Cellular immunology最新文献

Immunomodulation by galectin-9: Distinct role in T cell populations, current therapeutic avenues and future potential. galectin-9 的免疫调节作用：在 T 细胞群中的独特作用、当前的治疗途径和未来的潜力。

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-11-13 DOI: 10.1016/j.cellimm.2024.104890

Eva M Gossink, Paul J Coffer, Alessandro Cutilli, Caroline A Lindemans

{"title":"Immunomodulation by galectin-9: Distinct role in T cell populations, current therapeutic avenues and future potential.","authors":"Eva M Gossink, Paul J Coffer, Alessandro Cutilli, Caroline A Lindemans","doi":"10.1016/j.cellimm.2024.104890","DOIUrl":"https://doi.org/10.1016/j.cellimm.2024.104890","url":null,"abstract":"<p><p>Galectins, glycan-binding proteins, have been identified as critical regulators of the immune system. Recently, Galectin-9 (Gal-9) has emerged as biomarker that correlates with disease severity in a range of inflammatory conditions. However, Gal-9 has highly different roles in the context of immunoregulation, with the potential to either stimulate or suppress the immune response. Neutralizing antibodies targeting Gal-9 have been developed and are in early test phase investigating their therapeutic potential in cancer. Despite ongoing research, the mechanisms behind Gal-9 action remain not fully understood, and extrapolating the implications of targeting this molecule from previous studies is challenging. Here, we examine the pleiotropic function of Gal-9 focusing on conventional T lymphocytes, providing a current overview of its immunostimulatory and immunosuppressive roles. In particular, we highlight that Gal-9 differentially regulates immune responses depending on the context. Considering this complexity, further investigation of Gal-9's intricate biology is necessary to define therapeutic strategies in immune disorders and cancer treatment aimed at inducing or inhibiting Gal-9 signaling.</p>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"407 ","pages":"104890"},"PeriodicalIF":3.7,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686098","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}

引用次数: 0

Ubiquitination and degradation of MHC-II by Tim-3 inhibits antiviral immunity Tim-3 对 MHC-II 的泛素化和降解抑制了抗病毒免疫。

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-11-07 DOI: 10.1016/j.cellimm.2024.104889

Jie Zhou , Zhonglin LV , Meichen Liu , Chunxiao Du , Lin Du , Zhenfang Gao , Ziying Jiang , Lanying Wang , Shuohua Wang , Meng Liang , Shun Xie , Yuxiang Li , Zhiding Wang , Ge Li , Yinxiang Wei , Gencheng Han

{"title":"Ubiquitination and degradation of MHC-II by Tim-3 inhibits antiviral immunity","authors":"Jie Zhou , Zhonglin LV , Meichen Liu , Chunxiao Du , Lin Du , Zhenfang Gao , Ziying Jiang , Lanying Wang , Shuohua Wang , Meng Liang , Shun Xie , Yuxiang Li , Zhiding Wang , Ge Li , Yinxiang Wei , Gencheng Han","doi":"10.1016/j.cellimm.2024.104889","DOIUrl":"10.1016/j.cellimm.2024.104889","url":null,"abstract":"<div><div>We previously reported that Tim-3, an immune checkpoint inhibitor, inhibits MHC-II expression, but the molecular mechanisms involved and the implications for antiviral immunity remain to be determined. Here, we found that during H1N1 infection, Tim-3 inhibits MHC-II expression in macrophages/microglia in vitro. Tim-3 interacts with MHC-II via its intracellular tail and induces proteasomal dependent degradation of MHC-II. In H1N1 infected macrophages/microglia, Tim-3 promotes the K48-linked ubiquitination of MHC-II via MARCH8, a ubiquitin E3 ligase that can be upregulated by Tim-3. In H1N1 infected mice, specific knockout of Tim-3 in macrophages leads to a decreased viral load, attenuates tissue damage and increases the survival rate. We have thus identified a novel mechanism by which Tim-3 mediates virus immune escape. Manipulating the Tim-3-MHC-II signaling pathway may provide a novel treatment for viral infections.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"407 ","pages":"Article 104889"},"PeriodicalIF":3.7,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638491","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}

引用次数: 0

Gastrodenol suppresses NLRP3/GSDMD mediated pyroptosis and ameliorates inflammatory diseases Gastrodenol 可抑制 NLRP3/GSDMD 介导的脓毒症，改善炎症性疾病

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-11-01 DOI: 10.1016/j.cellimm.2024.104888

Peipei Chen , Yunshu Wang , Huaiping Tang , Zhuo Liu , Jing Wang , Tingting Wang , Yun Xu , Sen-Lin Ji

