Transplant immunology最新文献

{"title":"Kidney transplantation from a systemic lupus erythematosus donor and 1-year follow-up: A case report","authors":"Dawei Zhou ,&nbsp;Junto Leung ,&nbsp;Yan Xiong ,&nbsp;Shaojun Ye ,&nbsp;Wei Zhou ,&nbsp;Qifa Ye ,&nbsp;Yanfeng Wang","doi":"10.1016/j.trim.2024.102077","DOIUrl":"10.1016/j.trim.2024.102077","url":null,"abstract":"<div><p>Systemic lupus erythematosus (SLE) is usually regarded as a relative contraindication for deceased kidney donation. The pathological variations because of the changes in the immune environment after kidney transplantation (KT) are unclear, and the recovery of renal function is poorly understood. We present a case of KT from a deceased donor with SLE who was followed-up for one year. Although SLE-related hemangioma developed during the perioperative period, it was cured after interventional treatment. A pre-planned biopsy was performed one year after KT, and it was found that most of the pathological changes and immunofluorescent markers of lupus had resolved. Renal function was stable, and urinary protein and occult blood levels reduced one year after KT.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102077"},"PeriodicalIF":1.6,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141477476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of predictive markers of Pneumocystis jirovecii pneumonia in kidney transplant recipients","authors":"Jingrun Zhou ,&nbsp;Huaqin Pan ,&nbsp;Jiarui Zhang ,&nbsp;Linjie Luo ,&nbsp;Yumeng Cao ,&nbsp;Ling Wang ,&nbsp;Zhenshun Cheng ,&nbsp;Guqin Zhang","doi":"10.1016/j.trim.2024.102074","DOIUrl":"10.1016/j.trim.2024.102074","url":null,"abstract":"<div><h3>Background</h3><p>Kidney transplantation has emerged as the most effective treatment for patients with uremia. Advances in immunosuppressant medications have significantly reduced the risk of rejection. However, a notable increase in opportunistic infections, such as <em>Pneumocystis jirovecii</em> pneumonia (PJP), demands special attention in clinical practice. Our study aims to evaluate risk factors and identify predictive markers associated with PJP in kidney transplantation recipients.</p></div><div><h3>Methods</h3><p>We conducted a case-control study (1:2 ratio) involving kidney transplant recipients with and without PJP, matched based on the same surgical date. The study was carried out at Zhongnan Hospital of Wuhan University, China.</p></div><div><h3>Results</h3><p>Ninety-three participants were enrolled at Zhongnan Hospital of Wuhan University, comprising 31 with PJP and 62 without PJP. All patients tested negative for HIV. Our findings indicate that PJP patients exhibited lower levels of serum albumin (<em>P</em> = 0.001), reduced counts of total and CD3⁺ (<em>P</em> &lt; 0.001), CD4⁺ (<em>P</em> = 0.001), and CD8⁺ T lymphocytes (<em>P</em> &lt; 0.001), and a lower rate of prophylactic trimethoprim-sulfamethoxazole (TMP-SMZ) usage compared to non-PJP patients (<em>P</em> = 0.02). Conversely, urea levels in PJP patients were significantly higher than in non-PJP controls (<em>P</em> &lt; 0.001). We developed a model combining CD8⁺ T cell count (&lt; 241.11/μL, <em>P</em> &lt; 0.001) and ALB levels (&lt; 35.2 g/L, <em>P</em> = 0.003), which demonstrated excellent discriminatory power in distinguishing PJP from non-PJP cases, with an area under the curve (AUC) of 0. 920 (95% CI, 0.856–0.989).</p></div><div><h3>Conclusions</h3><p>Our study suggests that a baseline CD8⁺ T cell count (&lt; 241.11/μL) and serum ALB levels (&lt; 35.2 g/L) offer robust predictive value for the occurrence of PJP infections in kidney transplant recipients.