Immunology最新文献

{"title":"A Review on Biosensors for Quantification of MCP-1 as a Potential Biomarker in Diseases.","authors":"Zahra Jamalizadeh Bahaabadi, Mohammad Javad Javid-Naderi, Prashant Kesharwani, Sercan Karav, Amirhossein Sahebkar","doi":"10.1111/imm.13944","DOIUrl":"https://doi.org/10.1111/imm.13944","url":null,"abstract":"<p><p>Monocyte chemoattractant protein-1 (MCP-1) as a chemokine is essential for inflammation-related processes. It regulates immunological responses and cell migration, which contribute to inflammation. Many disorders are exacerbated by this chemokine, which attracts or grows other inflammatory cells, including monocytes/macrophages, at the site of infection or tissue injury. The elevated concentrations of MCP-1 are associated with the pathogenesis of many diseases, such as cancer, cardiovascular disease, kidney disease, and neuroinflammatory disease. Therefore, monitoring this inflammatory biomarker in the body has been recommended and strongly advised to make an accurate diagnosis and prognosis. Although MCP-1 is of great importance in disease processes, few biosensing approaches are specifically designed to detect this molecule. These are often electrochemical and optical techniques. Rapid and accurate diagnosis of inflammatory diseases by identifying biomarkers has had a great effect on the advancement of biosensors. Improved biosensor technology expansion prevents excessive prices and low sensitivity, enabling quick and correct diagnosis and tracking of disease processes. This review will concentrate on the biological functions of MCP-1, its significance in different disorders, and the features and applications of biosensors designed for MCP-1 detection and quantification.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Depressive Disorder Affects TME and Hormonal Changes Promoting Tumour Deterioration Development.","authors":"Jingjing Dong, Juan Du, Ruyun Liu, Xinghua Gao, Yixiao Wang, Lin Ma, Yong Yang, Jing Wu, Jianqiang Yu, Ning Liu","doi":"10.1111/imm.13933","DOIUrl":"https://doi.org/10.1111/imm.13933","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Cancer patients often suffer from depression, the presence of which promotes the deterioration of the cancer patient's condition and thus affects the patient's survival. However, the exact mechanisms underlying the relationship between depression and tumour progression remain unclear, and this complexity involves multi-system and multi-level interactions, with several key challenges remaining in current research. First, the extreme complexity of biological systems. Depression and tumors involve multiple pathways such as neuroendocrine, immune system, and metabolism, respectively, and there are nonlinear interactions between these pathways (e.g., HPA axis activation affects both immunosuppression and tumor angiogenesis), so it is difficult to isolate the predominant role of a single mechanism, and there are feedback loops (e.g., inflammatory factors (e.g., IL-6) can both induce depressive symptoms and promote tumor growth) form a \"feedback loop between depression and tumors\" that makes it difficult to determine the direction of causality. Second, the potential blind spot of mechanism research. There is insufficient direct evidence for the brain-tumor axis, and it is known that the vagus nerve or sympathetic nerves can directly modulate the tumor microenvironment (TME) (e.g., via β-adrenergic receptors), but there is a lack of technical support for in vivo imaging on how the CNS remotely affects tumors through the neural circuits; whereas depression-associated disturbances of the intestinal flora or in certain stages of tumor development (e.g., metastatic) or specific microenvironments (e.g., areas of hyper-infiltrating T-cells) may have long-term effects on the tumors, but such changes are difficult to capture in short-term experiments and cannot be precisely temporally resolved by existing technologies. However, there are limitations in current research methods. Existing studies have relied on mouse models of chronic stress (e.g., chronic unpredictable stress), but the \"depression-like behaviour\" of mice is fundamentally different from the clinical manifestations of depression in humans, and the TME (e.g., immune composition) is different from that of humans. Finally, for patients with cancer-associated depression, clinical treatment is usually a two-pronged strategy, but the combination of anticancer and antidepressant drugs has limitations, such as drug-drug interactions, safety issues, and the challenge of individualised treatment in clinical practice. Therefore, by elucidating the relationship between