Immunity, Inflammation and Disease最新文献

{"title":"APOBEC3C-Mediated NF-κB Activation Promotes Malignant Progression of Gliomas","authors":"Chao Zhang,&nbsp;Tao Yang,&nbsp;Yuhang Tang,&nbsp;Dong Yu,&nbsp;Shiqiang Hou,&nbsp;Ning Lin,&nbsp;Qun Li","doi":"10.1002/iid3.70224","DOIUrl":"https://doi.org/10.1002/iid3.70224","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To analyze the clinicopathological features, immunological characteristics, and prognostic value of APOBEC3C in gliomas, and to verify the specific mechanism by which it mediates the malignant progression of gliomas.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>mRNA-seq data from 693 glioma patients in the CGGA database and 697 glioma patients in the TCGA were analyzed, respectively. In addition, single-cell sequencing data were obtained from the CGGA database. Bioinformatics methods were applied to reveal the possible mechanisms of APOBEC3C-mediated malignant progression of gliomas. Moreover, western blot, transwell, and cell-scratch assays were used to explore the potential mechanisms of APOBEC3C-mediated glioma invasion and migration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>APOBEC3C was enriched in malignant glioma subtypes and was a potential biomarker for mesenchymal subtypes in glioma patients. It was closely associated with glioma inflammation and immunity. Additionally, APOBEC3C is a potential independent prognostic factor for glioma, and inhibition of APOBEC3C expression can suppress the EMT process in glioma cells through the NF-κB signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>APOBEC3C is a potential biomarker for glioma patients. It is closely related to the clinicopathology of glioma and may be a potential immunotherapy target for glioma patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144687961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Importance of Pan-Immune-Inflammation Value Score in Locally Advanced Rectal Cancer","authors":"Mahmut Uçar,&nbsp;Mukaddes Yılmaz,&nbsp;Eda Erdiş,&nbsp;Birsen Yücel","doi":"10.1002/iid3.70227","DOIUrl":"https://doi.org/10.1002/iid3.70227","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>In this study, we aimed to observe the prognostic significance of the pan-immune-inflammation value (PIV) score calculated at the time of diagnosis in patients with locally advanced rectal cancer, as well as its effect on treatment response, survival, and prognosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Material and Method</h3>\u0000 \u0000 <p>This retrospective, single-center observational study was designed to analyze patients with nonmetastatic (stages II–III) rectal cancer who received neoadjuvant treatment, categorized into two groups: PIV-L (<i>n</i> = 67, 50%) and PIV-H (<i>n</i> = 67, 50%). The median PIV score was used for cutoff determination. Survival analysis was applied. Univariate and multivariate Cox regression analyses were used to determine prognostic factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Preoperative clinical lymph node status (<i>p</i> = 0.011), liver metastasis (<i>p</i> = 0.028), carcinoembryonic antigen (CEA; <i>p</i> = 0.013), and cancer antigen 19.9 (CA19.9; <i>p</i> = 0.040) levels; pathological complete response (<i>p</i> = 0.035); tumor regression score (<i>p</i> = 0.030); postoperative lymph node status (<i>p</i> = 0.019); tumor deposits (<i>p</i> = 0.035); and budding (<i>p</i> = 0.043) were statistically different between the groups. The 5- and 10-year overall survival (OS) rates were 77% versus 69% and 62% versus 38% in the PIV-L and PIV-H groups, respectively (<i>p</i> = 0.032). While the PIV score was prognostic for OS in univariate analysis (HR: 1.85, 95% CI: 1.04–3.31, <i>p</i> = 0.035), a result of insignificance was obtained in multivariate analysis (HR: 1.76, 95% CI: 0.98–3.01 <i>p</i> = 0.056). The 5- and 10-year disease-free survival (DFS) rates were 67% versus 54% and 56% versus 39% in the PIV-L and PIV-H groups, respectively, with the PIV-H group showing a statistically significantly lower rate (<i>p</i> = 0.048). For DFS, the PIV score was found to be a statistically insignificant prognostic factor in univariate analysis (HR: 0.052, 95% CI: 0.99–2.86, <i>p</i> = 0.052) and recognized as an independent prognostic factor in multivariate analysis (HR: 1.87, 95% CI: 1.08–3.26, <i>p</i> = 0.026).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>A higher pretreatment PIV score was associated with poorer clinicopathological features, a worse treatment response, lower survival rates, and a poor prognosis for DFS.