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102074"},"PeriodicalIF":1.6,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141470916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CS12192: A novel selective and potent JAK3 inhibitor mitigates acute graft-versus-host disease in bone marrow transplantation","authors":"Shengjian Huang ,&nbsp;Qianjiao Yang ,&nbsp;You Zhou ,&nbsp;Lingjie Li ,&nbsp;Song Shan","doi":"10.1016/j.trim.2024.102075","DOIUrl":"10.1016/j.trim.2024.102075","url":null,"abstract":"<div><h3>Background</h3><p>Despite the significant role of JAK3 in various autoimmune diseases, including graft-versus-host disease (GVHD), there has been a lack of potent and selective JAK3 inhibitors specifically studied for GVHD. In our preclinical investigations, we evaluated a novel JAK3 inhibitor called CS12192, which is already undergoing clinical investigation in autoimmune diseases.</p></div><div><h3>Methods</h3><p>We evaluated the efficacy of CS12192 in GVHD through mixed lymphocyte reaction (MLR) in both mouse and human cells, as well as allogeneic bone marrow transplantation (BMT) in a murine model.</p></div><div><h3>Results</h3><p>CS12192, starting at a concentration of 0.5 μM, dose-dependently reduced the intracellular positivity for cytokines TNF-α and IFN-γ in CD4+ T cells (<em>p</em> &lt; 0.05 to <em>p</em> &lt; 0.0001) and CD8+ T cells (<em>p</em> &lt; 0.01 to <em>p</em> &lt; 0.0001) during mouse allogeneic MLR assays. This effect was observed for both single and double positivity of the cytokines. Moreover, In MLR assays with three different human donors, CS12192 also demonstrated a dose-dependent reduction in the proportion of IFN-γ positive CD4+ T cells (<em>p</em> &lt; 0.0001) and CD8+ T cells (<em>p</em> &lt; 0.01 to <em>p</em> &lt; 0.0001). Additionally, it suppressed T cell proliferation in the mouse MLR (<em>p</em> &lt; 0.05 to <em>p</em> &lt; 0.0001), but this effect was observed in only one human donor (<em>p</em> &lt; 0.001 to <em>p</em> &lt; 0.0001). Furthermore, the administration of CS12192 at 40 and 80 mg/kg BID significantly improved the survival rate in the BMT model, resulting in cumulative 62-day survival rates of 88.89% (<em>p</em> &lt; 0.01) and 100% (<em>p</em> &lt; 0.001), respectively, compared with prednisolone (<em>p</em> &lt; 0.05).</p></div><div><h3>Conclusions</h3><p>CS12192 is a novel, potent and selective JAK3 inhibitor demonstrating great potential to mitigate acute GVHD.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102075"},"PeriodicalIF":1.6,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141470917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lung transplantation: Current insights and outcomes","authors":"Claudio Napoli ,&nbsp;Giuditta Benincasa ,&nbsp;Alfonso Fiorelli ,&nbsp;Maria Grazia Strozziero ,&nbsp;Dario Costa ,&nbsp;Ferdinando Russo ,&nbsp;Vincenzo Grimaldi ,&nbsp;Konrad Hoetzenecker","doi":"10.1016/j.trim.2024.102073","DOIUrl":"10.1016/j.trim.2024.102073","url":null,"abstract":"<div><p>Until now, the ability to predict or retard immune-mediated rejection events after lung transplantation is still limited due to the lack of specific biomarkers. The pressing need remains to early diagnose or predict the onset of chronic lung allograft dysfunction (CLAD) and its differential phenotypes that is the leading cause of death. Omics technologies (mainly genomics, epigenomics, and transcriptomics) combined with advanced bioinformatic platforms are clarifying the key immune-related molecular routes that trigger early and late events of lung allograft rejection supporting the biomarker discovery. The most promising biomarkers came from genomics. Both unregistered and NIH-registered clinical trials demonstrated that the increased percentage of donor-derived cell-free DNA in both plasma and bronchoalveolar lavage fluid showed a good diagnostic performance for clinically silent acute rejection events and CLAD differential phenotypes. A further success arose from transcriptomics that led to development of Molecular Microscope® Diagnostic System (MMDx) to interpret the relationship between molecular signatures of lung biopsies and rejection events. Other immune-related biomarkers of rejection events may be exosomes, telomer length, DNA methylation, and histone-mediated neutrophil extracellular traps (NETs) but none of them entered in registered clinical trials. Here, we discuss novel and existing technologies for revealing new immune-mediated mechanisms underlying acute and chronic rejection events, with a particular focus on emerging biomarkers for improving precision medicine of lung transplantation field.