Immunity, Inflammation and Disease最新文献

{"title":"Impact of COVID-19 on Respiratory Virus Infections in Children, Japan, 2018–2023","authors":"Emi Takashita,&nbsp;Kohei Shimizu,&nbsp;Chiharu Kawakami,&nbsp;Tomoko Momoki,&nbsp;Miwako Saikusa,&nbsp;Hiroki Ozawa,&nbsp;Makoto Kumazaki,&nbsp;Shuzo Usuku,&nbsp;Nobuko Tanaka,&nbsp;Ryuichi Senda,&nbsp;Ichiro Okubo,&nbsp;Seiichiro Fujisaki,&nbsp;Shiho Nagata,&nbsp;Hiroko Morita,&nbsp;Hideka Miura,&nbsp;Kayo Watanabe,&nbsp;Mina Nakauchi,&nbsp;Yoko Matsuzaki,&nbsp;Shinji Watanabe,&nbsp;Hideki Hasegawa,&nbsp;Yoshihiro Kawaoka","doi":"10.1002/iid3.70176","DOIUrl":"https://doi.org/10.1002/iid3.70176","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>COVID-19, caused by SARS-CoV-2, was first documented in Japan in January 2020. We previously reported an increased risk of rhinovirus infections among children during the early phase of the COVID-19 pandemic. Here, we assessed the impact of COVID-19 on respiratory virus infections after SARS-CoV-2 spread nationwide.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed clinical specimens from 4012 patients with respiratory infections in Yokohama, Japan from January 2018 to April 2023.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 15 representative respiratory viruses we detected (influenza virus, rhinovirus, coxsackievirus, echovirus, enterovirus, human coronavirus 229E, HKU1, NL63, and OC43, human metapneumovirus, human parainfluenza virus, human parechovirus, RSV, human adenovirus, human bocavirus, human parvovirus B19, herpes simplex virus type 1, and varicella-zoster virus), influenza was most affected by the COVID-19 pandemic, with no influenza viruses detected for nearly 3 years.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The decrease in influenza infections following the emergence of SARS-CoV-2 may have contributed to the previously reported increase in rhinovirus infections. The rhinovirus outbreak, rather than SARS-CoV-2, may have contributed to the decrease in enveloped virus infections (RSV, parainfluenza viruses, metapneumovirus, and coronavirus 229E, HKU1, NL63, and OC43), possibly due to negative virus-virus interactions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70176","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595672","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":"Case Report: PFAPA (Periodic Fever, Aphthous Stomatitis, Pharyngitis, and Cervical Adenitis) Syndrome With a Novel TNFAIP3 Mutation","authors":"Jiewen Deng,&nbsp;Hui Guo,&nbsp;Ruina Kong,&nbsp;Jie Gao","doi":"10.1002/iid3.70178","DOIUrl":"https://doi.org/10.1002/iid3.70178","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis (PFAPA) syndrome has been considered as a childhood syndrome. Its etiopathogeny is unknown however, currently considered as auto-immune inflammatory disease. Recently, a few cases of adult-onset of PFAPA syndrome have been reported. However, there is no report about the adult-onset of PFAPA case with a novel <i>TNFAIP3</i> Mutation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective and Method</h3>\u0000 \u0000 <p>Followed by detailed clinical inquiry, related laboratory tests, genetic sequencing and treatment, we reported a case with the adult-onset of PFAPA syndrome with a novel TNFAIP3 mutation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We have found a novel mutation in the gene <i>TNFAIP3</i> in an adult patient with periodic fever, aphthous stomatitis, pharyngitis, and adenitis—the PFAPA syndrome, under the environmental factor-COVID-19 vaccination.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This case demonstrated adult-onset of PFAPA symptoms, including periodic fever of unknown origin, which can occur in adult patients with the familial hereditary <i>TNFAIP3</i> mutation and environmental factors. And the therapeutic measures provide some reference and practical significance for the treatment of PFAPA syndrome.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70178","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595674","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 Role of miR-144 in Inflammatory Diseases: A Review","authors":"Shukun Hong,&nbsp;Hongye Wang,&nbsp;Lujun Qiao","doi":"10.1002/iid3.70172","DOIUrl":"https://doi.org/10.1002/iid3.70172","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Inflammation, often caused by various stimuli, is a common response to tissue homeostasis disruptions and is considered a key driver of many pathological conditions. MicroRNA-144 (miR-144) has emerged as a critical regulator in inflammatory diseases, with its dysregulation implicated in various pathological conditions. Understanding its role and mechanisms is essential for developing therapeutic strategies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This article aimed to evaluate the role of miR-144 in inflammatory diseases through a literature review.