Cellular immunology最新文献

{"title":"Interactions of mesenchymal stromal/stem cells and immune cells following MSC-based therapeutic approaches in rheumatoid arthritis","authors":"Sajad Dehnavi ,&nbsp;Mahvash Sadeghi ,&nbsp;Jalil Tavakol Afshari ,&nbsp;Mojgan Mohammadi","doi":"10.1016/j.cellimm.2023.104771","DOIUrl":"10.1016/j.cellimm.2023.104771","url":null,"abstract":"<div><p>Rheumatoid arthritis (RA) is considered to be a degenerative and progressive autoimmune disorder. Although several medicinal regimens are used to treat RA, potential adverse events such as metabolic disorders and increased risk of infection, as well as drug resistance in some patients, make it essential to find an effective and safe therapeutic approach. Mesenchymal stromal/stem cells (MSCs) are a group of non-hematopoietic stromal cells with immunomodulatory and inhibitory potential. These cells exert their regulatory properties through direct cell-to-cell interactions and paracrine effects on various immune and non-immune cells. As conventional therapeutic approaches for RA are limited due to their side effects, and some patients became refractory to the treatment, MSCs are considered as a promising alternative treatment for RA. In this review, we introduced various experimental and clinical studies conducted to evaluate the therapeutic effects of MSCs on animal models of arthritis and RA patients. Then, possible modulatory and suppressive effects of MSCs on different innate and adaptive immune cells, including dendritic cells, neutrophils, macrophages, natural killer cells, B lymphocytes, and various subtypes of T cells, were categorized and summarized. Finally, limitations and future considerations for the efficient application of MSCs as a therapeutic approach in RA patients were presented.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"393 ","pages":"Article 104771"},"PeriodicalIF":4.3,"publicationDate":"2023-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41107003","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":"Serum IgA augments adhesiveness of cultured lung microvascular endothelial cells and suppresses angiogenesis","authors":"Kazufumi Takada ,&nbsp;Maho Suzukawa ,&nbsp;Sayaka Igarashi ,&nbsp;Yuuki Uehara ,&nbsp;Shizuka Watanabe ,&nbsp;Sahoko Imoto ,&nbsp;Masaki Ishii ,&nbsp;Yoshiteru Morio ,&nbsp;Hirotoshi Matsui ,&nbsp;Masahiro Akishita ,&nbsp;Ken Ohta","doi":"10.1016/j.cellimm.2023.104769","DOIUrl":"10.1016/j.cellimm.2023.104769","url":null,"abstract":"<div><p>Immunoglobulin A (IgA) is important in local immunity and is also abundant in the blood. This study aimed to evaluate the effects of serum IgA on cultured lung microvascular endothelial cells (HMVEC-Ls), which are involved in the pathogenesis of inflammatory lung diseases. Serum IgA induced adhesion molecules and inflammatory cytokine production from HMVEC-Ls, and enhanced adhesion of peripheral blood mononuclear cells to HMVEC-Ls. In contrast, migration, proliferation, and tube formation of HMVEC-Ls were significantly suppressed by serum IgA. Experiments with siRNAs and western blotting revealed that two known IgA receptors, β1,4-galactosyltransferase 1 (b4GALT1) and asialoglycoprotein receptor 1 (ASGR1), and mitogen-activated protein kinase and nuclear factor-kappa B pathways were partly involved in serum IgA-induced cytokine production by HMVEC-Ls. Collectively, serum IgA enhanced cytokine production and adhesiveness of HMVEC-L, with b4GALT1 and ASGR1 partially being involved, and suppressed angiogenesis. Thus, serum IgA may be targeted to treat inflammatory lung diseases.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"393 ","pages":"Article 104769"},"PeriodicalIF":4.3,"publicationDate":"2023-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41115511","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":"PD-1 negatively tunes macrophage immune activation by turning off JNK and STAT1 signaling: Exploited by Leishmania for its intra-macrophage survival","authors":"Shalini Roy ,&nbsp;Anand K Gupta ,&nbsp;Madhurima Banerjee ,&nbsp;Pijush K. Das ,&nbsp;Anindita Ukil","doi":"10.1016/j.cellimm.2023.104758","DOIUrl":"10.1016/j.cellimm.2023.104758","url":null,"abstract":"<div><p>The anti-inflammatory role of the programmed death-1 receptor (PD-1) is well appreciated. However, the mechanism of how PD-1 signaling inhibits the pro-inflammatory cytokine responses in macrophages, which is further exploited by <em>Leishmania</em> to foster their intracellular survival, was unknown. We found that among three major MAP kinases regulating immune activation, PD-1 signaling decreased only JNK phosphorylation without perturbing p38 and ERK. Inflammatory transcription factor STAT1 was also inhibited by PD-1. Association studies documented that SHP, the downstream phosphatase of PD-1, is directly responsible for the decreased phosphorylation of JNK and STAT1. JNK and STAT1 deactivation led to Elk-1/c-Fos inhibition, which significantly decreased IL-12 and TNF-α levels. Further investigation revealed c-Fos deactivation ultimately rendered transcription factor AP1 inactive and facilitating parasite-favorable anti-inflammatory environment.