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102073"},"PeriodicalIF":1.6,"publicationDate":"2024-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141421090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Model for end-stage liver disease-dependent prognostic capacity of platelet-to-lymphocyte ratio following liver transplantation for hepatocellular carcinoma","authors":"Chiyu He ,&nbsp;Wei Shen ,&nbsp;Zuyuan Lin ,&nbsp;Zhihang Hu ,&nbsp;Huigang Li ,&nbsp;Hao Chen ,&nbsp;Modan Yang ,&nbsp;Xinyu Yang ,&nbsp;Jianyong Zhuo ,&nbsp;Linhui Pan ,&nbsp;Xuyong Wei ,&nbsp;Li Zhuang ,&nbsp;Shusen Zheng ,&nbsp;Di Lu ,&nbsp;Xiao Xu","doi":"10.1016/j.trim.2024.102071","DOIUrl":"10.1016/j.trim.2024.102071","url":null,"abstract":"<div><h3>Background</h3><p>To improve liver organ allocation, the model for end-stage liver disease (MELD) score was adopted in candidates reflecting the severity of liver disease and the physical condition of patients. Inflammatory markers are prognostic factors for various cancers and play prognostic roles in patients after liver transplantation (LT) for hepatocellular carcinoma (HCC). Researchers focused more on pre-LT inflammatory markers, while the role of dynamic change of these inflammatory markers is still unknown. The purpose of this study was to estimate the prognostic value of pre-LT and post-LT inflammatory markers.</p></div><div><h3>Material and methods</h3><p>We collected the pre-LT complete blood count and the post-LT result with highest count of white blood cells within 48 h. Platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio and systemic immune-inflammation index were calculated, and their prognostic roles were analyzed for their MELD scores.</p></div><div><h3>Results</h3><p>This retrospective two-center cohort study enrolled 290 patients after LT for HCC. Multivariate analysis identified pre-LT PLR as independent risk factor for recurrence-free survival (RFS) [HR (95%CI): 1.002 (1.000–1.003), <em>p</em> = 0.023]. A high pre-LT PLR or post-LT PLR were associated with poorer RFS (<em>p</em> &lt; 0.001 and <em>p</em> = 0.004, respectively). Based on the MELD scores, the pre-LT PLR value was able to predict the RFS in high MELD group (p &lt; 0.001) but had no predictive power in low MELD group (<em>p</em> = 0.076). On the contrary, the post-LT PLR value was better to predict the overall RFS value in low MELD group (<em>p</em> = 0.007) but could not predict the overall RFS value in high MELD group (<em>p</em> = 0.136).</p></div><div><h3>Conclusions</h3><p>Both pre-LT PLR and post-LT PLR demonstrated prognostic value in patients following LT for HCC. Monitoring PLR values based on the MELD score can improve the predictive prognosis and more effectively guide the individual decisions for the postoperative intervention.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102071"},"PeriodicalIF":1.5,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141311828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Qi Huang Fang improves intestinal barrier function and intestinal microbes in septic mice through NLRP3 inflammasome-mediated cellular pyroptosis","authors":"Tingting Shu ,&nbsp;Jun Zhang ,&nbsp;Ruiying Hu ,&nbsp;Fang Zhou ,&nbsp;Hanyong Li ,&nbsp;Jing Liu ,&nbsp;Yanbo Fan ,&nbsp;Xucheng Li ,&nbsp;Peiwu Ding","doi":"10.1016/j.trim.2024.102072","DOIUrl":"10.1016/j.trim.2024.102072","url":null,"abstract":"<div><h3>Objective</h3><p>Sepsis has a high incidence, morbidity, and mortality rate and is a great threat to human safety. Gut health plays an important role in sepsis development. Qi Huang Fang (QHF) contains astragalus, rhubarb, zhishi, and atractylodes. It is used to treat syndromes of obstructive qi and deficiency of righteousness. This study aimed to investigate whether QHF improves intestinal barrier function and microorganisms in mice through NLRP3 inflammatory vesicle-mediated cellular focal death.