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70227","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144688153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanism of NLRP3 Inflammasome in Inflammatory Diseases and Tumors","authors":"Le-Lan Gong,&nbsp;He-Jiang Zhou,&nbsp;Quan-Ming Zhao,&nbsp;Ning Xu,&nbsp;Feng-Chang Huang,&nbsp;Ling-Yan Su,&nbsp;Wen-Liang Li","doi":"10.1002/iid3.70213","DOIUrl":"https://doi.org/10.1002/iid3.70213","url":null,"abstract":"<p>The nucleotide-binding and oligomerization domain-like receptors (NLRs) are pattern recognition receptors. Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), a member of the NLRs family, can form a protein complex with caspase-1, apoptosis-associated speck-like protein and caspase recruitment domain. And its assembly and activation cause inflammatory reaction and are closely related to the effects of antitumor immunity. The activation of NLRP3 inflammasome can induce polarization, hyperactivity or pyroptosis of immune cells, releasing interleukin-1β (IL-1β) and interleukin-18, which leads a cascade immunity or inflammatory responses. As an important component of the innate immune system, the NLRP3 inflammasome plays vital roles inflammatory diseases and tumors. In this review, we attempt to summarize the recent findings about the role of NLRP3 in the pathogenesis of tumors and inflammatory diseases such as diabetes, Alzheimer disease, and atherosclerosis.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70213","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amphiregulin Promotes Proliferation and Migration of the Damaged Endothelial Cells in Kawasaki Disease Cell Models","authors":"Jiawen Xu,&nbsp;Yihua Jin,&nbsp;Min Wang,&nbsp;Yijing Tao,&nbsp;Yujia Wang,&nbsp;Fangqi Gong","doi":"10.1002/iid3.70223","DOIUrl":"https://doi.org/10.1002/iid3.70223","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Amphiregulin (Areg), a member of the epidermal growth factor family, plays a critical role in tissue repair, inflammation, and immunity. Macrophages are an important source of Areg and are also among the key immune cells activated in Kawasaki disease (KD). Despite this, the role of Areg in KD has not been studied. Therefore, this study aims to investigate the expression of Areg in a KD model and to elucidate its effects on injured endothelial cells using a KD cell model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The serum of LCWE-induced KD mouse model was measured by ELISA. RAW264.7 cells were stimulated with LCWE, and the supernatant was collected. Then, MCAECs were treated with LCWE-induced RAW264.7 cells conditioned medium (RAW-CM) to simulate inflammatory damage in KD endothelial cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our study showed that the serum level of Areg increased in LCWE-induced mouse model. In vitro, LCWE increased the expression and secretion of Areg in RAW264.7 macrophages, an effect that was inhibited by ADAM-17 blockade. The conditioned medium (CM) from LCWE-stimulated RAW264.7 cells (RAW-CM) enhanced the proliferative capacity of endothelial cells, an effect that was partially inhibited by Areg antibodies. Recombinant Areg promoted the proliferation and migration of damaged endothelial cells, effects that were dependent on the activation of the AKT and ERK signaling pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study demonstrates that serum Areg level increased in LCWE-induced KD mouse model, and Areg promoted proliferation and migration abilities of injured endothelial cells. Our work suggests that Areg may be one of the reasons for the repair of injured endothelial cells in LCWE model vasculitis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70223","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144624519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory Responses Potentiate GAS M Protein Induced Cardiac Damage in an Experimental Model of Rheumatic Heart Disease","authors":"Rukshan A. M. Rafeek,&nbsp;Simone L. Reynolds,&nbsp;Manisha Pandey,&nbsp;David J. McMillan,&nbsp;Kadaba S. Sriprakash,&nbsp;Michael F. Good,&nbsp;Natkunam Ketheesan","doi":"10.1002/iid3.70221","DOIUrl":"https://doi.org/10.1002/iid3.70221","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Acute rheumatic fever (ARF) and Rheumatic heart disease (RHD) are autoimmune sequalae, that develops in a proportion of individuals exposed to group A streptococcal infection. The autoimmune pathology