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104758"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10314827","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":"Editorial: Processing, presentation, and recognition of T cell determinants: From molecular insights to clinical applications","authors":"Eddie A. James","doi":"10.1016/j.cellimm.2023.104756","DOIUrl":"10.1016/j.cellimm.2023.104756","url":null,"abstract":"","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104756"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10260836","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":"Haploinsufficiency of A20 caused by a novel pathogenic missense variant of TNFAIP3 and successfully treated with anti-TNF and immunosuppressive therapies","authors":"Sun Lina ,&nbsp;Han Ya'nan ,&nbsp;Yang Ying ,&nbsp;Wang Fengfan ,&nbsp;Hou Xin ,&nbsp;Ren Xiaoxia ,&nbsp;Fang Ying","doi":"10.1016/j.cellimm.2023.104753","DOIUrl":"10.1016/j.cellimm.2023.104753","url":null,"abstract":"<div><p>Loss-of-function of protein A20, encoded by <em>TNFAIP3</em>, leads to an early-onset haploinsufficiency of A20 (HA20). This study reports one Chinese child with HA20 and explores the genetic etiology of <em>TNFAIP3</em> variant. The patient exhibited transient recurrent episodes of fever, intermittent signs of arthritis, gastrointestinal symptoms and multiple colonic ulcers. Laboratory tests revealed elevated inflammatory indicators and mild to moderate anemia. Genetic analysis identified a heterozygous <em>de novo</em> variant in his <em>TNFAIP3</em> gene (c.740C＞T, p. P247L), which had never been reported before. The novel missense variation was validated to be pathogenic through causing insufficient expression of A20, over-activation of NF-κB signaling pathway and elevated levels of proinflammatory cytokines in response to stimulation by lipopolysaccharide. A combination of oral corticosteroids, TNF-α inhibitors and thalidomide freed him from symptoms and abnormal inflammatory indicators. Furthermore, continual improvement of the patient's condition was observed during a follow-up period of five months. We demonstrate a case with a <em>de novo</em> missense variant resulting in a loss-of-function of <em>TNFAIP3</em>, which expands the clinical spectrum of HA20. Cytokine antagonists and immunosuppressants may be effective drugs.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104753"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10260807","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":"Attenuated airways inflammation and remodeling in IL-37a and IL-37b transgenic mice with an ovalbumin-induced chronic asthma","authors":"Lele Cui ,&nbsp;Xiaofeng Qin ,&nbsp;Tingting Fu ,&nbsp;Chenduo Li ,&nbsp;Dan Wang ,&nbsp;Yue Hu ,&nbsp;Yan Li ,&nbsp;Yan Chen ,&nbsp;Ye Cui ,&nbsp;Jingjing Wang ,&nbsp;Huihui Yuan ,&nbsp;Zhe Lv ,&nbsp;Jie Liu ,&nbsp;Damo Xu ,&nbsp;Rongfei Wei ,&nbsp;Sun Ying ,&nbsp;Wei Wang","doi":"10.1016/j.cellimm.2023.104759","DOIUrl":"10.1016/j.cellimm.2023.104759","url":null,"abstract":"<div><h3>Background</h3><p>Asthma is a common chronic respiratory disease characterized by airways inflammation, hyperresponsiveness and remodeling. IL-37, an anti-inflammatory cytokine, consists of five splice isoforms, that is, a-e. Although it has been previously shown that recombinant human IL-37b is able to inhibit airway inflammation and hyperresponsiveness in animal models of asthma, the effects and difference of other IL-37 isoforms, such as IL-37a on features of asthma are unknown.</p></div><div><h3>Methods</h3><p>Animal models of chronic asthma were established using IL-37a and IL-37b transgenic mice with C57BL/6J background and wild-type (WT) mice sensitized and nasally challenged with ovalbumin (OVA). Airway hyperresponsiveness was measured using FlexiVent apparatus, while histological and immunohistological stainings were employed to measure airways inflammation and remodeling indexes, including goblet cell metaplasia, mucus production, deposition of collagen, hypertrophy of airway smooth muscles and pulmonary angiogenesis.