{"title":"Gastrodenol suppresses NLRP3/GSDMD mediated pyroptosis and ameliorates inflammatory diseases","authors":"Peipei Chen , Yunshu Wang , Huaiping Tang , Zhuo Liu , Jing Wang , Tingting Wang , Yun Xu , Sen-Lin Ji","doi":"10.1016/j.cellimm.2024.104888","DOIUrl":"10.1016/j.cellimm.2024.104888","url":null,"abstract":"<div><div>Pyroptosis, a form of inflammatory programmed cell death, plays a pivotal role in the pathogenesis of various diseases. This process is primarily mediated by the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3). Gastrodenol (Bismuth tripotassium dicitrate, GAS) is a mineral compound which is used to treat duodenal and gastric ulcers associated with Helicobacter pylori. In this study, GAS was found to exhibit protective effects against classical pyroptosis in macrophages. Specifically, GAS effectively inhibits the activation of the NLRP3 inflammasome, Gasdermin D (GSDMD)-mediated pyroptosis, and the secretion of pro-inflammatory cytokines. Mechanistically, GAS inhibited NLRP3 oligomerization and reduced the oligomerization of adaptor protein apoptosis-associated speck like protein containing a caspase activation and recruitment domain (ASC) by directly binding to NLRP3. The interaction between GAS and NLRP3 is primarily mediated through hydrogen bonding and hydrophobic forces. Hydrogen bonds are formed with PHE-727, LEU-723, and ASP-700. Remarkably, GAS treatment attenuated pyroptosis-mediated inflammatory diseases, including experimental autoimmune encephalomyelitis (EAE), lipopolysaccharide (LPS)-induced septic, and monosodium urate (MSU)-induced peritonitis in mice. To conclude, this is the first report that discovered clinical old medicine GAS as a potent inhibitor of pyroptosis and propose a novel therapeutic strategy for the prevention and treatment of NLRP3-GSDMD mediated diseases.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104888"},"PeriodicalIF":3.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560638","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}

引用次数: 0

Drug screening identifies pyrrolidinedithiocarbamate ammonium ameliorating DSS-induced mouse ulcerative colitis via suppressing Th17 differentiation 药物筛选发现吡咯烷二硫代氨基甲酸铵可通过抑制 Th17 分化改善 DSS 诱导的小鼠溃疡性结肠炎

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-10-22 DOI: 10.1016/j.cellimm.2024.104887

Yu-e Guo , Jie Lv , Ping Shu , Xi Li , Ying Li , Junhong Guo , Guofang Chen , Yuping Li , Bo Lu , Wei Zhang , Yin Liu

{"title":"Drug screening identifies pyrrolidinedithiocarbamate ammonium ameliorating DSS-induced mouse ulcerative colitis via suppressing Th17 differentiation","authors":"Yu-e Guo , Jie Lv , Ping Shu , Xi Li , Ying Li , Junhong Guo , Guofang Chen , Yuping Li , Bo Lu , Wei Zhang , Yin Liu","doi":"10.1016/j.cellimm.2024.104887","DOIUrl":"10.1016/j.cellimm.2024.104887","url":null,"abstract":"<div><div>T helper 17 (Th17) cells play crucial roles in various autoimmune diseases, including ulcerative colitis (UC), which is characterized by widespread inflammation in the mucosa of the colon and rectum. To identify small-molecule compounds capable of inhibiting CD4<sup>+</sup> T cell differentiation into Th17 cells, we established a screening system. Through drug screening, we found that pyrrolidinedithiocarbamate ammonium (PDTC) effectively inhibits Th17 differentiation. In a dextran sulfate sodium (DSS)-induced UC mouse model, administration of PDTC significantly ameliorated colitis. PDTC treatment decreased the production of proinflammatory mediators and inhibited the proportion of Th17 cells in colitis-afflicted mice by suppressing NF-κB activation. These findings showed that PDTC can alleviate colitis by inhibiting NF-κB activation. The therapeutic effects of PDTC observed in a mouse model of UC provided a rationale for its application in clinical settings.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104887"},"PeriodicalIF":3.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142526061","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}

引用次数: 0

Complement system component 3 deficiency modulates the phenotypic profile of murine macrophages 补体系统成分 3 缺乏可调节小鼠巨噬细胞的表型特征

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-10-22 DOI: 10.1016/j.cellimm.2024.104886