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Electronic databases including PubMed, Web of Science, Springer Link, China Knowledge Resource Integrated Database, and Wanfang Data were searched for relevant literature. The following keywords were used and combined differently according to the rules of the databases: “miR-144,” “inflammation,” “inflammatory,” and “immune response.” Studies investigating miR-144 in the context of inflammation were included. Data were extracted to assess miR-144's expression patterns and its association with disease severity and outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>miR-144 was found to be differentially expressed in a range of inflammatory diseases, including sepsis, infectious diseases, respiratory diseases, cardiovascular diseases, digestive diseases, neuropsychiatric diseases, arthritis, and pregnancy complications. The expression patterns varied depending on the disease, with both upregulation and downregulation observed. miR-144 was implicated in the modulation of inflammatory responses through direct and indirect targeting of key proteins and pathways. The review also highlighted the potential of miR-144 as a diagnostic and prognostic biomarker.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>miR-144 plays a significant role in the pathogenesis of inflammatory diseases and holds promise as a biomarker. Its expression patterns and regulatory mechanisms offer insights into disease processes and may guide future therapeutic strategies. However, further clinical studies are needed to validate miR-144's utility as a biomarker and to explore its therapeutic potential in a clinical setting.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70172","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595075","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 Exosomes Derived From Bone Marrow Mesenchymal Stem Cells Alleviate Inflammatory Injury in Heart Failure Disease by Enhancing the Expression of KLF4","authors":"Yutong Han,&nbsp;Yang Bi,&nbsp;Donghai Zhang,&nbsp;Yubao Liu","doi":"10.1002/iid3.70161","DOIUrl":"https://doi.org/10.1002/iid3.70161","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The aim of this study is to investigate the impact and mechanism of action of exosomes derived from bone marrow mesenchymal stem cells (BMSCs) in the treatment of heart failure (HF).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The analysis of gene sequencing data set was employed to identify potential therapeutic target proteins for HF. Subsequently, H9C2 cells and Sprague-Dawley (SD) rats were utilized as experimental models to simulate doxorubicin hydrochloride (Doxorubicin, Dox)-induced myocardial injury. This approach was employed to investigate the expression changes of inflammatory factors, including TNF-α, IL-6, IL-1β, sST2, and Gal-3, as well as the alterations in their expression following exosome treatment. Meanwhile, the mechanism of exosomes in relieving HF and inhibiting inflammation were investigated using constructed KLF 4 knockout cell lines and SD rats.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>BMSC-derived exosomes were capable of enhancing the expression level of KLF4 in cardiomyocytes, decreasing the expression levels of myocardial damage markers BNP and hs-TnI, as well as inflammatory factors TNF-α, IL-6, IL-1β, sST2, and Gal-3, thereby alleviating HF injury. In vitro and in vivo experiments have shown that exosomal treatment decreases the expression of BNP and hs-TnI, which are indicators of myocardial injury, along with the release of inflammatory cytokines in cardiomyocytes. Concurrently, the expression of KLF4 was downregulated, leading to a significant reduction in this physiological modulation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>BMSC-derived exosomes exhibit superior therapeutic potential for HF by enhancing the expression of KLF4 and mitigating inflammation in myocardial tissue.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70161","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554323","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":"Aurantio-Obtusin Suppresses Airway Inflammation and Serum ICAM-1 Expression in Guinea Pig Allergic Asthma Model","authors":"Mavis Sersah Nyarko,&nbsp;Cynthia Amaning Danquah,&nbsp;Aaron Opoku Antwi,&nbsp;Benjamin Obukowho Emikpe,&nbsp;Newman Osafo","doi":"10.1002/iid3.70160","DOIUrl":"https://doi.org/10.1002/iid3.70160","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Aurantio-obtusin is a trihydroxyanthraquinone found in the seeds of <i>Cassia tora</i> and <i>Cassia obtusifolia</i>. Its neuroprotective, anti-inflammatory, anti-allergic, and antioxidant potential has been documented in multiple studies. While previous reports mention its potential as an antiasthma agent, its effects on allergen-induced airway inflammation have not been explored.