Immunology letters最新文献

{"title":"IL-21 drives skin and lung inflammation and fibrosis in a model for systemic sclerosis","authors":"In Gyu Um ,&nbsp;Jin Seok Woo ,&nbsp;Young Joon Lee ,&nbsp;Seon-Yeong Lee ,&nbsp;Ha Yeon Jeong ,&nbsp;Hun Sik Na ,&nbsp;Jeong Su Lee ,&nbsp;A. Ram Lee ,&nbsp;Sung- Hwan Park ,&nbsp;Mi-La Cho","doi":"10.1016/j.imlet.2024.106924","DOIUrl":"10.1016/j.imlet.2024.106924","url":null,"abstract":"<div><h3>Background</h3><p>Systemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy, abnormal inflammation, and fibrosis of the skin and internal organs, notably the skin and lungs, significantly impairing quality of life. There is currently no cure for SSc, and its etiology remains largely unknown, presenting a primary barrier to effective treatment. We investigated the role of interleukin-21 (IL-21) in the pathogenesis of SSc.</p></div><div><h3>Methods</h3><p>We assessed the expression levels of fibrosis-related genes in human dermal fibroblasts exposed to IL-21 and TGF beta. We also induced SSc in wild-type C57BL/6 mice and IL-21 knockout (KO) mice with a C57BL/6 background using bleomycin (Bleomycin). Histological analyses were conducted on skin and lung tissues from these mice. The distribution and expression levels of fibrosis-related proteins in the tissues were examined via immunohistochemistry and quantitative real-time PCR. Furthermore, we measured the frequency of Th1, Th2, and Th17 cells among splenocytes through flow cytometry.</p></div><div><h3>Results</h3><p>IL-21 activation led to STAT3 phosphorylation more than TGF beta in dermal fibroblasts. In IL-21 KO mice with BLM-induced SSc, skin thickness and lung fibrosis were reduced. The absence of IL-21 in these mice resulted in suppressed expression of fibrosis-related genes, including <em>Col1a1, Col1a2, Col3a1, CTGF, α-SMA, STAT3</em>, and <em>TGFβ</em>, in the skin and lungs. It also led to a decreased frequency of Th1, Th2, and Th17 cells, as well as a lower Th17/Treg ratio among splenocytes, factors known to contribute to the development of SSc.</p></div><div><h3>Conclusions</h3><p>IL-21 contributes to the development of SSc by promoting the expression of fibrosis-related genes and modulating the levels of CD4+ <em>T</em> cells.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106924"},"PeriodicalIF":3.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142228981","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":"Silencing TRIM8 alleviates allergic asthma and suppressing Th2 differentiation through inhibiting NF-κB/NLRP3 signaling pathway","authors":"Yao Tang ,&nbsp;Yan Zhao ,&nbsp;Yuanyuan Guan ,&nbsp;Longge Xue ,&nbsp;Jingsong Guo ,&nbsp;Tingrui Zhao ,&nbsp;Yuqing Guan ,&nbsp;Songlin Tong ,&nbsp;Chunli Che","doi":"10.1016/j.imlet.2024.106923","DOIUrl":"10.1016/j.imlet.2024.106923","url":null,"abstract":"<div><h3>Background and aim</h3><p>Allergic asthma is a primary type of asthma and characterized by T helper 2 (Th2) cells -mediated inflammation. Tripartite motif containing 8 (TRIM8) protein is involved in immunoreaction and inflammatory response in many diseases. However, its role in allergic asthma remains unclear. Medical databank showed that TRIM8 was increased in lung of ovalbumin (OVA)-challenged mice. This study aimed to elucidate the effects of TRIM8 on allergic asthma and Th2 development.</p></div><div><h3>Methods</h3><p>Asthma were induced by OVA challenge in mice, and the adenovirus vector loaded with TRIM8 knockdown sequence was delivered into asthma mice by nasal inhalation. The percentage of Th2 cells in lung was assessed by flow cytometric analysis, and the contents of Th2 cytokines (interleukin (IL)-4, IL-5 and IL-13) in bronchoalveolar lavage fluid (BALF) were assessed with ELISA. In vitro Th2 induction was performed in CD4⁺ cells from mouse spleen, the expression of Th2 molecules (IL-4, IL-5 and GATA binding protein 3 (GATA3)) were measured by real-time PCR. In addition, the nuclear factor-kappa B (NF-κB)/nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing 3 (NLRP3) signaling was determined.