</p></div><div><h3>Results</h3><p>Compared to WT mice, both IL-37a and IL-37b transgenic mice had significant reduced airway hyperresponsiveness and the declined total numbers of inflammatory cells, predominant eosinophils into airways and lung tissues. Furthermore, all features of airways remodeling, including degrees of mucus expression, collagen deposition, hypertrophy of smooth muscles, thickness of airways and neovascularization markedly decreased in IL-37 transgenic mice compared with OVA-treated WT mice.</p></div><div><h3>Conclusion</h3><p>Our data suggest that both IL-37a and IL-37b isoforms are able to not only ameliorate airways inflammation and airways hyperresponsiveness, but also greatly reduce airways structural changes of animal models of chronic asthma.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104759"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10261900","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":"The effects of age, origin, and biological sex on rodent mast cell (BMMC and MC/9) and basophil (RBL-2H3) phenotype and function","authors":"Ashley Wagner ,&nbsp;Syed Benazir Alam ,&nbsp;Marianna Kulka","doi":"10.1016/j.cellimm.2023.104751","DOIUrl":"10.1016/j.cellimm.2023.104751","url":null,"abstract":"<div><p>Mast cells initiate allergic inflammatory immune responses and play a role in disease by releasing various inflammatory and immunomodulatory mediators. Several mast cell-lines and primary cultured cells have been used as mast cell models with inconsistent results among research groups. Bone marrow-derived mast cells (BMMC) cultured from mouse bone marrow progenitor cells are often used as a representative model of mucosal mast cell behaviour, however their reported phenotype is variable due to inconsistent culture protocols. RBL-2H3 is a rat basophilic histamine-releasing cell line that has some characteristics of both mast cells and basophils but is not a true representation of either cell type. The murine mast cell line MC/9 is an IL-3-dependent mucosal mast cell model but has limited mast cell characteristics. In this study, we have compared the response of BMMC (derived from C57BL/6 male or female mice), two sources of RBL-2H3 (purchased directly from ATCC and a lab curated culture), and MC/9 (ATCC) at several critical stages to some common stimuli (IgE/Ag, A23187) and analyzed mast cell morphology, expression level of common mast cell surface markers (CD117 and FcεRI), protease expression, and function (growth kinetics, viability, ROS production, degranulation, cytokine release and FcεRI signaling). The objective of this study was to provide insight into the effects of culture conditions, biological sex, and age of the cells on variability among reported phenotypes and, to determine optimal conditions for activation of these cells. Our data show that factors that are often overlooked such as source, age and biological sex of mast cells play an integral role in phenotypic outcomes and may account for the reported variability in their function.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104751"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10623908","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":"Crosstalk between peripheral immunity and central nervous system in Alzheimer’s disease","authors":"Hanchen Yang ,&nbsp;Qi Qin ,&nbsp;Meng Wang ,&nbsp;Yunsi Yin ,&nbsp;Ruiyang Li ,&nbsp;Yi Tang","doi":"10.1016/j.cellimm.2023.104743","DOIUrl":"10.1016/j.cellimm.2023.104743","url":null,"abstract":"<div><p>The significance of peripheral immunity in the pathogenesis and progression of Alzheimer’s diseases (AD) has been recognized. Brain-infiltrated peripheral immune components transporting across the blood–brain barrier (BBB) may reshape the central immune environment. However, mechanisms of how these components open the BBB for AD occurrence and development and correlations between peripheral and central immunity have not been fully explored. Herein, we formulate a hypothesis whereby peripheral immunity as a critical factor allows AD to progress. Peripheral central immune cell crosstalk is associated with early AD pathology and related risk factors. The damaged BBB permits peripheral immune cells to enter the central immune system to deprive its immune privilege promoting the progression toward developing AD. This review summarizes the influences of risk factors on peripheral immunity, alongside their functions, highlighting the concept of peripheral and central immunity as an integrated system in AD pathogenesis, which has received scant attention before.