Cellular immunology最新文献

{"title":"Rac1 plays a crucial role in MCP-1-induced monocyte adhesion and migration","authors":"Chandreyee Datta ,&nbsp;Pradip Das ,&nbsp;Surbhi Swaroop,&nbsp;Ashish Bhattacharjee","doi":"10.1016/j.cellimm.2024.104843","DOIUrl":"https://doi.org/10.1016/j.cellimm.2024.104843","url":null,"abstract":"<div><p>Monocyte migration is an important process in inflammation and atherogenesis. Identification of the key signalling pathways that regulate monocyte migration can provide prospective targets for prophylactic treatments in inflammatory diseases. Previous research showed that the focal adhesion kinase Pyk2, Src kinase and MAP kinases play an important role in MCP-1-induced monocyte migration. In this study, we demonstrate that MCP-1 induces iPLA₂ activity, which is regulated by PKCβ and affects downstream activation of Rac1 and Pyk2. Rac1 interacts directly with iPLA₂ and Pyk2, and plays a crucial role in MCP-1-mediated monocyte migration by modulating downstream Pyk2 and p38 MAPK activation. Furthermore, Rac1 is necessary for cell spreading and F-actin polymerization during monocyte adhesion to fibronectin. Finally, we provide evidence that Rac1 controls the secretion of inflammatory mediator vimentin from MCP-1-stimulated monocytes. Altogether, this study demonstrates that the PKCβ/iPLA₂/Rac1/Pyk2/p38 MAPK signalling cascade is essential for MCP-1-induced monocyte adhesion and migration.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104843"},"PeriodicalIF":3.7,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141434313","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":"Immunological characteristics of CD103+CD161+ T lymphocytes on chronic rhinosinusitis with nasal polyps","authors":"Danqi Sun ,&nbsp;Kai Wang ,&nbsp;Youmou Chen ,&nbsp;Beiying Zhang ,&nbsp;Jun Tang ,&nbsp;Wei Luo ,&nbsp;Jia Liu ,&nbsp;Sifei Yu","doi":"10.1016/j.cellimm.2024.104842","DOIUrl":"10.1016/j.cellimm.2024.104842","url":null,"abstract":"<div><p>Chronic rhinosinusitis with nasal polyps (CRSwNPs) is a heterogeneous disease characterized by local inflammation of the upper airway and sinus mucosa. T cell-mediated immune responses play irreplaceable roles in the pathogenesis of nasal polyps. CD161⁺ T cells have been implicated in the pathology of several diseases through cytokine production and cytotoxic activity. However, the immunological characteristics of CD161⁺ T cells in nasal mucosa are still not well understood, particularly in CRSwNPs. Our research revealed a notable enrichment of CD161⁺ T cells in nasal tissues compared to peripheral blood, with a significantly more infiltration of CD161⁺ T cells in CRSwNPs compared to control nasal samples. Phenotypical analysis found that CD161⁺ T cells predominantly co-expressed tissue-resident memory surface markers CD103, CD69, and CD45RO. CD161⁺CD103⁺ T cells demonstrated complicated effector functions, marked by elevated levels of PD-1, CTLA-4, IL-17, and IFN-γ and diminished expression of FoxP3 and CD25. Interestingly, despite CD161⁺ T cells was more abundant in polyp tissues compared to normal control tissues, and then further categorizing polyp samples into distinct groups based on clinical characteristics, only the recurrent CRSwNP group showed a significant reduction in CD161⁺CD8⁺ T cells compared to the primary CRSwNP group. This finding suggested the necessity for further research to comprehensively understand the underlying mechanisms and the broader significance of CD161⁺ T cells in the advancement and relapse of CRSwNPs.