</p></div><div><h3>Results</h3><p>TRIM8 was highly expressed in the lung tissues of asthmatic mice and Th2-induced CD4⁺ cells. OVA challenge-induced Th2 development and Th2 cytokine secretion were restrained by silencing of TRIM8 in vivo. Similarly, the Th2 differentiation in vitro was also suppressed by TRIM8 knockdown. TRIM8 inhibited the NF-κB/NLRP3 activity by blocking transforming growth factor-beta-activated kinase 1 (TAK1), and the effects of TRIM8 were abrogated by overexpression of NLRP3.</p></div><div><h3>Conclusions</h3><p>Silencing TRIM8 relieved the asthmatic injury in mice and excessive Th2 development via inhibiting the NF-κB/NLRP3 pathway. It is indicated that TRIM8 may contribute to the airway inflammation in allergic asthma via activating the NF-κB/NLRP3 signaling pathway. The current study provided a novel potential target for allergic asthma treatment.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106923"},"PeriodicalIF":3.3,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142228980","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":"Acute effects of TLR3 agonist Poly(I:C) on bone marrow hematopoietic progenitor cells in mice","authors":"Xin Shu ,&nbsp;Yuxuan Xie ,&nbsp;Manling Shu ,&nbsp;Xiangying Ou ,&nbsp;Juan Yang ,&nbsp;Zhenyu Wu ,&nbsp;Xuan Zhang ,&nbsp;Jinfu Zhang ,&nbsp;Huihong Zeng ,&nbsp;Lijian Shao","doi":"10.1016/j.imlet.2024.106927","DOIUrl":"10.1016/j.imlet.2024.106927","url":null,"abstract":"<div><p>Hematopoietic progenitor cells (HPCs) in bone marrow with limited abilities for self-renewal and differentiation continuously supply hematopoietic cells through life. When suffering infection or inflammation, HPCs will actively proliferate to provide differentiated hematopoietic cells to maintain hematopoietic homeostasis. Poly(I:C), an agonist of TLR3, can specifically activate Type I interferon (IFN-I) signaling which exerts anti-inflammatory effects and influence hematopoiesis after infection. However, the effects of Poly(I:C)-induced IFN-I on the bone marrow hematopoietic system still deserve attention. In this study, our results revealed the efficacy of the IFN-I model, with a remarkably decrease in HPCs and a sharp elevation in LSKs numbers after single dose of Poly(I:C) injection. Apoptotic ratios of HPCs and LSKs significantly increased 48 h after Poly(I:C) treatment. Application of Poly(I:C) prompted the transition of HPCs and LSKs from G0 to G1 phases, potentially leading to the accelerated exhaustion of HPCs. From the cobblestone area-forming cell (CAFC) assay, we speculate that Poly(I:C) impairs the differentiation capacity of HPCs as well as their colony-forming ability. RT-qPCR and immunohistochemistry revealed significant upregulation of IFN-I associated genes and proteins following Poly(I:C) treatment. In conclusion, a single dose of Poly(I:C) induced an acute detrimental effect on HPCs within 48 h potentially due to TLR3 engagement. This activation cascaded into a robust IFN-I response emanating from the bone marrow, underscoring the intricate immunological dynamics at play following Poly(I:C) intervention.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106927"},"PeriodicalIF":3.3,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142228979","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":"Intestinal epithelial vitamin D receptor defense against inflammatory bowel disease via regulating microfold cells","authors":"Xiaomeng Sun ,&nbsp;Yuxuan Wu ,&nbsp;Chenhua Han ,&nbsp;Na Zhang ,&nbsp;Xin Chen ,&nbsp;Yunzi Chen","doi":"10.1016/j.imlet.2024.106925","DOIUrl":"10.1016/j.imlet.2024.106925","url":null,"abstract":"<div><p>Vitamin D receptor (VDR) is involved in the pathogenesis of inflammatory bowel disease (IBD). However, the mechanism of