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>Our study reports on the mechanisms by which aurantio-obtusin exerts its effects on underlying inflammation in experimentally-induced allergic asthma. The effect of aurantio-obtusin pretreatment on molecular and histological changes in guinea pig lungs when challenged with aerosolized ovalbumin was assessed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our results showed that aurantio-obtusin significantly reduced ovalbumin (OVA)-induced increase in serum OVA-specific immunoglobulin E (OVA-sIgE) and intercellular adhesion molecule (ICAM)-1. Aurantio-obtusin further suppressed inflammatory cytokine expression (IL-8, TNF-α, IL-6 and thymic stromal lymphopoietin) as well as malondialdehyde, a product of oxidative stress in bronchial lavage. The histopathological assessment showed a reduced transit of inflammatory cells and reduced deposition of collagen in the lungs of aurantio-obtusin-treated guinea pigs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Overall, the data suggests that aurantio-obtusin mitigated ovalbumin-induced airway inflammation by impeding the production of OVAsIgE and suppressing levels of key pro-inflammatory cytokines. Our findings suggest that aurantio-obtusin has potential benefits in the management of allergic airway inflammation in type 2 asthma.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143513604","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":"MiR-146a Reduces Inflammation in Experimental Pancreatitis via the TRAF6–NF-κB Signaling Pathway in Mice","authors":"Xiaoyu Yang,&nbsp;Yuping Ren,&nbsp;Xueyang Li,&nbsp;Liang Xia,&nbsp;Jianhua Wan","doi":"10.1002/iid3.70163","DOIUrl":"https://doi.org/10.1002/iid3.70163","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The initial inflammatory response plays a pivotal role in the development of acute pancreatitis. MiR-146a is believed to play a key role in negatively regulating inflammation and potentially contributes to anti-inflammatory activity in acute pancreatitis, though its mechanism remains largely unexplored.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This study aimed to explore the effects of miR-146a on AP in mice and clarify its regulatory mechanisms in pancreatic inflammation and damage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Adult male BALB/C mice were used. Adeno-associated virus (AAV) vectors were used to modulate miR-146a expression in mice via tail vein injection. AP was induced by intraperitoneal injection of caerulein, caerulein + LPS, or <span>l</span>-arginine. Histological analysis, immunohistochemistry staining, immunofluorescence staining, measurements of amylase and lipase activities, and qRT-PCR were performed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Overexpression of miR-146a reduced pancreatic damage and inflammation in caerulein-induced AP. It decreased serum amylase and lipase levels, mitigated pathological features such as interstitial edema and inflammatory cell infiltration in the pancreas and lung, and reduced neutrophil infiltration and proinflammatory cytokine expression. MiR-146a attenuated the activation of the NF-κB signaling pathway by inhibiting the degradation of IκBα and the expression of phosphorylated-p65 and reducing the nuclear translocation of NF-κB p65. Similar protective effects of miR-146a were observed in AP models induced by <span>l</span>-arginine and caerulein combined with LPS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>MiR-146a alleviates acute pancreatitis in mice by targeting TRAF6 and suppressing the activation of the NF-κB signaling pathway. These findings suggest that miR-146a could be a potential therapeutic target for AP.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70163","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143513605","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":"Natural Resistance to HIV Infection: Role of Immune Activation","authors":"María M. Naranjo-Covo,&nbsp;Daniel S. Rincón-Tabares,&nbsp;Lizdany Flórez-Álvarez,&nbsp;Juan C. Hernandez,&nbsp;Wildeman Zapata-Builes","doi":"10.1002/iid3.70138","DOIUrl":"https://doi.org/10.1002/iid3.70138","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Introduction&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Although repeated exposure to HIV-1 can result in infection, some individuals remain seronegative without clinical or serologic evidence of infection; these individuals are known as HIV-1-exposed seronegative individuals. This population has been extensively studied to understand the mechanisms associated with natural resistance to HIV infection. Two main hypotheses have been proposed to explain this resistance: some researchers associated resistance with a low activation phenotype characterized by a decrease in the activation and proliferation of immune system cells linked with infection control and decreased production of cytokines and pro-inflammatory molecules, whereas others suggest that resistance is related to immune system activation and the expression of high levels of chemokines, pro-inflammatory cytokines and antiviral molecules.