Tiago Francisco da Silva , Thaís Akemi Amamura , Iuri Cordeiro Valadão , Milena Carvalho Carneiro , Vanessa Morais Freitas , Ana Paula Lepique , Lourdes Isaac

{"title":"Complement system component 3 deficiency modulates the phenotypic profile of murine macrophages","authors":"Tiago Francisco da Silva , Thaís Akemi Amamura , Iuri Cordeiro Valadão , Milena Carvalho Carneiro , Vanessa Morais Freitas , Ana Paula Lepique , Lourdes Isaac","doi":"10.1016/j.cellimm.2024.104886","DOIUrl":"10.1016/j.cellimm.2024.104886","url":null,"abstract":"<div><div>The Complement System is composed of more than 40 proteins that act in innate and adaptive immunity. C3 is the most abundant one and C3-deficient patients are more susceptible to recurrent and severe infections. Several studies have demonstrated the importance of C3 in controlling infections. However, its role in leukocyte biology is still poorly understood. This study aimed to evaluate several cellular parameters in macrophages from C3-deficient mice and compare them to similar cells from wild-type counterparts. We observed that in the absence of C3, the population of F4/80<sup>low</sup> macrophages in the peritoneal cavity of thioglycolate-treated mice is diminished, probably due to the lack of chemotactic factors like C3a and low levels of C5a. Using fluorescence microscopy analysis, we observed that macrophages from C3-deficient mice exhibited morphological alterations when compared to similar cells from wild-type mice. We observed a significant increase in the expression of CD11c, which is part of CR4 (CD11c/CD18), in macrophages from C3-deficient compared to cells from wild-type mice. Treatment with 12-<em>o</em>-tetradecanoylphorbol-13-acetate, stimulated ROS production and MAPK activation by macrophages. However, these parameters were lower in macrophages from C3-deficient mice when compared to wild-type counterparts. In addition, the phagocytosis of iC3b-opsonized Zymosan particles was diminished in macrophages from C3-deficient mice. Our results suggest that C3 deficiency in C57Black/6 mice may influence specific morphological and functional parameters of macrophages, cells of fundamental importance for both the innate and acquired immune responses.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104886"},"PeriodicalIF":3.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142526060","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}

引用次数: 0

IL-10: A Key Regulator and potential therapeutic target in uveitis IL-10：葡萄膜炎的关键调节因子和潜在治疗靶点。

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-10-18 DOI: 10.1016/j.cellimm.2024.104885

Chengzhi Liu, Xinyu Wang, Xusheng Cao

{"title":"IL-10: A Key Regulator and potential therapeutic target in uveitis","authors":"Chengzhi Liu, Xinyu Wang, Xusheng Cao","doi":"10.1016/j.cellimm.2024.104885","DOIUrl":"10.1016/j.cellimm.2024.104885","url":null,"abstract":"<div><div>Uveitis is a prevalent inflammatory eye disease that primarily affects working-age individuals and can lead to blindness if untreated. Interleukin-10 (IL-10) is a multifunctional cytokine with broad immunosuppressive properties and plays a significant role in various pathological and physiological processes. However, its specific role and underlying mechanisms in uveitis remain incompletely understood. This review aims to shed light on the biological characteristics of IL-10, its involvement in the uveitis pathophysiology, and its potential as a novel therapeutic target. By examining existing literature, the review analyzes IL-10 expression levels and regulatory mechanisms in different types of uveitis, discussing its role in immune regulation. Despite IL-10 being expressed variably across various forms of autoimmune uveitis, studies consistently highlight its protective role, prompting research into ways to enhance its bioavailability in the eye. IL-10 is often upregulated in infectious uveitis, contributing to pathogen immune evasion. Furthermore, primary intraocular lymphoma (PIOL), which shares clinical similarities with uveitis, also shows upregulated IL-10 levels, whereas IL-6 is more commonly elevated in uveitis. This differential expression suggests that IL-6 and IL-10 could be diagnostic markers to distinguish between PIOL and uveitis. Future research should continue to focus on elucidating the molecular mechanisms of IL-10 in uveitis, exploring its potential therapeutic applications, and developing targeted treatments that leverage the immunomodulatory effects of IL-10 to prevent and manage this sight-threatening condition.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104885"},"PeriodicalIF":3.7,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495999","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}

引用次数: 0

House dust mite allergen directly activates ILC2 cells via the TLR4 signaling pathway in allergic airway diseases 在过敏性气道疾病中，屋尘螨过敏原通过 TLR4 信号通路直接激活 ILC2 细胞。

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-10-18 DOI: 10.1016/j.cellimm.2024.104884