</p></div><div><h3>Methods</h3><p>A mouse model of sepsis was constructed by cecal ligation and puncture (CLP) of specific pathogen-free (SPF)-grade C57BL/6 mice after continuous gavage of low, medium, and high doses of astragalus formula or probiotics for 4 weeks. Twenty-four hours postoperatively, the mechanism of action of QHF in alleviating septic intestinal dysfunction and restoring intestinal microecology, thereby alleviating intestinal injury, was evaluated by pathological observation, immunohistochemistry, western blotting, ELISA, and 16S rDNA high-throughput sequencing.</p></div><div><h3>Results</h3><p>Different doses of QHF and probiotics ameliorated intestinal injury and reduced colonic apoptosis in mice to varying degrees (<em>P</em> &lt; 0.05). Meanwhile, different doses of QHF and probiotics were able to reduce the serum levels of IL-6, IL-1β, and TNF-α (<em>P</em> &lt; 0.05); down-regulate the protein expression of NLRP3, caspase-1, and caspase-11 (<em>P</em> &lt; 0.05); and up-regulate the protein expression of zonula occluden-1 (ZO-1) and occludin (<em>P</em> &lt; 0.05), which improved the intestinal barrier function in mice. In addition, QHF decreased the relative abundance of harmful bacteria (Firmicutes<em>,</em> Muribaculaceae<em>,</em> Campilobacterota<em>, Helicobacter,</em> and <em>Alistipes</em>) and increased the relative abundance of beneficial bacteria (Bacteroidetes and Actinobacteria) (<em>P</em> &lt; 0.05).</p></div><div><h3>Conclusion</h3><p>QHF improves intestinal barrier function and gut microbiology in mice <em>via</em> NLRP3 inflammasome-mediated cellular pyroptosis.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102072"},"PeriodicalIF":1.5,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141301711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapy with regulatory T-cell infusion in autoimmune diseases and organ transplantation: A review of the strengths and limitations","authors":"Mahdieh Naghavi Alhosseini ,&nbsp;Padideh Ebadi ,&nbsp;Mohammad Hossein Karimi ,&nbsp;Graziella Migliorati ,&nbsp;Luigi Cari ,&nbsp;Giuseppe Nocentini ,&nbsp;Mozhdeh Heidari ,&nbsp;Saeede Soleimanian","doi":"10.1016/j.trim.2024.102069","DOIUrl":"10.1016/j.trim.2024.102069","url":null,"abstract":"<div><p>In the last decade, cell therapies have revolutionized the treatment of some diseases, earning the definition of being the “third pillar” of therapeutics. In particular, the infusion of regulatory T cells (Tregs) is explored for the prevention and control of autoimmune reactions and acute/chronic allograft rejection. Such an approach represents a promising new treatment for autoimmune diseases to recover an immunotolerance against autoantigens, and to prevent an immune response to alloantigens. The efficacy of the in vitro expanded polyclonal and antigen-specific Treg infusion in the treatment of a large number of autoimmune diseases has been extensively demonstrated in mouse models. Similarly, experimental work documented the efficacy of Treg infusions to prevent acute and chronic allograft rejections. The Treg therapy has shown encouraging results in the control of type 1 diabetes (T1D) as well as Crohn's disease, systemic lupus erythematosus, autoimmune hepatitis and delaying graft rejection in clinical trials. However, the best method for Treg expansion and the advantages and pitfalls with the different types of Tregs are not fully understood in terms of how these therapeutic treatments can be applied in the clinical setting. This review provides an up-to-date overview of Treg infusion-based treatments in autoimmune diseases and allograft transplantation, the current technical challenges, and the highlights and disadvantages of this therapeutic approaches.”