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Aims&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Our study aims to review and analyze the most relevant evidence supporting the role of the activation level of the immune system during natural resistance to HIV-1 infection.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A search was conducted via the PubMed, SciELO and ScienceDirect databases. The literature search was performed in a nonsystematic manner. Articles published in the last five decades addressing immune activation mechanisms in natural resistance to HIV were reviewed.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A low-activation phenotype, characterized by a high frequency of Treg cells; reduced expression of CD25, CD38, and HLA-DR; and lower production of pro-inflammatory cytokines in peripheral and mucosal tissues, plays a key role in reducing the number of activated cells susceptible to infection, but it minimizes chronic inflammation, facilitating viral entry and spread. In contrast, the activation phenotype is associated with high expression of markers such as CD25, CD38, and HLA-DR, along with elevated high levels of interferon-stimulated genes and pro-inflammatory cytokines. This profile could promote infection control while increasing the number of virus-susceptible cells.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The complexity of the immune response during HIV exposure, reflected in the conflicting evidence concerning whether low or high immune activation offers protection against infection, suggests that there may be multiple pathways to HIV-1 resistance, influenced by factors such as the type of","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70138","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489906","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":"Fluvastatin Promotes Treg Cell Production in Allogeneic Immune Reaction and Suppresses Inflammatory Response","authors":"Xianxian Chen,&nbsp;Dong Huang,&nbsp;Li Zhao,&nbsp;Donghai Tang,&nbsp;Yu Tian,&nbsp;Chunxiao Ren,&nbsp;Fen Yan,&nbsp;Kailin Xu,&nbsp;Kai Zhao","doi":"10.1002/iid3.70165","DOIUrl":"https://doi.org/10.1002/iid3.70165","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Statins, a class of HMG-CoA reductase inhibitors, exhibit prophylactic benefits against immune rejection induced by allogeneic hematopoietic stem cell transplantation (allo-HSCT). Despite the protective function is confirmed, the precise mechanism to induce immune tolerance of statin in the initial stages of transplantation remains incompletely understood. Given that Treg cells play a critical role in preventing graft versus host response and Foxp3 as a transcription factor of Treg can be induced by statins, we hypothesize that the immunosuppressive effects of statins are partially mediated through regulation of Treg cells expansion.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>T cells were stimulated in vitro under anti-CD3/anti-CD28/IL-2/TGF-β condition or allo-reactive system with or without the addition of statins. The induction of Tregs were detected using flow cytometry. Allo-HSCT models were established by transferring donor cells alone or combined with recipient treated by fluvastatin. The proportions of Treg and phenotypes of effector T cells were identified. Cytokine secretion and antigen-presenting cell (APC) function were tested in irradiated mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Statins induced higher Treg production in classical and allogeneic cell co-culture conditions in vitro. In the early stage of models treated with fluvastatin only in donors or combined treatment of donors and recipients, a similar phenomenon was observed with elevated levels of Foxp3⁺ Treg along with increased expression of CCR7, CD62L, and S1P1 on allo-reactive T cells. Fluvastatin treatment suppressed the secretion of pro-inflammatory cytokines IFN-γ and TNF-α by CD4⁺ and CD8⁺ T cells in irradiated mice. Furthermore, fluvastatin also contributed to restraining the numbers and activation of APCs, including dentritic cells (DCs) and macrophages in vitro and in vivo.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our finding demonstrated that statin exposure modulates immune responses during the initial phase of allo-HSCT by promoting Treg expansion and suppressing inflammatory reactions, which supply a promising strategy for aGVHD prevention.