Yan Li , Zhennan Qu , Xue Wang , Qiqi Wang , Zhe Lv , Wei Wang , Sun Ying , Luo Zhang , Feng Lan

{"title":"House dust mite allergen directly activates ILC2 cells via the TLR4 signaling pathway in allergic airway diseases","authors":"Yan Li , Zhennan Qu , Xue Wang , Qiqi Wang , Zhe Lv , Wei Wang , Sun Ying , Luo Zhang , Feng Lan","doi":"10.1016/j.cellimm.2024.104884","DOIUrl":"10.1016/j.cellimm.2024.104884","url":null,"abstract":"<div><h3>Background</h3><div>Unlike T cells and B cells, the activation process of group 2 innate lymphoid cells (ILC2s) is mainly driven by epithelial cell derived cytokines rather than specific antigen recognition. Whether antigens have a direct role in activating ILC2s remains poorly understood.</div></div><div><h3>Methods</h3><div>Following stimulation, type 2 cytokine secretions and cell death were assessed in house dust mite (HDM)-stimulated ILC2s. To investigate the underlying mechanisms, RNA-sequencing (RNA-seq) was performed on HDM-stimulated ILC2s. The validation experiments were done through <em>in vitro</em> stimulation assays and an HDM-induced asthmatic murine model, using specific inhibitors targeting receptor and relevant proteins of signaling pathways.</div></div><div><h3>Results</h3><div>HDM stimulation increased the secretion of IL-5 and IL-13 cytokines from ILC2s, inhibited apoptosis of ILC2, and promoted the proliferation of ILC2s. As confirmed by RNA-seq, HDM stimulation upregulated genes in ILC2s, including those responsible for type 2 cytokines, ILC2s-specific transcriptional factors, and related receptors. Both toll-like receptor (TLR) 1 and TLR4 were constitutively expressed on ILC2s, however, only TLR4 was predominantly upregulated upon HDM stimulation. TAK242, a specific TLR4 inhibitor, significantly blocked the effect of HDM on ILC2s, in terms of type 2 cytokine secretions and cell death. Using specific inhibitors in pathways, we confirmed that HDM promoted ILC2s activation via TLR4-ERK, p38, and NF-κB signaling pathways.</div></div><div><h3>Conclusions</h3><div>Allergen HDM directly activates ILC2s through TLR4 mediated-ERK/p38/NF-κB signaling pathway. These findings provide new insights into how antigens propagate type 2 immune response via ILC2s, contributing to chronic inflammations in allergic airway diseases.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104884"},"PeriodicalIF":3.7,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495998","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}

引用次数: 0

B cell-intrinsic IFN-γ promotes excessive CD11c+ age-associated B cell differentiation and compromised germinal center selection in lupus mice 狼疮小鼠体内的 B 细胞内源性 IFN-γ 促进了 CD11c+ 年龄相关 B 细胞的过度分化，并损害了生殖中心的选择能力

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-10-18 DOI: 10.1016/j.cellimm.2024.104883

Shujun Liu , Wenqian Zhang , Shihao Tian , Yan Zhang , Zhinan Yin , Gonghua Huang , Huihui Zhang , Fubin Li

{"title":"B cell-intrinsic IFN-γ promotes excessive CD11c+ age-associated B cell differentiation and compromised germinal center selection in lupus mice","authors":"Shujun Liu , Wenqian Zhang , Shihao Tian , Yan Zhang , Zhinan Yin , Gonghua Huang , Huihui Zhang , Fubin Li","doi":"10.1016/j.cellimm.2024.104883","DOIUrl":"10.1016/j.cellimm.2024.104883","url":null,"abstract":"<div><div>CD11c<sup>+</sup> age-associated B cells (ABCs) have emerged as a key component in protective and autoreactive B cell responses. Lupus is an autoimmune disorder linked to reduced efficacy of vaccines and increased susceptibility to infections. Previously, we reported that excessive CD11c<sup>+</sup> ABCs not only significantly contribute to autoantibody production but also promote aberrant T cell activation and compromised affinity-based germinal center selection in response to immunization in lupus mice. Yet, the regulation of CD11c<sup>+</sup> ABC differentiation is not fully understood. In this study, we show that B cell-intrinsic IFN-γ is required for excessive CD11c<sup>+</sup> ABC differentiation in lupus mice. B cell-intrinsic IFN-γ is mainly produced by CD11c<sup>+</sup> ABCs. IFN-γ-deficiency leads to decreased expression of ABC characteristic genes. We further show that ablating IFN-γ can normalize T cell overactivation and rescue antigen-specific GC responses in lupus mice. Our study offers insight into the crucial role of B cell-intrinsic IFN-γ in promoting excessive CD11c<sup>+</sup> ABC differentiation, which compromises affinity-based germinal center selection and affinity maturation in lupus, providing a potential strategy to normalize vaccine responses in lupus.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104883"},"PeriodicalIF":3.7,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142526059","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}