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104842"},"PeriodicalIF":4.3,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141409576","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":"Extra-pulmonary control of respiratory defense","authors":"Filiz T. Korkmaz,&nbsp;Lee J. Quinton","doi":"10.1016/j.cellimm.2024.104841","DOIUrl":"https://doi.org/10.1016/j.cellimm.2024.104841","url":null,"abstract":"<div><p>Pneumonia persists as a public health crisis, representing the leading cause of death due to infection. Whether respiratory tract infections progress to pneumonia and its sequelae such as acute respiratory distress syndrome and sepsis depends on numerous underlying conditions related to both the causative agent and host. Regarding the former, pneumonia burden remains staggeringly high, despite the effectiveness of pathogen-targeting strategies such as vaccines and antibiotics. This demands a greater understanding of host features that collaborate to promote immune resistance and tissue resilience in the infected lung. Such features inside the pulmonary compartment have drawn much attention, where major advances have been made related to resident and recruited immune activity. By comparison, extra-pulmonary processes guiding pneumonia susceptibility are relatively elusive, constituting the focus of this review. Here we will highlight examples of when, how, and why tissues outside of the lungs dispatch signals that modulate local immunity in the airspaces. Topics include the liver, gut, bone marrow, brain and more, all of which contribute in direct and indirect ways to pneumonia outcome. When tuned appropriately, it has become clear that these responses can serve protective roles, and this will be considered distinctly from what would otherwise be aberrant responses characteristic of pneumonia-induced organ injury and sepsis. Further advances in this area may reveal novel targetable areas for clinical intervention that are not confined to the intra-pulmonary space.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104841"},"PeriodicalIF":4.3,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141324034","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":"Nasal mucosa-derived mesenchymal stem cells prolonged the survival of septic rats by protecting macrophages from pyroptosis","authors":"Linzhi Zhang,&nbsp;Zhe Wang,&nbsp;Xuan Sun,&nbsp;Wanjing Rong,&nbsp;Wenwen Deng,&nbsp;Jiangnan Yu,&nbsp;Ximing Xu,&nbsp;Qingtong Yu","doi":"10.1016/j.cellimm.2024.104840","DOIUrl":"https://doi.org/10.1016/j.cellimm.2024.104840","url":null,"abstract":"<div><p>Sepsis is characterized by an exacerbated inflammatory response, driven by the overproduction of cytokines, a phenomenon known as a cytokine storm. This condition is further compounded by the extensive infiltration of M1 macrophages and the pyroptosis of these cells, leading to immune paralysis. To counteract this, we sought to transition M1 macrophages into the M2 phenotype and safeguard them from pyroptosis. For this purpose, we employed ectodermal mesenchymal stem cells (EMSCs) sourced from the nasal mucosa to examine their impact on both macrophages and septic animal models. The co-culture protocol involving LPS-stimulated rat bone marrow macrophages and EMSCs was employed to examine the paracrine influence of EMSCs on macrophages. The intravenous administration of EMSCs was utilized to observe the enhancement in the survival rate of septic rat models and the protection of associated organs. The findings indicated that EMSCs facilitated M2 polarization of macrophages, which were stimulated by LPS, and significantly diminished levels of pro-inflammatory cytokines and NLRP3. Furthermore, EMSCs notably restored the mitochondrial membrane potential (MMP) of macrophages through paracrine action, eliminated excess reactive oxygen species (ROS), and inhibited macrophage pyroptosis. Additionally, the systemic integration of EMSCs substantially reduced injuries to multiple organs and preserved the fundamental functions of the heart, liver, and kidney in CLP rats, thereby extending their survival.