depression and tumour bidirectional effects, this review relatively clarifies how depression affects TME to promote tumour progression by influencing changes in immunosuppression, hormonal changes, glutamate/glutamate receptors, and intestinal flora. Further, some potential therapeutic strategies are proposed for the clinical treatment of this group of patients through the above pathological mechanism; at the same time, it was found that a","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of Regulatory T Cells After Virus Infection and Vaccination.","authors":"MansourehKarimi Kakh, Mehrnoosh Doroudchi, AtefeGhamar Talepoor","doi":"10.1111/imm.13927","DOIUrl":"https://doi.org/10.1111/imm.13927","url":null,"abstract":"<p><p>Vaccines have been proven to be one of the safest and most effective ways to prevent and combat diseases. However, the main focus has been on the evaluation of the potency of effector mechanisms and the lack of adverse effects of vaccine candidates. Recently, the importance of induced regulatory mechanisms of the immune system after vaccination has come to light. With the increase in our knowledge about these regulatory mechanisms including the regulatory T cells (Tregs), we have come to understand the significance of this arm of the immune system in controlling immunopathology and/or diminishing the effectiveness of vaccines, especially viral vaccines. Tregs play a dual role during infectious diseases by limiting immune-mediated pathology and also contributing to chronic pathogen persistence by decreasing effector immunity and clearance of infection. Tregs may also affect immune responses after vaccination primarily by inhibiting antigen presenting cell function such as cytokine secretion and co-stimulatory molecule expression as well as effector T (Teff) and B cell function. In this article, we review the current knowledge on the induction of Tregs after several life-threatening virus infections and their available vaccines to bring them to the spotlight and emphasise that studying viral-induced antigen-specific Tregs will help us improve the effectiveness and decrease the immunopathology or side effects of viral vaccines. Trial Registration: ClinicalTrials.gov identifier: NCT04357444.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased CD8^dim and Decreased CD8^bright T Cells as Immunological Signature for Multibacilary Leprosy Patients.","authors":"Yuri Scheidegger de Castro, Letícia Silva Nascimento, Juliana Azevedo da Silva, Rebeka da Conceição Souza, Gabriel Nogueira Araújo, Sandra Chalhub de Oliveira, Edilbert Pellegrini Nahn Junior, Alba Lucínia Peixoto-Rangel","doi":"10.1111/imm.13937","DOIUrl":"https://doi.org/10.1111/imm.13937","url":null,"abstract":"<p><p>Leprosy, a chronic infectious disease caused by Mycobacterium leprae, manifests in a spectrum of clinical forms and severity. This study investigated the percentage of CD8⁺ T cells and their subpopulations (CD8^bright and CD8^dim T cells) in leprosy patients stratified by clinical forms, bacterial load, and age. No significant differences were observed in the overall percentage of CD8⁺ T cells among healthy controls and leprosy patients. However, an increased percentage of CD8^dim T cells and a decreased percentage of CD8^bright T cells were associated with severe multibacillary and lepromatous forms of leprosy, independent of bacillary load. Further, these cellular profiles correlated more strongly with disease severity than with age, in spite of elderly multibacillary patients exhibiting significant reductions in CD8^bright T cells and increases in CD8^dim T cells compared to young or middle-aged paucibacillary patients, but not compared to young and middle-aged multibacillary patients. These findings suggest that CD8^bright and CD8^dim T cell profiles are critical indicators of disease progression and severity in leprosy, highlighting their potential as biomarkers for clinical evaluation.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Alveolar Macrophages Detect SARS-CoV-2 Envelope Protein Through TLR2 and TLR4 and Secrete Cytokines in Response.","authors":"Conor Grant, Emily Duffin, Finbarr O'Connell, Parthiban Nadarajan, Colm Bergin, Joseph Keane, Mary P O'Sullivan","doi":"10.1111/imm.13922","DOIUrl":"https://doi.org/10.1111/imm.13922","url":null,"abstract":"<p><p>Alveolar macrophages (AMs) are the most numerous immune cells of the lung and are the resident, sentinel lung immunocytes that summon trafficking immune cells to the compartment. Immune profiling of AMs from COVID-19 patients implicates AMs in the immune circuits that drive pulmonary inflammation in severe COVID-19 infection. However, little is