Expert Review of Clinical Immunology最新文献

Objective: This study evaluated the potential diagnostic utility of pepsin, trypsin, and mucin 5B (MUC5B) in hearing impairment in patients with laryngopharyngeal reflux (LPR)-related chronic secretory OM (CSOM).

Methods: Patients with LPR-related CSOM were enrolled and assigned into the normal hearing (NH), and mild (Mi-HI) and moderate-to-severe hearing impairment (Mo-HI) groups. Pepsin, trypsin, and MUC5B contents were determined by ELISA, with their correlations with Eustachian tube dysfunction questionnaire-7 (ETDQ-7) score and inflammatory factors (interleukin [IL]-2, IL6, IL-8), and diagnostic performance in hearing impairment assessed by Pearson, Spearman, and ROC curves. Factors influencing hearing impairment were identified using logistic regression models.

Results: Pepsin, trypsin, and MUC5B contents were upregulated in patients' middle ear effusion as hearing impairment worsened. The three indicators correlated to EDTQ-7 and inflammatory factors, and exhibited high diagnostic value for hearing impairment in LPR-related CSOM patients. Remarkably, their combination created significantly higher diagnostic value than a single indicator. Abundantly-increased pepsin, trypsin, and MUC5B amplified hearing impairment incidence.

Conclusion: Pepsin, trypsin, and MUC5B are independent risk factors for hearing impairment in LPR-related CSOM patients. Their combination assists hearing impairment diagnosis in patients, providing a tool in clinical practice to stratify patients and offering a theoretical basis for exploring therapeutic targets.

Background: Periostin is a novel biomarker associated with a range of inflammatory conditions, particularly those involving pulmonary inflammation and fibrotic processes. This research aimed to investigate the association between periostin concentrations, severity of COVID-19, and patient mortality.

Research design and methods: Our study comprised 127 participants: 36 healthy controls (Group-1), 37 COVID-19 patients with uncomplicated disease (Group-2), 28 with mild pneumonia (Group-3), and 26 with severe pneumonia (Group-4). Periostin levels in all participants were measured using the ELISA method.

Results: Periostin concentrations were significantly elevated in COVID-19 patients compared to healthy controls (p < 0.001). Periostin concentrations were significantly elevated in patients with severe COVID-19 pneumonia compared to those with mild pneumonia or uncomplicated disease (p < 0.05). According to our study analysis, periostin level independently predicted severe pneumonia in COVID-19 (Odds Ratio: 1.085; 95% CI: 1.035-1.137; p = 0.001). Serum periostin threshold of 67.5 ng/mL predicted severe pneumonia with 69.2% sensitivity and 66.2% specificity. Lastly, every 1 ng/mL increase in periostin was linked to 1.21-fold higher mortality risk in COVID-19 patients with severe pneumonia (Hazard Ratio: 1.216; 95% CI: 1.006-1.471; p = 0.044).

Conclusion: Our findings suggest that periostin level may help assessing disease severity and predicting mortality in COVID-19. Additional studies with expanded patient groups are needed.

Introduction: In patients with cirrhosis and ascites, failure of intestinal barriers and cirrhosis-associated immune dysfunction contribute to the translocation of bacteria and microbial products to the peritoneal cavity, which promotes infection, perpetuates inflammation and accelerates acute-on-chronic liver failure. Resident peritoneal immune cells are repeatedly exposed to bacterial products, and their activation status is linked to complications of spontaneous bacterial peritonitis.

Areas covered: This narrative review summarizes the recent research on human peritoneal immunity in decompensated cirrhosis, focusing on the altered composition and functional states of human peritoneal macrophages, resident and migrating T cells, and neutrophils and their involvement in peritoneal inflammation and infection.

Expert opinion: Peritoneal immune cells in decompensated cirrhosis show compartmentalized chronic activation and dysfunction, contributing to inflammation and infection risk. Given the direct accessibility of these cells, targeting peritoneal macrophage priming and differentiation, innate immune memory, inflammatory mediators and intercellular peritoneal cross-talk offer potential strategies to prevent infections and mitigate inflammation. To fine-tune the delicate balance between hyperinflammation and anergy, further research is necessary to translate immunomodulatory approaches into effective clinical interventions.

Introduction: Alopecia areata (AA) is an autoimmune non-scarring hair loss that involves collapse of hair follicle immune privilege. Genetic susceptibility, environmental stressors, and aberrant interaction between dendritic cells, CD4⁺ and CD8⁺ lymphocytes, drives follicular destruction and disrupts hair cycling. Pro-inflammatory cytokines, including IL-15 and IFNγ, and downstream JAK-STAT pathway activation, are central to disease progression.