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104840"},"PeriodicalIF":4.3,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141328385","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":"Dopamine β-hydroxylase shapes intestinal inflammation through modulating T cell activation","authors":"Qiaoling Sun ,&nbsp;Heng Li ,&nbsp;Jing Lv ,&nbsp;Weilin Shi ,&nbsp;Yanfeng Bai ,&nbsp;Ke Pan ,&nbsp;Alice Chen","doi":"10.1016/j.cellimm.2024.104839","DOIUrl":"https://doi.org/10.1016/j.cellimm.2024.104839","url":null,"abstract":"<div><h3>Background</h3><p>Inflammatory bowel disease (IBD) is a chronic and relapsing disease characterized by immune-mediated dysfunction of intestinal homeostasis. Alteration of the enteric nervous system and the subsequent neuro-immune interaction are thought to contribute to the initiation and progression of IBD. However, the role of dopamine beta-hydroxylase (DBH), an enzyme converting dopamine into norepinephrine, in modulating intestinal inflammation is not well defined.</p></div><div><h3>Methods</h3><p>CD4⁺CD45RB^highT cell adoptive transfer, and 2,4-dinitrobenzene sulfonic acid (DNBS) or dextran sodium sulfate (DSS)-induced colitis were collectively conducted to uncover the effects of DBH inhibition by nepicastat, a DBH inhibitor, in mucosal ulceration, disease severity, and T cell function.</p></div><div><h3>Results</h3><p>Inhibition of DBH by nepicastat triggered therapeutic effects on T cell adoptive transfer induced chronic mouse colitis model, which was consistent with the gene expression of DBH in multiple cell populations including T cells. Furthermore, DBH inhibition dramatically ameliorated the disease activity and colon shortening in chemically induced acute and chronic IBD models, as evidenced by morphological and histological examinations. The reshaped systemic inflammatory status was largely associated with decreased pro-inflammatory mediators, such as TNF-α, IL-6 and IFN-γ in plasma and re-balanced Th1, Th17 and Tregs in mesenteric lymph nodes (MLNs) upon colitis progression. Additionally, the conversion from dopamine (DA) to norepinephrine (NE) was inhibited resulting in increase in DA level and decrease in NE level and DA/NE showed immune-modulatory effects on the activation of immune cells.</p></div><div><h3>Conclusion</h3><p>Modulation of neurotransmitter levels via inhibition of DBH exerted protective effects on progression of murine colitis by modulating the neuro-immune axis. These findings suggested a promising new therapeutic strategy for attenuating intestinal inflammation.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104839"},"PeriodicalIF":4.3,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141286546","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":"Unlocking the power of Zc3h12c: Orchestrating Macrophage activation and elevating the innate immune response","authors":"Yinxia Zhao ,&nbsp;Maoli Zhu ,&nbsp;Songfang Wu ,&nbsp;Meixian Ou ,&nbsp;Yang Xi ,&nbsp;Zhen Liu ,&nbsp;Rui Hu ,&nbsp;Xiaowei Li ,&nbsp;Ting Xu ,&nbsp;Xiaoqing Xiang ,&nbsp;Ying Zhou ,&nbsp;Shuijun Li","doi":"10.1016/j.cellimm.2024.104837","DOIUrl":"10.1016/j.cellimm.2024.104837","url":null,"abstract":"<div><p>The activation of macrophages, essential for the innate defense against invading pathogens, revolves around Toll-like receptors (TLRs). Nevertheless, a comprehensive understanding of the molecular mechanisms governing TLR signaling in the course of macrophage activation remains to be fully clarified. Although Zc3h12c was originally identified as being enriched in organs associated with macrophages, its precise function remains elusive. In this study, we observed a significant induction of Zc3h12c in macrophages following stimulation with TLR agonists and pathogens. Overexpression of Zc3h12c significantly mitigated the release of TNF-α and IL-6 triggered by lipopolysaccharide (LPS), whereas depletion of Zc3h12c increased the production of the cytokines mentioned above. Notably, the expression of IFN-β was not influenced by Zc3h12c. Luciferase reporter assays revealed that Zc3h12c could suppress the TNF-α promoter activity. Moreover, Zc3h12c exerted a notable inhibitory effect on JNK, ERK, p38, and NF-κB signaling induced by LPS. In summary, the findings of our study suggest that Zc3h12c functions as a robust suppressor of innate immunity, potentially playing a role in the pathogenesis of infectious diseases.