VDR in IBD is still unclear. Microfold cells (M cells) mediated antigen-sampling pathway is central in developing immune responses to pathogenic and commensal bacteria and related to IBD. We found that Intestinal epithelial cell-specific knockdown of VDR(VDR^IEC-KO) increases the susceptibility of mice to experimental colitis induced by sodium dextran sulfate(DSS) by producing more M cells. Knockdown VDR in intestinal epithelial cells increased RANKL-induced microfold cells and promoted the ability of microfold cells to uptake S. Typhimurium (S. T.). Mechanistically, we demonstrated that knockdown VDR promoted the differentiation and maturation of M cells via the Spi-B-dependent pathway. We conclude that M cells may be a potential target of VDR for treating intestinal mucosal barrier dysfunction in IBD.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106925"},"PeriodicalIF":3.3,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142228978","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":"Autoantibody mediated deficiency of IL-36-receptor antagonist in a subset of patients with psoriasis and psoriatic arthritis","authors":"Marie-Christin Hoffmann ,&nbsp;Natalie Fadle ,&nbsp;Evi Regitz ,&nbsp;Igor Age Kos ,&nbsp;Onur Cetin ,&nbsp;Vadim Lesan ,&nbsp;Klaus-Dieter Preuss ,&nbsp;Marina Zaks ,&nbsp;Elisabeth Stöger ,&nbsp;Vincent Zimmer ,&nbsp;Philipp Klemm ,&nbsp;Gunter Assmann ,&nbsp;Jochen Pfeifer ,&nbsp;Joerg Thomas Bittenbring ,&nbsp;Moritz Bewarder ,&nbsp;Thomas Vogt ,&nbsp;Claudia Pföhler ,&nbsp;Bernhard Thurner ,&nbsp;Christoph Kessel ,&nbsp;Lorenz Thurner","doi":"10.1016/j.imlet.2024.106926","DOIUrl":"10.1016/j.imlet.2024.106926","url":null,"abstract":"<div><h3>Objective</h3><p>Psoriatic arthritis (PsA) is known as a seronegative form of spondylarthropathy. The interleukin-36 cytokine family may have a major role in disease pathogenesis and particularly the related cutaneous manifestations. In light of our recent observations on (transient) autoantibody phenotypes neutralizing endogenous anti-inflammatory receptor antagonists (progranulin, IL-1Ra) in different inflammatory conditions, we set out to investigate the potential role of such antibodies targeting IL-36 cytokine family members in PsA and psoriasis without arthritic manifestations (Pso).</p></div><div><h3>Methods</h3><p>In the present study we screened for hypothetic autoantibodies against the anti-inflammatory mediators IL-36 receptor antagonist (IL-36Ra) and anti-inflammatory IL-38 in PsA, Pso and inflammatory and healthy controls. Serum samples of patients with PsA (<em>n</em> = 254), Pso (<em>n</em> = 100), systemic lupus erythematosus (SLE, <em>n</em> = 50), rheumatoid arthritis (RA, <em>n</em> = 100), ulcerative colitis (UC, <em>n</em> = 50), Crohn´s disease (CD, <em>n</em> = 50), and healthy controls (<em>n</em> = 237) were screened for autoantibodies against IL-36Ra and IL-38 as well as IL-36Ra levels by ELISA. Biochemical analysis for immune complexes and atypic protein isoforms as well as IL-36 signaling reporter assays were performed.</p></div><div><h3>Results</h3><p>Anti-IL-36Ra antibodies were detected in five out of 100 (5.0 %) patients with Pso, in 12 of 254 (4.72 %) patients with PsA and in one of 50 (2 %) patients with CD, but in none of the other investigated inflammatory or healthy controls. The IL-36Ra autoantibodies belonged to the IgG1 subclass and their titers ranged between 1:200 to 1:1600. They resulted in immune-complex formation, depletion of serum IL-36Ra levels and were functional in terms of facilitating unrestricted IL-36 signaling.</p></div><div><h3>Conclusion</h3><p>IL-36Ra autoantibodies were found in subgroups of patients with Pso and PsA and may drive respective pathology.