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104743"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10256933","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":"Piperine suppresses inflammatory fibroblast-like synoviocytes derived from rheumatoid arthritis patients Via NF-κB inhibition","authors":"Qoyama Noel Baito,&nbsp;Halmat M. Jaafar,&nbsp;Talar Ahmad Merza Mohammad","doi":"10.1016/j.cellimm.2023.104752","DOIUrl":"10.1016/j.cellimm.2023.104752","url":null,"abstract":"<div><p>Rheumatoid Arthritis (RA) is a common autoimmune disease recognized by hyperplasia of synoviocytes and chronic joint inflammation. Activation of fibroblast-like synoviocytes (FLSs) is one of the main features of RA which can trigger inflammation leading to articular cartilage and joint destruction. Aberrant activation of NF-κB signaling cascade was found to be responsible for the high proliferation and defective apoptosis of FLSs and subsequent inflammation in RA. Piperine is a principal constituent of piper species frequently used as antitumor and anti-inflammatory natural compound. In this study we aimed to assess the anti-inflammatory effect of piperine on RA-FLS through NF-κB inhibition.</p><p>FLSs were isolated from 68 RA patients and 30 healthy controls and were exposed to piperine. The main assays were MTT assay, flow cytometric analysis, PI staining, reverse transcription-PCR (RT-PCR), and ELISA.</p><p>Results showed that piperine can induce the apoptosis and reduce the proliferation of RA-FLSs in vitro. Moreover, piperine directly reduced the phosphorylation of NF-kB and the expression of NF-κB target genes related to RA-FLSs proliferation (c-Myc and Cycline D1), apoptosis inhibition (Bcl2 and Bcl-xl) and inflammation (COX2, IL-1β, TNF-α,IL-6, CCL5 and CXCL10) while increasing the expression of apoptosis related ones (Bax) in vitro. Piperine also reduced the protein levels of cytokines and chemokines secreted by FLSs as a result of NF-κB inhibition.</p><p>In conclusion, our results provide evidence for the anti-inflammatory capacity of piperine through inhibition of NF-κB pathway in FLSs proposing this compound as a suitable alternative for chemical treatment of RA.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104752"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10314434","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":"Phloretin suppresses intestinal inflammation and maintained epithelial tight junction integrity by modulating cytokines secretion in in vitro model of gut inflammation","authors":"Smita Kapoor ,&nbsp;Yogendra S. Padwad","doi":"10.1016/j.cellimm.2023.104754","DOIUrl":"10.1016/j.cellimm.2023.104754","url":null,"abstract":"<div><p>Ulcerative colitis is a type of inflammatory bowel disease which in long run can lead to colorectal cancer (CRC). Chronic inflammation can be a key factor for the occurrence of CRC thus mitigating an inflammation can be a preventive strategy for the occurrence of CRC. In this study we have explored the anti-inflammatory potential of phloretin, in <em>in vitro</em> gut inflammation model, developed by co-culture of Caco2 (intestinal epithelial) cells and RAW264.7 macrophages (immune cells). Phloretin is a dihydrochalcone present in apple, pear and strawberries. An anti-inflammatory effect of phloretin in reducing LPS induced inflammation and maintenance of transepithelial electric resistance (TEER) in Caco2 cells was examined. Paracellular permeability assay was performed using Lucifer yellow dye to evaluate the effect of phloretin in inhibiting gut leakiness caused by inflammatory mediators secreted by activated macrophages. Phloretin attenuated LPS induced nitric oxide levels, oxidative stress, depolarization of mitochondrial membrane potential in Caco2 cells as evidenced by reduction in reactive oxygen species (ROS), and enhancement of MMP, and decrease in inflammatory cytokines IL8, TNFα, IL1β and IL6. It exhibited anti-inflammatory activity by inhibiting the expression of NFκB, iNOS and Cox2. Phloretin maintained the epithelial integrity by regulating the expression of tight junction proteins ZO1, occludin, Claudin1 and JAM. Phloretin reduced LPS induced levels of Cox2 along with the reduction in Src expression which further regulated an expression of tight junction protein occludin. Phloretin in combination to sodium pyruvate exhibited potential anti-inflammatory activity via targeting NFkB signaling. Our findings paved a way to position phloretin as nutraceutical in preventing the occurrence of colitis and culmination of disease into colitis associated colorectal cancer.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"391 ","pages":"Article 104754"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10313942","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}