引用次数: 0

Unveiling the impact of TREM-2+ Macrophages in metabolic disorders 揭示 TREM-2+ 巨噬细胞在代谢紊乱中的影响。

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-10-04 DOI: 10.1016/j.cellimm.2024.104882

Mike Telemaco Contreras Colmenares, Amanda de Oliveira Matos, Pedro Henrique dos Santos Dantas, José Rodrigues do Carmo Neto, Marcelle Silva-Sales, Helioswilton Sales-Campos

{"title":"Unveiling the impact of TREM-2+ Macrophages in metabolic disorders","authors":"Mike Telemaco Contreras Colmenares, Amanda de Oliveira Matos, Pedro Henrique dos Santos Dantas, José Rodrigues do Carmo Neto, Marcelle Silva-Sales, Helioswilton Sales-Campos","doi":"10.1016/j.cellimm.2024.104882","DOIUrl":"10.1016/j.cellimm.2024.104882","url":null,"abstract":"<div><div>The Triggering Receptor Expressed on Myeloid cells 2 (TREM-2) has been widely known by its anti-inflammatory activity. It can be activated in response to microbes and tissue damage, leading to phagocytosis, autophagy, cell polarization and migration, counter inflammation, and tissue repair. So far, the receptor has been largely explored in neurodegenerative disorders, however, a growing number of studies have been investigating its contribution in different pathological conditions, including metabolic diseases, in which (resident) macrophages play a crucial role. In this regard, TREM-2 + macrophages have been implicated in the onset and development of obesity, atherosclerosis, and fibrotic liver disease. These macrophages can be detected in the brain, white adipose tissue, liver, and vascular endothelium. In this review we discuss how different murine models have been demonstrating the ability of such cells to contribute to tissue and body homeostasis by phagocytosing cellular debris and lipid structures, besides contributing to lipid homeostasis in metabolic diseases. Therefore, understanding the role of TREM-2 in metabolic disorders is crucial to expand our current knowledge concerning their immunopathology as well as to foster the development of more targeted therapies to treat such conditions.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104882"},"PeriodicalIF":3.7,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380121","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}

引用次数: 0

Netosis and trained immunity in tick-borne diseases: a possible pathogenetic role 蜱传疾病中的净毒和训练有素的免疫力：可能的致病作用。

IF 3.7 4区医学

Cellular immunology Pub Date : 2024-10-02 DOI: 10.1016/j.cellimm.2024.104881

Giusto Davide Badami , Bartolo Tamburini , Leila Mohammadnezhad , Rita Vaz-Rodrigues , Lidia La Barbera , José de la Fuente , Guido Sireci

{"title":"Netosis and trained immunity in tick-borne diseases: a possible pathogenetic role","authors":"Giusto Davide Badami , Bartolo Tamburini , Leila Mohammadnezhad , Rita Vaz-Rodrigues , Lidia La Barbera , José de la Fuente , Guido Sireci","doi":"10.1016/j.cellimm.2024.104881","DOIUrl":"10.1016/j.cellimm.2024.104881","url":null,"abstract":"<div><div>Various types of pathogens transmitted by ticks elicit distinct immune responses just like the emerging α-Gal syndrome that is associated with allergic reactions to tick bites. The mechanisms of Neutrophil Extracellular Traps release (called NETosis) and trained immunity in response to tick-borne microbes have not been extensively investigated. In our paper, we explored the intricate interplay of NETosis and trained immunity within the realm of infectious diseases triggered by tick bites and their possible pathogenetic role in autoimmunity. We conducted an extensive literature search to identify studies for this review, considering articles and reviews published in English within the last years. Additionally, we scrutinized the references of all included papers and relevant review articles to ensure comprehensive coverage. We shed light on a plausible correlation between these innate immune responses and their potential implication in certain pathological conditions, with a specific focus on some autoimmune diseases. These findings offer new perspectives for a more profound comprehension of the immunopathogenesis of certain autoimmune-like signs where clinicians should include Tick-Borne Diseases (TBDs) in their differential diagnoses, in those geographical areas of tick infestation.</div></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"405 ","pages":"Article 104881"},"PeriodicalIF":3.7,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379144","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}

引用次数: 0