known about human AM responses to SARS-CoV-2 proteins, such as the spike protein and envelope protein. We aimed to understand if human AMs recognize SARS-CoV-2 proteins and how they respond. We found that human AMs do not sense SARS-CoV-2 spike protein but do sense envelope protein via the pattern recognition receptors TLR2 and TLR4, secreting IL-1β, IFNγ, IL-12p70, IL-6, and TNFα in response. AMs from donors over the age of 70 years produced significantly more cytokines than those from younger patients following stimulation with SARS-CoV-2 envelope protein. AMs from current smokers had lower cytokine secretion. This is the first report of human AMs producing cytokines in response to SARS-CoV-2 proteins and the first to correlate those responses with clinical risk factors. These results may partly explain why older adults are at such high risk of severe lung inflammation in COVID-19.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-Antigen-Specific B Cells Induced Regulatory CD4⁺ T Cells Through Decreasing T Cell Activation.","authors":"Chien-Hui Chien, Tsai-Ying Yeh, Bor-Luen Chiang","doi":"10.1111/imm.13940","DOIUrl":"https://doi.org/10.1111/imm.13940","url":null,"abstract":"<p><p>Our previous findings demonstrated that naïve B cells elicit suppressive CD4⁺ regulatory T (Treg) cells, named as Treg-of-B cells. However, the capability of antigen-specific B cells in that process remains unclear. Using ovalbumin (OVA) as a model antigen, the present study showed that B cells from OVA-immunised mice decreased that ability. Instead, OVA-activated OVA-specific (OB1) B cells induced effector-like T-of-OB1 cells without regulatory function. Phenotypically, Treg-of-B cells reduced the production of interferon (IFN)-γ, interleukin (IL)-17 and IL-2 and expressed CD62L, PD1 and endothelial cell adhesion molecule 1 (PECAM1). Functionally, adoptive transfer of Treg-of-B cells significantly attenuated Th1 cell-mediated delayed-type hypersensitivity (DTH) responses and inhibited IFN-γ-producing Th1 cells, while T-of-OB1 cells did not. Mechanistically, activated antigen-specific B cells increased the expression of costimulatory molecules and promoted higher T cell activation, contributing to effector T cell phenotype. Conversely, Treg-of-B cells exhibited lower T cell activation, possibly mediated through the expression of PECAM1, Dusp2, Dusp5, Ptpn7, Ptpn22 and Ms4a4b. These findings suggest that non-antigen-specific B cells elicit CD4⁺ Treg cells, potentially via attenuating T cell activation, whereas that capacity is absent in antigen-specific B cells. This distinction underscores the critical role of B cell antigen specificity in immune regulation and inflammation.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory Mechanisms of ILC2 in Lung Development: Emerging Insights Into Bronchopulmonary Dysplasia Pathogenesis.","authors":"Jie Zhu, Jia Tang, Mi Yan, Qinyi Yu, Guangli Ren, Zhangxue Hu","doi":"10.1111/imm.13942","DOIUrl":"https://doi.org/10.1111/imm.13942","url":null,"abstract":"<p><p>Bronchopulmonary dysplasia (BPD) is a severe lung disease affecting preterm infants. The incidence rate in preterm infants aged < 25 weeks is > 70% and it causes irreversible lung damage. BPD is a high-risk factor for respiratory system infections in adults and allergic diseases, such as asthma, which cause a heavy burden on society and families. Pathological features of BPD include pulmonary inflammation and disorders of alveolar and vascular development, which lead to insufficient ventilation. The group 2 innate lymphoid cells (ILC2) are recruited to the lungs during the critical window period of lung development and regulate lung development partly by secreting interleukin (IL)-5 and IL-13; however, the specific mechanism remains unclear. In this review, we summarise the stage of lung development, pathophysiological characteristics of BPD, the role of ILC2 in lung development, and its specific mechanism to provide evidence supporting ILC2 as a key immune cell in lung development, and has potential in BPD therapy.