in people with migraine. [ABSTRACT FROM AUTHOR]

Background and objectives Juvenile idiopathic arthritis (JIA), an autoimmune disease, has been proposed to be comorbid with obstructive sleep apnoea (OSA). We aimed at testing the hypothesis that patients with JIA may presented with high risk of OSA in a cohort study. Subjects and methods This is a cohort study including patients with JIA from 1999 to 2013 identified from a longitudinal health registry. A matched non-JIA control group was also included. The primary outcome variable was presence of OSA. A Cox proportional hazard model was developed to estimate the risk of OSA in patients with JIA. A cumulative probability model was adopted to assess the time-dependent effect of JIA on OSA development, implying a causal link of the association. Results A total of 2791 patients with JIA were included, and 11 164 individuals without JIA were selected as matched controls. A total of 95 included subjects had OSA: 31 in the JIA group and 64 in the control group. Patients with JIA were more likely to have OSA compared with controls (adjusted hazard ratio, aHR = 1.922, 95% confidence interval [CI] = 1.244–2.970). The incidence of developing OSA was particularly high among patients with JIA-associated deformity that presented at age 18–30 years (aHR = 1.993, 95% CI = 1.277–3.113) and males (aHR = 1.786, 95% CI = 1.097–2.906). The risk of developing OSA increased over 60 months (aHR = 2.523, 95% CI = 1.322–4.815) of follow-up after the JIA diagnosis. Conclusions Patients with JIA have a significantly increased risk of developing OSA compared with matched individuals without JIA. [ABSTRACT FROM AUTHOR]

The combination of radiotherapy and immunotherapy improves the survival rate of patients with malignancies developed through escape from T-cell-mediated immune surveillance. Immune checkpoint inhibitors, such as anti-programmed cell death protein-ligand 1 (anti-PD-L1) antibody, are used to rescue exhausted T cells. Simultaneously, dendritic cells (DCs) which are antigen-presenting cells that can initiate T-cell activation, are used to induce a tumor-specific immune response. However, the synergistic antitumor efficacy of the aforementioned combinational immunotherapy with intratumoral injection of low-dose DCs has not been reported, and the underlying therapeutic mechanism requires further investigation. Herein, we present the special case of a psoriatic patient with cutaneous squamous cell carcinoma (cSCC) in the right inguinal region, these two diseases characterized by opposing contradiction, further complicating treatments and side-effect management efforts. To treat the intractable SCC without exaggerating psoriasis, we developed the triple-regimen therapy (TRT) with the intratumoral injection of low-dose autologous DCs and anti-PD-L1 combined with radiotherapy. The injected DCs were obtained simply through leukapheresis without prior G-CSF administration for mobilization nor tumor-antigen loading for expansion. The patient received three radiation doses (24, 18, and 18 Gy) combined with three intratumoral injections of anti-PD-L1 antibody (40, 60, and 120 mg) plus autologous DCs (80% of the DC subpopulation being CD16+ myeloid DC with approximate amounts of 7.3 × 104, 2.5 × 106, and 1.7 × 107) within 10 weeks. The efficacy of the TRT was encouraging in shrinking tumor mass with remarkable SUVmax reduction (approximately 42%) on FDG PET-Scan despite relatively low-dose DCs were available. The low-dose intratumoral immunotherapy induced mild cutaneous side effects as expected. The transcriptomes were compared between pre-TRT and post-TRT biopsies to analyze underlying mechanical pathways of the TRT protocol. Over 10 highly significantly enriched T-cell-related pathways (P < 0.0001) were identified in post-TRT biopsies. In addition, the activation of both innate and adaptive immunity was significantly enriched in post-TRT peripheral blood samples. We develop the easily accessible TRT which produces both local anti-tumor T-cell responses and systemic antitumor immunity for treating cSCC patients, especially for those with autoimmune disease. [ABSTRACT FROM AUTHOR]

Abstract: Mesenchymal stem cells (MSCs) are multi-potent with numerous mesenchymal-lineage differentiation potential and immunomodulatory capabilities. However, the immunoregulatory properties of MSCs are not clearly defined. The objective of the present study was to elucidate the role(s) of MSCs in IL-17 production and the subsequent effect(s) on neutrophil activation. We have demonstrated that human bone marrow-derived MSCs (BM-MSCs) instruct anti-CD3/anti-CD28 antibody-activated CD4+ CD45RO+ memory T cells, but not other CD4+ subsets or CD8+ T cells, to produce IL-17 after cell–cell contact. After the addition of IL-17, neutrophil phagocytic activity was increased. This is the first report on the ability of BM-MSCs to induce IL-17 production in memory CD4+ T cells that, in turn, promotes enhanced phagocytic activity of neutrophils. These results suggest that MSCs regulate the functional activation of neutrophils via their role in modulating IL-17 from CD4+ CD45RO+ memory T cells. [Copyright &y& Elsevier]

Purpose: The innate immune response, particularly the reaction of polymorphonuclear neutrophils (PMNs), is crucial in shaping the outcomes of chronic inflammation, fibrosis, or osseointegration following biomaterial implantation. Peri-implantitis or peri-mucositis, inflammatory conditions linked to dental implants, pose a significant threat to implant success. We developed a single-cell analysis approach using a murine model to assess the immune response to implant materials, offering a practical screening tool for potential dental implants., Methods: We performed bioinformatics analysis and established a peri-implant inflammation model by inserting two titanium implants into the maxillary region, to examine the immune response., Results: Bioinformatics analysis revealed that titanium implants triggered a host immune response, primarily mediated by PMNs. In the in vivo experiments, we observed a rapid PMN-mediated response, with increased infiltration around the implants and on the implant surface by day 3. Remarkably, PMN attachment to the implants persisted for 7 days, resembling the immune profiles seen in human implant-mediated inflammation., Conclusions: Our findings indicate that persistent attachment of the short-living PMNs to titanium implants can serve as an indicator or traits of peri-implant inflammation. Therefore, analyzing gingival tissue at the single-cell level could be a useful tool for evaluating the biocompatibility of candidate dental implants.