</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102069"},"PeriodicalIF":1.5,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141284862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunosenescence, immunotolerance and rejection: clinical aspects in solid organ transplantation","authors":"","doi":"10.1016/j.trim.2024.102068","DOIUrl":"10.1016/j.trim.2024.102068","url":null,"abstract":"<div><p>As a consequence of increased lifespan and rising number of elderly individuals developing end-stage organ disease, the higher demand for organs along with a growing availability for organs from older donors pose new challenges for transplantation. During aging, dynamic adaptations in the functionality and structure of the biological systems occur. Consistently, immunosenescence (IS) accounts for polydysfunctions within the lymphocyte subsets, and the onset of a basal but persistent systemic inflammation characterized by elevated levels of pro-inflammatory mediators. There is an emerging consensus about a causative link between such hallmarks and increased susceptibility to morbidities and mortality, however the role of IS in solid organ transplantation (SOT) remains loosely addressed. Dissecting the immune-architecture of immunologically-privileged sites may prompt novel insights to extend allograft survival. A deeper comprehension of IS in SOT might unveil key standpoints for the clinical management of transplanted patients.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"86 ","pages":"Article 102068"},"PeriodicalIF":1.6,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0966327424000844/pdfft?md5=d62789ea327de9c7de59d9e7dd16b831&pid=1-s2.0-S0966327424000844-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141284861","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":"Thrombomodulin as a potential diagnostic marker of acute myocardial infarction and correlation with immune infiltration: Comprehensive analysis based on multiple machine learning","authors":"Guoqing Liu ,&nbsp;Lixia Huang ,&nbsp;Xiangwen Lv ,&nbsp;Yuting Guan ,&nbsp;Lang Li","doi":"10.1016/j.trim.2024.102070","DOIUrl":"https://doi.org/10.1016/j.trim.2024.102070","url":null,"abstract":"<div><h3>Background</h3><p>Acute myocardial infarction (AMI) is a global health problem with high mortality. Early diagnosis can prevent the development of AMI and provide valuable information for subsequent treatment. Angiogenesis has been shown to be a critical factor in the development of infarction and targeting this process may be a potential protective strategy for preventing myocardial injury and improving the prognosis of AMI patients. This study aimed to screen and verify diagnostic markers related to angiogenesis in AMI and to investigate the molecular mechanisms of action associated with AMI in terms of immune cell infiltration.</p></div><div><h3>Methods</h3><p>The GSE66360 and the GSE60993 datasets were both downloaded from the GEO database and were used as the training cohort and the external validation cohort, respectively. Angiogenesis-related genes (ARGs) were downloaded from the MSigDB database. The hub ARGs were identified via LASSO, RF, and SVM-RFE algorithms. ROC curves were used to assess the accuracy of the hub ARGs. The potential mechanisms of the hub ARGs were analyzed by GSEA. The ssGSEA algorithm was used to determine differences in immune cell infiltration and immune function. The CIBERSORT algorithm was used for immune cell infiltration analysis. In addition, we constructed a ceRNA network map of differentially expressed ARGs.</p></div><div><h3>Results</h3><p>We identified the thrombomodulin <em>(THBD)</em> gene from ARGs as a potential diagnostic marker for AMI based on the LASSO, SVM-RFE, and RF algorithms. <em>THBD</em> was differentially expressed and had a potential diagnostic value (area under the curve [AUC] = 0.931 and 0.765 in the training and testing datasets, respectively). GSEA showed that the MAPK signaling pathway was more enriched in the high-expression group of <em>THBD</em> (<em>P</em> &lt; 0.05). Immune cell infiltration analysis demonstrated that <em>THBD</em> was mainly positively correlated with monocytes (<em>R</em> = 0.48, <em>P</em> = 0.00055) and neutrophils (<em>R</em> = 0.36, <em>P</em> = 0.013). Finally, in the ceRNA regulatory network, <em>THBD</em> was closely associated with 9 miRNAs and 42 lncRNAs involved in AMI.