of ARF/RHD is multifactorial. Both host and pathogen-associated factors including genetic predisposition, inflammatory responses, tissue cross-reactive antibodies and T-cells contribute to disease development and progression. Hitherto, the role of inflammatory responses in ARF/RHD has never been demonstrated in animal models. In this study for the first time, using the Rat Autoimmune valvulitis model of RHD, we demonstrate the requirement for inflammatory responses in promoting cardiac damage in ARF/RHD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>To determine the role of inflammatory responses we used <i>Bordetella pertussis</i> toxin (BPTx) as an adjuvant to enhance the inflammatory responses initiated by GAS M protein.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Lewis rats injected with GAS rM5 emulsified in Complete Freund's Adjuvant (CFA) and co-adjuvant BPTx, had enhanced valvulitis and inflammatory changes as shown by; (a) elevated levels of circulating inflammatory cytokines; (b) functional changes characterized by a prolonged P-R interval in electrocardiography, (c) enhanced cross-reactive antibody production against cardiac and connective tissue proteins; and (d) increased infiltration of IFN-γ+ and IL-17A+ secreting leukocytes into myocardium and valvular tissues.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These studies have established that in addition to exposure to GAS M protein, BPTx accelerate the inflammatory and autoimmune processes leading to cardiac damage. These observations substantiate the hypothesis that, in susceptible individuals robust inflammatory responses facilitate the progression of ARF/RHD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70221","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144598425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leucine-Rich Repeat Containing 15 Promotes the Inflammatory Response in Rheumatoid Arthritis by Regulating NF-κB Pathway","authors":"Miaomiao Xin,&nbsp;Guangtao Xia,&nbsp;Xin Guan,&nbsp;Guangmin Xi,&nbsp;Min Fu","doi":"10.1002/iid3.70220","DOIUrl":"https://doi.org/10.1002/iid3.70220","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>To explore the influence and molecular mechanism of leucine-rich repeat containing 15 (LRRC15) in rheumatoid arthritis (RA) model induced by collagen-induced arthritis (CIA) in rats and interleukin-1 beta (IL-1β) treated fibroblast-like synoviocytes (FLSs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>LRRC15 expression was analyzed using reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blot analysis, and immunohistochemistry. Hematoxylin-eosin (H&amp;E) and safranin-O-green staining were performed to assess the pathological changes in the joint tissues of rats. The messenger ribonucleic acid (mRNA) and protein expression of interferon gamma (IFN-γ), interleukin (IL)-6, IL-1β, and IL-10 was detected by RT-qPCR, enzyme-linked immunosorbent assay (ELISA), and western blot. Cell proliferation and migration was surveyed using cell counting kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU), and Transwell assays. Western blot was applied to detect the protein changes of nuclear factor kappaB (NF-κB) subunit p65, phosphorylated (p)-p65, inhibitor of kappa Bα (IκBα), phosphorylated inhibitor kappa Bα (p-IκBα), and nuclear factor erythroid 2-related factor 2 (Nrf2).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In CIA rats and IL-1β-treated FLSs, LRRC15 expression was upregulated. In vivo, <i>Lrrc15</i> silencing prevented joint damage, inhibited the expression of IFN-γ, IL-6, IL-1β, and p65, and increased the expression of IL-10 and IκBα. In vitro, <i>Lrrc15</i> silencing inhibited the proliferation, migration, and the expression of IFN-γ, IL-6, IL-1β, p-p65, and p-IκBα, and increased the expression of IL-10, IκBα, and Nrf2 in FLSs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p><i>Lrrc15</i> silencing relieved joint damage and inflammatory response in RA, and this may be associated with the inhibition of the NF-κB pathway.