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106926"},"PeriodicalIF":3.3,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0165247824001007/pdfft?md5=93335ba1a513060ba43aaf9f1933485b&pid=1-s2.0-S0165247824001007-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142241830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PARP1 inactivation increases regulatory T / Th17 cell proportion in intestinal inflammation. Role of HMGB1","authors":"Roberta Vitali ,&nbsp;Flavia Novelli ,&nbsp;Francesca Palone ,&nbsp;Salvatore Cucchiara ,&nbsp;Laura Stronati ,&nbsp;Claudio Pioli","doi":"10.1016/j.imlet.2024.106912","DOIUrl":"10.1016/j.imlet.2024.106912","url":null,"abstract":"<div><p>Inflammatory bowel diseases (IBD) are chronic relapsing disorders with increasing prevalence. Knowledge gaps still limit the possibility to develop more specific and effective therapies. Using a dextran sodium sulfate colitis mouse model, we found that inflammation increased the total number and altered the frequencies of leukocytes within colon mesenteric lymph nodes (cMLNs). Although the inflammation reduced the frequency of regulatory T (Treg) cells, their absolute numbers were increased. Increased frequency of colitogenic Th17 cells was also observed. Noteworthy, untreated mice lacking Poly(ADP-ribose)-Polimerase-1 functional gene (PARP-1KO) displayed higher frequency of Treg cells and lower percentage of Th17 cells in cMLNs. In colitic PARP-1KO mice the inflammation driven expansion of the Foxp3 Treg population was more pronounced than in WT mice. Conversely, colitis increased Th17 cells to a lower extent in PARP-1KO mice compared with WT mice, resulting in a more protective Treg/Th17 cell ratio. Consequently PARP-1KO mice developed less severe colitis with reduced expression of inflammatory cytokines. In ex vivo experiments PARP-1KO and WT CD11c dendritic cells (DCs) promoted naïve CD4 T cell differentiation differently, the former sustaining more efficiently the generation of Treg cells, the latter that of Th17 cells. Addition of HMGB1 B box or of dipotassium glycyrrhizate, which sequesters extracellular HMGB1, revealed a role for this alarmin in the regulation exerted by PARP-1 on the stimulating vs. tolerogenic function of DCs during colitis. Moreover, a higher percentage of CD11c DC from PARP-1KO mice expressed CD103, a marker associated with the ability of DC to induce Treg cells, compared with WT DC. Conversely, PARP-1KO DC were including a reduced percentage of CX3CR1+ DC, described to induce Th17 cells. These findings were observed in both splenic and colon lamina propria DC.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106912"},"PeriodicalIF":3.3,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0165247824000865/pdfft?md5=1e040df6d88298414481fb5d2ba69836&pid=1-s2.0-S0165247824000865-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced TRIM expression correlates with anomalous CD4 T cell activation in systemic lupus Erythematosus and its clinical diagnostic potential","authors":"Ayibaota Bahabayi ,&nbsp;Yaoyi Zhu ,&nbsp;Yuying Nie ,&nbsp;Jiaxin Ren ,&nbsp;Ainizati Hasimu ,&nbsp;Qi Li ,&nbsp;Zhonghui Zhang ,&nbsp;Xingyue Zeng ,&nbsp;Yuzhe Hu ,&nbsp;Pingzhang Wang ,&nbsp;Chen Liu","doi":"10.1016/j.imlet.2024.106913","DOIUrl":"10.1016/j.imlet.2024.106913","url":null,"abstract":"<div><h3>Objective</h3><p>This study seeks to elucidate the expression, function, and clinical relevance of the T cell receptor interacting molecule (TRIM) within circulating CD4+<em>T</em> cell subsets in systemic lupus erythematosus (SLE) patients.</p></div><div><h3>Methods</h3><p>We assessed TRIM expression across distinct subpopulations of human peripheral blood mononuclear cells (PBMCs) through the analysis of publicly available single-cell RNA sequencing data. In addition, TRIM expression was investigated within CD4+<em>T</em> cell subsets of peripheral blood and spleens in mice. PBMCs were isolated from both SLE patients, healthy controls (HCs) and rheumatoid arthritis (RA) patients with subsequent measurement and comparative analysis of TRIM expression and functional molecules using flow cytometry. To gauge the clinical relevance of TRIM in SLE, correlation and ROC curve analyses were performed.