Areas covered: Though variably effective, conventional treatments including corticosteroids, contact sensitizers, phototherapy, and systemic immunosuppressants remain standard therapeutic approaches for AA in many clinics. However, insights into Th1, Th2, and Th17 cell activity, along with the cytokine signals involved (IFNγ, IL-15, IL-4/13, IL-17/23), and an emerging understanding of immune checkpoints in AA (PD-1/PD-L1, CD28/CD80/CD86/CTLA4, OX40/OX40L), are shaping the clinical investigation of new AA treatments; particularly JAK inhibitors and biologics targeting specific signaling pathways.

Expert opinion: Heterogeneity in AA clinical presentation, molecular pathogenesis, and variable treatment responses suggests a biomarker-driven patient stratification system is needed to optimize drug selection, reduce trial-and-error therapy, and minimize side-effect risk. In the longer term, approaches that couple rapid immunosuppression with strategies to regenerate follicular immune privilege and tolerize autoreactive memory T cells are likely to shift AA therapeutic approaches away from chronic immune suppression toward true disease-modifying or curative interventions.

Background: This study evaluated clinician adherence to unrestricted antinuclear antibody (ANA) and subserology test requests, comparing rheumatologists and other specialists, and assessed the financial impact of inappropriate orders.

Research design and methods: We analyzed 43,691 patients tested for ANA IIF from January 2022 to June 2024. ENA profile immunoblot requests without appropriate ANA IIF positivity were categorized by specialty.

Results: Rheumatologists ordered 11,581 ANA IIF tests (26.51%), while non-rheumatology physicians ordered 32,110 (73.49%). Of ANA IIF-negative results, 55.82% had ENA immunoblots, with rheumatologists (73.97%) and non-rheumatologists (50.42%) contributing to unnecessary requests. After implementing reflex testing, specialist training, and ELISA, the ENA immunoblot claim rate decreased from 58.44% to 20% within one year, resulting in an annual savings of €121,000.

Conclusions: Reflex testing and laboratory-guided algorithms reduce unnecessary orders, maintain diagnostic accuracy, and achieve significant cost savings through enhanced collaboration between clinicians and laboratories.

Introduction: Langerhans Cell Histiocytosis (LCH) is a rare neoplastic disorder characterized by monoclonal proliferation and tissue infiltration by pathological dendritic cells, often associated with abnormal activation of the MAPK signaling pathway and BRAF V600E mutation. The diagnosis is established through clinical, radiological, and histopathological evaluation. It can manifest in various organs, notably bones, skin, and the hypothalamic-pituitary axis. The assessment of central nervous system (CNS) involvement in LCH includes both parenchymal and non-parenchymal structures, including craniofacial bones, hypothalamic-pituitary axis, and meninges.

Areas covered: We used the PubMed database and reviewed relevant English-language literature published from 1989 to 2024. The sources included original researches, reviews and case reports, excluding editorials and letters to the editor. This review focuses on the existing evidence regarding the imaging, clinical, and pathological aspects of CNS, cranial and spinal bones involvement in LCH and its differential diagnosis.

Expert opinion: Imaging plays an essential role in properly diagnosing, guiding biopsy and monitoring treatment. Computed tomography (CT) is particularly helpful for evaluating bone involvement, while magnetic resonance imaging (MRI) is preferred for assessing parenchymal brain and meningeal lesions. The disease can present in either tumoral or neurodegenerative forms, manifesting with varied symptoms depending on the affected region.

Introduction: The rising global prevalence of eosinophilic esophagitis (EoE) has made it a major topic of interest in both Clinical Immunology and Gastroenterology. Despite advances in understanding its physiopathology, optimal long-term management remains challenging due to disease heterogeneity and variable treatment responses. An integrated, patient-centered approach can be valuable in clinical practice, improving outcomes by tailoring treatment strategies to individual patient needs.

Areas covered: This review explores the current therapeutic options of EoE, including proton pump inhibitors (PPIs), topical corticosteroids, elimination diets, and biologic agents, focusing on treatment efficacy, limitations, and patient-centered factors such as quality of life, treatment adherence, and comorbid atopic conditions. The article also examines recent guidelines and the rationale behind personalized therapy approaches. A comprehensive review of the current literature on personalized therapy for EoE has been conducted, highlighting recent developments in treatment strategies and individualized patient care approaches.

Expert opinion: There is no one-size-fits-all therapeutic strategy for EoE. Given the complexity of patient profiles, including immunologic phenotypes, psychological attitudes, and socioeconomic factors, therapeutic choices must be personalized. Shared decision-making is essential to align treatment plans with patient values and improve both clinical outcomes and long-term adherence.