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144598759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty Acids and Inflammatory Protein Biomarkers From Coronavirus Disease 2019 Patients","authors":"Niharika Bala,&nbsp;Alaa H. Habib,&nbsp;Marianne Kozuch,&nbsp;Nancy D. Denslow,&nbsp;Neha S. Dhaliwal,&nbsp;Anna H. Owings,&nbsp;Sarah C. Glover,&nbsp;Abdel A. Alli","doi":"10.1002/iid3.70218","DOIUrl":"https://doi.org/10.1002/iid3.70218","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The coronavirus disease 2019 (COVID-19) is a viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and associated with systemic inflammation. Inflammation is an important process that follows infection and facilitates the body's innate immune response and repair of damaged tissue. Polyunsaturated fatty acids play an important role in the inflammatory process. These lipids can target transcription factors to modulate gene expression and protein function.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Here, we performed a fatty acid methyl ester (FAME) analysis and immunoassays to evaluate whether differences in basal levels of different types of biomarkers can be detected in freshly frozen plasma samples from patients with and without COVID-19.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>FAME analysis showed a decrease in arachidic acid and myristic acid, but an increase in caprylic acid, palmitic acid, and eicosenoic acid in the plasma of COVID-19 patients compared to non-COVID-19 patients. Multiple chemokines including IP-10, MCP-1, and MIP-1 beta were increased in the COVID-19 group compared to the non-COVID-19 group. Similarly, cytokines including IL-1 alpha and IL-8, and cell adhesion and inflammatory response markers including ICAM-1 and E-selectin were greater in the plasma of COVID-19 patients compared to non-COVID-19 patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>A baseline signature of specific polyunsaturated fatty acids, cytokines, and chemokines present in the plasma after COVID-19 viral infection may serve as biomarkers that can be useful in various applications including determination of severity of infection, indication of disease prognosis, and consideration for therapeutic options.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70218","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disparities in Seasonal Influenza Vaccination in Europe","authors":"Katinka M. Giezeman-Smits,&nbsp;Bram Palache,&nbsp;Gerrit A. van Essen,&nbsp;Miloš Jeseňák,&nbsp;Enrique Castro-Sánchez,&nbsp;Anna Elisabeth Steinberg,&nbsp;Joris van Vugt","doi":"10.1002/iid3.70186","DOIUrl":"https://doi.org/10.1002/iid3.70186","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Seasonal influenza remains a major public health challenge in Europe, associated with high morbidity, mortality, and socioeconomic burden. Despite the proven efficacy and cost-effectiveness of vaccination, coverage rates vary substantially across European countries and population groups, often falling short of the World Health Organization's target of 75% for older adults.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This narrative review aims to identify and explore disparities in seasonal influenza vaccination coverage across European countries and among different population subgroups. It also seeks to examine the underlying causes of these disparities and propose actionable strategies to improve equity in vaccine uptake.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A literature search was conducted using the PubMed database for English-language articles published within the last 5 years. Keywords included: comorbidity, disparity, Europe, inequality, influenza, knowledge, ethnic disparity, seasonal influenza vaccination, socioeconomic disparity, vaccination coverage, and vaccine hesitancy. Additional references were identified from the retrieved articles.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Widespread disparities in influenza vaccination were observed across various demographic and professional groups. These included disparities by geographic location, ethnicity, socioeconomic status, sex and gender, age, comorbidities, and occupation—particularly among healthcare professionals. Contributing factors included limited knowledge or education, negative attitudes or behaviors toward vaccination, vaccine hesitancy and fatigue, and restricted access to vaccination services. Structural barriers and institutional trust issues also played key roles.