</p></div><div><h3>Results</h3><p>In both healthy humans and mice, TRIM was higher expressed within CD4+<em>T</em> cell subsets, especially in naive CD4+<em>T</em> cells. TRIM+ Tregs exhibited lower Helios+ cells and CD45RA-FoxP3hi cells percentages compared to TRIM- Treg cells. TRIM+<em>T</em> cells demonstrated reduced granzyme B and perforin secretion and increased IFN-γ secretion in comparison to TRIM- T cells. Notably, the proportion of TRIM+CD4+<em>T</em> cells was diminished in SLE patients. The downregulation of TRIM+ in CD4+<em>T</em> cells positively correlated with diminished complement C3 and C1q levels and inversely correlated with CRP. The identification of TRIM-associated CD4 T cell subsets aids in distinguishing SLE patients from HCs and those with RA.</p></div><div><h3>Conclusions</h3><p>Reduced TRIM expression is linked to abnormal CD4+<em>T</em> cell activation in SLE. TRIM-associated CD4+<em>T</em> cells may be implicated in the pathogenesis of SLE and hold potential for clinical diagnostic purposes.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106913"},"PeriodicalIF":3.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132616","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":"Aloe-emodin relieves allergic contact dermatitis pruritus by inhibiting mast cell degranulation","authors":"Yan Yang ,&nbsp;Jianmei Sun ,&nbsp;Huan You ,&nbsp;Yuling Sun ,&nbsp;Yizhi Song ,&nbsp;Zhouyang Shen ,&nbsp;Tongtong Liu ,&nbsp;Donglang Guan ,&nbsp;Yuan Zhou ,&nbsp;Shuo Cheng ,&nbsp;Changming Wang ,&nbsp;Guang Yu ,&nbsp;Chan Zhu ,&nbsp;Zongxiang Tang","doi":"10.1016/j.imlet.2024.106902","DOIUrl":"10.1016/j.imlet.2024.106902","url":null,"abstract":"<div><p>Urushiol-induced allergic contact dermatitis (ACD) is a chronic inflammatory skin disease in which skin barrier dysfunction leads to pruritus and eczematous lesions. ACD is triggered by immune imbalance. Aloe emodin is an anthraquinone derivative extracted from rhubarb, aloe and other traditional Chinese medicines. It has a wide range of pharmacological effects, including anti-inflammatory, anti-tumor, and anti-allergic effects. The purpose of our study was to demonstrate the effectiveness of aloe-emodin on urushiol-induced acute pruritus and allergic contact dermatitis. The results showed that urushiol could stimulate keratinocytes to release chemokines CXCL1, CXCL2, CCL2, TSLP, and TNF-α, which recruit or activate mast cells. Aloe-emodin treatment inhibited inflammatory-response-induced mast cell degranulation in skin lesions and suppressed the expression of inflammatory cytokines, such as interleukin-4, and interleukin-6. Therefore, the results indicate that aloe-emodin can improve urushiol-induced acute pruritus and allergic contact dermatitis in mice by inhibiting mast cell degranulation.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"270 ","pages":"Article 106902"},"PeriodicalIF":3.3,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055474","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":"Acute and prolonged effects of interleukin-33 on cytokines in human cord blood-derived mast cells","authors":"Sherin Bakhashab ,&nbsp;Ghalya H Banafea ,&nbsp;Farid Ahmed ,&nbsp;Reem Alsolami ,&nbsp;Hans-Juergen Schulten ,&nbsp;Kalamegam Gauthaman ,&nbsp;Muhammad Imran Naseer ,&nbsp;Peter Natesan Pushparaj","doi":"10.1016/j.imlet.2024.106908","DOIUrl":"10.1016/j.imlet.2024.106908","url":null,"abstract":"<div><p>Mast cells are multifaceted cells localized in tissues and possess various surface receptors that allow them to respond to inner and external threat signals. Interleukin-33 (IL-33) is a cytokine released by structural cells in response to parasitic infections, mechanical damage, and cell death. IL-33 can activate mast cells, causing them to release