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70165","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489846","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":"Changes of Peripheral T Cells in Systemic Lupus Erythematosus Patients","authors":"Juanfeng Lao,&nbsp;Rongjun Huang,&nbsp;Rongcai Wu,&nbsp;Yulin Yuan","doi":"10.1002/iid3.70156","DOIUrl":"https://doi.org/10.1002/iid3.70156","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Efficient indicators for evaluating the imbalance of lymphocyte function were crucial to clinical therapy in systemic lupus erythematosus (SLE) patients. This study aimed to find biomarkers to assess lymphocyte-mediated immune response in SLE patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 81 SLE patients (non-active: <i>n</i> = 35, active: <i>n</i> = 46) and 70 healthy donors were recruited in the study. Peripheral blood was obtained, and flow cytometry was used to detect circulating lymphocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Data showed that the counts of CD3⁺T, CD4⁺T, CD8⁺ T, and NK cells were decreased in active SLE patients compared with non-active SLE patients and healthy donors. The counts of peripheral T cells were increased in responders but decreased in non-responders among active patients. In addition, an increase in B cell counts was found in active SLE patients compared with those in the other two groups. Active SLE patients showed higher percentages of memory T cells but lower naive T cells than those in non-active SLE patients and healthy controls. Activation molecules (CD38 and HLA-DR) and inhibitory molecule PD-1 expressions on T cells were significantly higher but percentages of CD28⁺CD8⁺T cells were lower in active SLE patients compared with those in the other two groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study indicated that monitoring the alterations of circulating lymphocyte counts and surface molecules may be helpful to assess disease activity of SLE patients, even discriminate active and non-active patients, which was beneficial to choose the best treatment option in clinical therapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143455940","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":"Identification of Natural Killer Cell-Associated Clusters in Skin Melanoma and the Impact on Prognosis and Drug Sensitivity","authors":"Jun Zhou,&nbsp;Renhui Cai,&nbsp;Danqun Zhang,&nbsp;Caifeng Chen","doi":"10.1002/iid3.70143","DOIUrl":"https://doi.org/10.1002/iid3.70143","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Skin melanoma exhibits significant heterogeneity in clinical outcomes and treatment responses among patients. This study aimed to investigate natural killer (NK) cell clusters in skin melanoma, their impact on patient prognosis, and their value as biomarkers for tailoring treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used data from TCGA, GSE19234, GSE65904, GSE244982, and GSE78220. A gene classifier was developed to identify two distinct clusters of melanoma patients. Survival analysis, NK cell infiltration levels, and responses to immune and targeted therapies were evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Unsupervised clustering revealed two distinct melanoma patient clusters with significant differences in NK cell activity and clinical outcomes. Cluster 1 showed higher NK cell infiltration, better overall survival (OS) (<i>p</i> &lt; 0.0001), and greater activity in NK-cell-related pathways. In contrast, Cluster 2, characterized by lower NK cell activity and higher exhaustion markers, had poorer OS. Drug sensitivity analysis indicated that Cluster 1 was more responsive to most melanoma treatments, whereas Cluster 2 had higher sensitivity to trametinib (<i>p</i> &lt; 0.001). The developed gene classifier had an AUC of 0.913 and effectively differentiated between clusters. Additionally, Cluster 1 showed better responses to immunotherapy with a higher rate of complete and partial responses (<i>p</i> &lt; 0.001). These findings were validated in external databases.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study identifies two distinct NK-cell-related clusters in melanoma with differential prognoses and treatment responses. These findings underscore the importance of integrating NK-cell-related profiles into personalized treatment strategies, offering a pathway to optimize therapeutic outcomes based on specific immune profiles.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 2","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70143","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143423633","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}