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104837"},"PeriodicalIF":4.3,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141135177","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":"Oridonin attenuates liver ischemia–reperfusion injury by suppressing PKM2/NLRP3-mediated macrophage pyroptosis","authors":"Xin-yi Wu ,&nbsp;Min-jie Zhao ,&nbsp;Wei Liao ,&nbsp;Tao Liu ,&nbsp;Jun-Yan Liu ,&nbsp;Jun-hua Gong ,&nbsp;Xing Lai ,&nbsp;Xue-song Xu","doi":"10.1016/j.cellimm.2024.104838","DOIUrl":"10.1016/j.cellimm.2024.104838","url":null,"abstract":"<div><h3>Background</h3><p>The NOD-like receptor protein 3 (NLRP3) mediated pyroptosis of macrophages is closely associated with liver ischemia reperfusion injury (IRI). As a covalent inhibitor of NLRP3, Oridonin (Ori), has strong anti-inflammasome effect, but its effect and mechanisms for liver IRI are still unknown.</p></div><div><h3>Methods</h3><p>Mice and liver macrophages were treated with Ori, respectively. Co-IP and LC-MS/MS analysis of the interaction between PKM2 and NLRP3 in macrophages. Liver damage was detected using H&amp;E staining. Pyroptosis was detected by WB, TEM, and ELISA.</p></div><div><h3>Results</h3><p>Ori ameliorated liver macrophage pyroptosis and liver IRI. Mechanistically, Ori inhibited the interaction between pyruvate kinase M2 isoform (PKM2) and NLRP3 in hypoxia/reoxygenation（H/R）-induced macrophages, while the inhibition of PKM2/NLRP3 reduced liver macrophage pyroptosis and liver IRI.</p></div><div><h3>Conclusion</h3><p>Ori exerted protective effects on liver IRI via suppressing PKM2/NLRP3-mediated liver macrophage pyroptosis, which might become a potential therapeutic target in the clinic.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104838"},"PeriodicalIF":4.3,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141137935","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":"Triptolide promotes differentiation of human monocytes into immunosuppressive MDSCs","authors":"Haozhou Wang ,&nbsp;Hui Yang ,&nbsp;Xiaodong Zhang ,&nbsp;Xiaoguang Zhou","doi":"10.1016/j.cellimm.2024.104836","DOIUrl":"10.1016/j.cellimm.2024.104836","url":null,"abstract":"<div><h3>Background</h3><p>Myeloid-derived suppressor cells (MDSCs) negatively modulate immune activity. Prior investigations have shown much promise in using MDSCs-assisted immunotherapy for organ transplantation patients. Additionally, owing to its immunosuppressive activity, MDSCs can also be used to manage immune-associated disorders.</p></div><div><h3>Methods</h3><p>Granulocyte-macrophage colony-stimulating factor (GM-CSF) was employed to stimulate myeloid progenitor cell differentiation. Triptolide (PG490) was introduced toward the later phases of in vitro MDSCs induction. Lastly, real-time PCR (RT-PCR) and flow cytometry were used to assess transcript expression and cell phenotype, and a mouse skin transplantation model was established to evaluate the MDSCs-mediated immune suppression in vivo.</p></div><div><h3>Results</h3><p>Co-stimulation with PG490 and GM-CSF potently induced myeloid-derived monocytes to form MDSCs, with remarkable immune-suppressive activity. The underlying mechanism involved downregulation of T cell proliferation, activation, enhancement of inflammatory cytokine release, as well as T cell conversion to Treg cells. PG490 strongly enhanced iNOS expression in MDSCs, and iNOS inhibition successfully reversed the immune-suppression. The PG490- and GM-CSF-induced MDSCs substantially extended survival duration of murine skin grafts, thereby validating their strong immune-suppressive activity in vivo.</p></div><div><h3>Conclusions</h3><p>Herein, we presented a new approach involving MDSCs-based immunosuppression in vitro. PG490 and GM-CSF co-treatment strongly induced immuno-suppressive activity in MDSCs both in vitro and in vivo. Our findings highlight the promise of applying MDSCs-based therapy in clinical organ transplantation treatment.