an array of mediators. This study aimed to identify the different cytokines released by human cord blood-derived mast cells (hCBMCs) in response to acute and prolonged stimulation with IL-33. For this purpose, a hCBMC model was established and stimulated with 10 ng and 20 ng of recombinant human IL-33 (rhIL-33) for 6 h and 24 h. Total RNA was hybridized using a high-density oligonucleotide microarray. A multiplex assay was performed to assess the released cytokines. Acute exposure to rhIL-33 increased the expression of IL-1α, IL-1β, IL-6, and IL-13, whereas prolonged exposure increased the expression of IL-5 and IL-10, and cytokines were detected in the culture supernatant. WebGestalt analysis revealed that rhIL-33 induces pathways and biological processes related to the immune system and the acute inflammatory response. This study demonstrates that rhIL-33 can activate hCBMCs to release pro- and anti-inflammatory cytokines, eliciting distinct acute and prolonged responses unique to hCBMCs.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"269 ","pages":"Article 106908"},"PeriodicalIF":3.3,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0165247824000828/pdfft?md5=cb2f00bc7f8589edd43ccdc2e5978bf2&pid=1-s2.0-S0165247824000828-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141995698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and characterization of circulating and adipose tissue infiltrated CD20+ T cells from subjects with obesity that undergo bariatric surgery","authors":"Aryane Cruz Oliveira Pinho ,&nbsp;Pedro Barbosa ,&nbsp;André Lazaro ,&nbsp;José G. Tralhão ,&nbsp;Maria João Pereira ,&nbsp;Artur Paiva ,&nbsp;Paula Laranjeira ,&nbsp;Eugenia Carvalho","doi":"10.1016/j.imlet.2024.106911","DOIUrl":"10.1016/j.imlet.2024.106911","url":null,"abstract":"<div><p>T cells play critical roles in adipose tissue (AT) inflammation. The role of CD20⁺ <em>T</em> cell in AT dysfunction and their contributing to insulin resistance (IR) and type 2 diabetes progression, is not known. The aim was to characterize CD20⁺ <em>T</em> cells in omental (OAT), subcutaneous (SAT) and peripheral blood (PB) from subjects with obesity (OB, <em>n</em> = 42), by flow cytometry. Eight subjects were evaluated before (T1) and 12 months post (T2) bariatric/metabolic surgery (BMS). PB from subjects without obesity (nOB, <em>n</em> = 12) was also collected. Higher percentage of CD20⁺ <em>T</em> cells was observed in OAT, compared to PB or SAT, in OB-T1. CD20 expression by PB CD4⁺ <em>T</em> cells was inversely correlated with adiposity markers, while follicular-like CD20⁺ <em>T</em> cells were positively correlated with impaired glucose tolerance (increased HbA1c). Notably, among OB-T1, IR establishment was marked by a lower percentage and absolute number of PB CD20⁺ <em>T</em> cells, compared nOB. Obesity was associated with higher percentage of activated CD20⁺ <em>T</em> cells; however, OAT-infiltrated CD20⁺ <em>T</em> cells from OB-T1 with diabetes displayed the lowest activation. CD20⁺ <em>T</em> cells infiltrating OAT from OB-T1 displayed a phenotype towards IFN-γ-producing Th1 and Tc1 cells. After BMS, the percentage of PB CD4⁺CD20⁺ <em>T</em> cells increased, with reduced Th1 and increased Th17 phenotype. Whereas in OAT the percentage of CD20⁺ <em>T</em> cells with Th1/17 and Tc1/17 phenotypes increased. Interestingly, OAT from OB pre/post BMS maintained higher frequency of effector memory CD20⁺ <em>T</em> cells. In conclusion, CD20⁺ <em>T</em> cells may play a prominent role in obesity-related AT inflammation.</p></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"269 ","pages":"Article 106911"},"PeriodicalIF":3.3,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0165247824000853/pdfft?md5=6f6c4b2601b82c4cf5897f26533c63d5&pid=1-s2.0-S0165247824000853-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987892","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}