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Addressing disparities in influenza vaccination coverage in Europe requires multi-level, stakeholder-specific strategies. These should include education campaigns, improved access through alternative delivery settings (e.g., pharmacies, schools), targeted communication to high-risk and underserved populations, and systemic changes to support healthcare providers. Tackling these issues will help reduce preventable morbidity and mortality, enhance herd immunity, and foster healthier ageing across European populations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 7","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70186","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Circ_0087199 Depletion Attenuates Lipopolysaccharides-Induced Human Periodontal Ligament Cell Injury Through the miR-527/TLR4 Axis","authors":"","doi":"10.1002/iid3.70219","DOIUrl":"https://doi.org/10.1002/iid3.70219","url":null,"abstract":"<p><b>RETRACTION:</b> J. Wang, N. Huo, C. Cai, Y. Zhang and R. Xiao, “Circ_0087199 Depletion Attenuates Lipopolysaccharides-Induced Human Periodontal Ligament Cell Injury Through the miR-527/TLR4 Axis,” <i>Immunity, Inflammation and Disease</i> 12, no. 1 (2024): e1153, https://doi.org/10.1002/iid3.1153.</p><p>The above article, published online on 24 January 2024 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley &amp; Sons Ltd. The retraction has been agreed upon due to the unclear rationale for the study and the inability of readers to reproduce the results based on the information provided in the article. Despite the authors’ claim that the data would be available upon request, they did not respond to our request for the data. The editors consider the results and conclusions unreliable. The authors were informed of the decision to retract but did not respond to requests for comment.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 6","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70219","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144492719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The M2 Macrophages Importance Role in Psoriasis","authors":"Ahmed Hussein Hasan Alshihmani,&nbsp;Mahmoud Mahmoudi,&nbsp;Ramiar Kamal Kheder,&nbsp;Afsane Fadaee,&nbsp;Seyed-Alireza Esmaeili","doi":"10.1002/iid3.70211","DOIUrl":"https://doi.org/10.1002/iid3.70211","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Psoriasis is a chronic autoimmune skin condition that is increasingly prevalent globally, causing significant challenges for affected individuals. The disease is influenced by a combination of genetic factors, environmental triggers, immune system dysfunction, and its systemic nature with comorbidities like cardiovascular diseases and depression. Macrophages, essential immune cells, play a critical role in the pathogenesis of psoriasis, displaying various functions and activation states.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aims to investigate the impact of M2 macrophages on the progression and management of psoriasis, particularly their ability to support tissue healing and reduce inflammation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>M1 macrophages are involved in early inflammation and pro-inflammatory responses when activated by LPS and IFN-γ, while M2 macrophages are activated by IL-4 and IL-13 to promote anti-inflammatory and tissue repair processes. Imbalance in M1 and M2 polarization can worsen autoimmune conditions such as psoriasis, underscoring the need to regulate macrophage phenotypes for effective disease management. Recent research suggests that targeting M2 macrophages could be a promising therapeutic approach for treating psoriasis, especially through advanced biologic treatments such as anti-IL-17 and anti-IL-23 therapies. Enhancing the function of M2 macrophages has been shown to reduce inflammation and improve outcomes in psoriatic conditions, potentially lowering the risk of comorbidities through early intervention and personalized treatment. Biomarkers like CD163(+) M2 macrophages are associated with disease progression, while treatments that enhance M2 macrophage function, such as PSORI-CM02 and Treg-of-B cell therapies, show potential in alleviating psoriasis symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Understanding the crucial role of M2 macrophages in psoriasis could pave the way for innovative treatment approaches that regulate immune responses and enhance patient care. Further exploration of macrophage biology in psoriasis may provide fresh perspectives on personalized therapeutic options for managing psoriasis and other inflammatory skin conditions, ultimately improving patient care and quality of life for individuals with this chronic skin condition.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 6","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70211","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144323550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}