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104836"},"PeriodicalIF":4.3,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141042417","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":"Characterization of the immune suppressive functions of eosinophils","authors":"Bomiao Qing ,&nbsp;Minyao Li ,&nbsp;Dan Peng ,&nbsp;Junyi Wang ,&nbsp;Shuo Song ,&nbsp;Lihua Mo ,&nbsp;Guoping Li ,&nbsp;Pingchang Yang","doi":"10.1016/j.cellimm.2024.104829","DOIUrl":"https://doi.org/10.1016/j.cellimm.2024.104829","url":null,"abstract":"<div><p>Eosinophils account for a significant portion of immune cells in the body. It is well known that eosinophils play a role in the pathogenesis of many diseases. In which the interaction between eosinophils and other immune cells is incompletely understood. The aim of this study is to characterize the immune suppressive functions of eosinophils. In this study, an irway allergy mouse model was established. Eosinophils were isolated from the airway tissues using flow cytometry cell sorting. The RAW264.7 cell line was used to test the immune suppressive functions of eosinophils. We observed that eosinophils had immune suppressive functions manifesting inhibiting immune cell proliferation and cytokine release from other immune cells. The eosinophil's immune suppressive functions were mediated by eosinophil-derived molecules, such as eosinophil peroxidase (EPX) and major basic protein (MBP). The expression of Ras-like protein in the brain 27a (Rab27a) was detected in eosinophils, which controlled the release of MBP and EPX by eosinophils. Eosinophil mediators had two contrast effects on inducing inflammatory responses or rendering immune suppressive effects, depending on the released amounts. Administration of an inhibitor of Rab27a at proper dosage could alleviate experimental airway allergy. To sum up, eosinophils have immune suppressive functions and are also inflammation inducers. Rab27a governs the release of EPX and MBP from eosinophils, which leads to immune suppression or inflammation. Modulation of Rab27a can alleviate airway allergy responses by modulating eosinophil’s immune suppressive functions, which has the translational potential for the management of eosinophil-related diseases.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104829"},"PeriodicalIF":4.3,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140947884","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":"Group2 innate lymphoid cells ameliorate renal fibrosis and dysfunction associated with adenine-induced CKD","authors":"Ryuichi Nagashima ,&nbsp;Hiroki Ishikawa ,&nbsp;Yoshihiro Kuno ,&nbsp;Chikara Kohda ,&nbsp;Koji Eshima ,&nbsp;Masayuki Iyoda","doi":"10.1016/j.cellimm.2024.104828","DOIUrl":"https://doi.org/10.1016/j.cellimm.2024.104828","url":null,"abstract":"<div><p>Renal fibrosis is a common pathway of chronic kidney disease (CKD) progression involving primary kidney injury and kidney diseases. Group 2 innate lymphoid cells (ILC2s) mediate type 2 immune responses irrespective of antigen presentation and play a reno-protective role in kidney injury and disease. In the present study, we observed a decrease in kidney-resident ILC2s in CKD and found that enrichment of ILC2s in the kidney ameliorates renal fibrosis. In CKD kidney, ILC2s preferentially produced IL-13 over IL-5 in response to IL-33 stimulation, regardless of ST2L expression. Moreover, GATA3 expression was decreased in ILC2s, and T-bet+ ILC1s and RORγt+ ILC3s were increased in CKD kidney. Adoptive transfer of kidney ILC2s into adenine-induced CKD model mouse improved renal function and fibrosis. Renal fibroblasts cultured with IL33-activated kidney ILC2s suppressed myofibroblast trans-differentiation through <em>Acta2</em> and <em>Fn-1</em> regulation. These results suggest that kidney ILC2s prevent CKD progression via improvement of renal fibrosis. Our findings also suggest that ILC2s may contribute to the development of new therapeutic agents and strategies for tissue fibroses.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"401 ","pages":"Article 104828"},"PeriodicalIF":4.3,"publicationDate":"2024-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140947885","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}