</p></div><div><h3>Conclusion</h3><p>THBD can be used as a potential diagnostic marker for AMI. This study provides new insights for future AMI diagnosis and molecular mechanism research. Moreover, immune cell infiltration plays an essential role in the occurrence and development of AMI.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102070"},"PeriodicalIF":1.5,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141249897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intraperitoneal injection of mesenchymal stem cells-conditioned media (MSCS-CM) treated monocyte can potentially alleviate motor defects in experimental autoimmune encephalomyelitis female mice; An original experimental study","authors":"Bahman Jalali Kondori ,&nbsp;Amir Abdolmaleki ,&nbsp;Mahdi Raei ,&nbsp;Akbar Ghorbani Alvanegh ,&nbsp;Hadi Esmaeili Gouvarchin Ghaleh","doi":"10.1016/j.trim.2024.102067","DOIUrl":"10.1016/j.trim.2024.102067","url":null,"abstract":"<div><h3>Introduction</h3><p>Multiple sclerosis (MS), as a destructive pathology of myelin in central nervous system (CNS), causes physical and mental complications. Experimental autoimmune encephalomyelitis (EAE) is laboratory model of MS widely used for CNS-associated inflammatory researches. Cell therapy using macrophage M2 (MPM2) is a cell type with anti-inflammatory characteristics for all inflammatory-based neuropathies. This experimental study investigated the probable therapeutic anti-inflammatory effects of intraperitoneal (IP) injection of MPM2 on alleviation of motor defect in EAE-affected animals.</p></div><div><h3>Materials and methods</h3><p>24 C57/BL6 female mice were divided into four groups of EAE, EAE + Dexa, EAE + PBS, and EAE + MP2. EAE was induced through deep cervical injection of spinal homogenate of guinea pigs. MPM2 cells were harvested from bone marrow and injected (10⁶cells/ml) in three days of 10, 13 and 16 post-immunizations (p.i). Clinical score (CS), anti-inflammatory cytokines (IL-4, IL-10), pro-inflammatory gene expression (TNF-α, IL-1β) and histopathological investigations (HE, Nissl and Luxol Fast Blue) were considered. Data were analyzed using SPSS software (v.19) and <em>p</em> &lt; 0.05 was considered significant level.</p></div><div><h3>Results</h3><p>During EAE induction, the mean animal weight was decreased (<em>p</em> &lt; 0.05); besides, following MPM2 injection, the weight gain was applied (<em>p</em> &lt; 0.05) in EAE + MPM2 groups than control. Increased (p &lt; 0.05) levels of CS was found during EAE induction in days 17–28 in EAE animals; besides, CS was decreased (p &lt; 0.05) in EAE + MPM2 group than EAE animals. Also, in days 25–28 of experiment, the CS was decreased (p &lt; 0.05) in EAE + MPM2 than EAE + Dexa. Histopathological assessments revealed low density of cell nuclei in corpus callosum, microscopically. LFB staining also showed considerable decrease in white matter density of corpus callosum in EAE group. Acceleration of white matter density was found in EAE + MPM2 group following cell therapy procedure. Genes expression of TNF-α, IL-1β along with IL-4 and IL-10 were decreased (<em>p</em> &lt; 0.05) in EAE + MPM2 group.</p></div><div><h3>Conclusion</h3><p>IP injection of MPM2 to EAE-affected female mice can potentially reduce the CNS inflammation, neuronal death and myelin destruction. MPM2 cell therapy can improve animal motor defects.</p></div>","PeriodicalId":23304,"journal":{"name":"Transplant immunology","volume":"85 ","pages":"Article 102067"},"PeriodicalIF":1.5,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141262882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}