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intestinal Butyrate Ameliorates Rheumatoid Arthritis Through Promoting the Expression of Cortistatin in Ileum via HDAC3-Vitamin D Receptor Pathway.","authors":"Minghui Liao, Yanrong Zhu, Qi Cui, Mengfan Yue, Jialin Li, Lei Gao, Yue He, Yilei Guo, Wenjie Zhang, Zhifeng Wei, Yufeng Xia, Yue Dai","doi":"10.1111/imm.13939","DOIUrl":"https://doi.org/10.1111/imm.13939","url":null,"abstract":"<p><p>Butyrate, administered orally or via drinking water, can effectively ameliorate experimental rheumatoid arthritis (RA) in mice despite its limited bioavailability. The discrepancy urges us to explore the involvement and role of intestinal anti-RA factors in the action of butyrate. In this study, we found that substituting drinking water with butyrate (75 mM) could promote the expression of cortistatin (CST) in the ileal epithelium of mice with collagen-induced arthritis (CIA), but butyrate did not alter the expression of other anti-RA neuropeptides in the intestine and the expression of CST in the spleen and brain. The anti-RA efficacy of butyrate was remarkably reduced following adeno-associated virus (AAV)-mediated knockdown of CST. Transcription factor screening revealed that butyrate upregulated CST expression via the vitamin D receptor (VDR). Notably, butyrate-induced VDR and CST expression in intestinal epithelial cells was diminished by α-cyano-4-hydroxycinnamic acid (CHC) rather than siRNA targeting G protein-coupled receptors (GPCRs), suggesting that butyrate functions through an intracellular pathway. Furthermore, butyrate significantly reduced HDAC activity in intestinal epithelial cells and HDAC3 plasmid transfection attenuated the upregulation of butyrate against VDR and CST expression. Chromatin immunoprecipitation assay showed that butyrate selectively enhanced histone acetylation in the P3 and P4 regions of the VDR promoter. In summary, intestinal butyrate exerts an anti-RA effect through selectively promoting the expression of CST in ileal epithelial cells via the HDAC3-VDR pathway.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unravelling the Impact of Outer Membrane Protein, OmpA, From S. Typhimurium on Aberrant AID Expression and IgM to IgA Class Switching in Human B-Cells.","authors":"Rahul Chaudhari, Mallar Dasgupta, Prashant Kodgire","doi":"10.1111/imm.13938","DOIUrl":"https://doi.org/10.1111/imm.13938","url":null,"abstract":"<p><p>Salmonella enterica serovar Typhimurium is a Gram-negative bacterium that causes gastrointestinal infection and poses significant public health risks worldwide. This study aims to explore how S. Typhimurium manipulates B-cell function through outer membrane protein A (OmpA). We investigate the effect of OmpA on Raji human B-cells, leading to the induction of activation-induced cytidine deaminase (AID) protein, which plays an important role in generating antibody diversity in B-cells, via initiating the process of somatic hypermutation (SHM) and class switch recombination (CSR). Our key findings demonstrate that OmpA is crucial for inducing aberrant AID expression in B-cells, leading to increased CSR. Interestingly, the increased AID expression was likely due to overexpression of cMYC, an activator for AID expression. Not only was the expression of cMYC elevated, but its occupancy on the aicda locus was raised. Furthermore, increased AID expression induced CSR events, specifically switching to IgA. In summary, our study suggests that OmpA plays a potential role in modulating B-cell regulation and controlling the adaptive immune system. These functional attributes of OmpA implicate its potential as a therapeutic target for combating S. Typhimurium pathogenesis.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a Novel Multi-Epitope Vaccine Against Streptococcus anginosus Infection via Reverse Vaccinology Approach.","authors":"Linglan Xu, Nan Xie, Yiqing Liu, Hongmei Tang, Tian Li, Jiaofeng Peng, Ranhui Li","doi":"10.1111/imm.13936","DOIUrl":"https://doi.org/10.1111/imm.13936","url":null,"abstract":"<p><p>Streptococcus anginosus is an opportunistic pathogen known for its capability to cause a broad range of infections, posing a significant and growing global health concern. Alongside enhancing diagnostic capabilities and bolstering public health initiatives, developing a safe and effective vaccine represents a promising strategy to tackle this health challenge. In this paper, we employed an array of bioinformatics tools to engineer a subunit vaccine that exhibits high immunogenicity against S. anginosus. After constructing the multi-epitope vaccine, we subsequently predicted its secondary and tertiary protein structures. After refining and validating the modelled structure, we utilised advanced computational approaches, including molecular docking and dynamic simulations, to evaluate the binding affinity, compatibility, and stability of the vaccine-adjuvant complexes. Eventually, in silico cloning was conducted to optimise protein expression and production. The multi-epitope subunit vaccine we developed showed properties in antigenicity and immunity theoretically. The computational study revealed that this vaccine demonstrates significant efficacy against S. anginosus.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}