Immunology letters最新文献

{"title":"Reassuring humoral and cellular immune responses to SARS-CoV-2 vaccination in participants with systemic sclerosis","authors":"","doi":"10.1016/j.imlet.2024.106929","DOIUrl":"10.1016/j.imlet.2024.106929","url":null,"abstract":"<div><div>Individuals with systemic sclerosis (SSc) are particularly susceptible to SARS-CoV-2 infections, yet it remains to be determined if they generate humoral and cellular responses comparable to controls following SARS-CoV-2 vaccinations. Herein, we collected blood and serum after second, third, and fourth SARS-CoV-2 vaccinations in patients with SSc and controls. Following each dose, participants with SSc mounted comparable serum anti-RBD IgG, anti-RBD IgA, and spike-specific CD4⁺ and CD8⁺ <em>T</em> cell responses to those found in controls. At 3 months post dose 2, the frequencies of Th1, Th2, Th17, and Treg spike-specific CD4⁺ <em>T</em> cells in participants with SSc did not differ from controls. At 2–6 weeks post dose 3, participants with SSc displayed reduced frequencies, but not numbers, of Th17-polarized spike-specific CD4⁺ <em>T</em> cells. Thus, participants with SSc did not display significantly weaker humoral or cellular responses to SARS-CoV-2 vaccination than controls, enabling reassurance of vaccine immunogenicity in participants with SSc.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286178","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":"NK cell receptors in anti-tumor and healthy tissue protection: Mechanisms and therapeutic advances","authors":"","doi":"10.1016/j.imlet.2024.106932","DOIUrl":"10.1016/j.imlet.2024.106932","url":null,"abstract":"<div><div>Natural Killer (NK) cells are integral to the innate immune system, renowned for their ability to target and eliminate cancer cells without the need for antigen presentation, sparing normal tissues. These cells are crucial in cancer immunosurveillance due to their diverse array of activating and inhibitory receptors that modulate their cytotoxic activity. However, the tumor microenvironment can suppress NK cell function through various mechanisms. Over recent decades, research has focused on overcoming these tumor escape mechanisms. Initially, efforts concentrated on enhancing T cell activity, leading to impressive results with immunotherapeutic approaches aimed at boosting T cell responses. Nevertheless, a substantial number of patients do not benefit from these treatments and continue to seek effective alternatives. In this context, NK cells present a promising avenue for developing new treatments, given their potent cytotoxic capabilities, safety profile, and activity against T cell-resistant tumors, such as those lacking HLA-I expression. Recent advancements in immunotherapy include strategies to restore and amplify NK cell activity through immune checkpoint inhibitors, cytokines, adoptive NK cell therapy, and CAR-NK cell technology. This review provides a comprehensive overview of NK cell receptors, the tumor escape mechanisms that hinder NK cell function, and the evolving field of NK cell-based cancer immunotherapy, highlighting ongoing efforts to develop more effective and targeted cancer treatment strategies.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0165247824001068/pdfft?md5=d43348cfcc26cd5b9229bd583314ccfb&pid=1-s2.0-S0165247824001068-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286180","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":"Gene Therapy Strategies for RAG1 Deficiency: Challenges and Breakthroughs.","authors":"Giorgio Gilioli, Arjan Lankester, Sander de Kivit, Frank J T Staal, Lisa M Ott de Bruin","doi":"10.1016/j.imlet.2024.106931","DOIUrl":"https://doi.org/10.1016/j.imlet.2024.106931","url":null,"abstract":"<p><p>Mutations in the recombination activating genes (RAG) cause various forms of immune deficiency. Hematopoietic stem cell transplant (HSCT) is the only cure for patients with severe manifestations of RAG deficiency; however, outcomes are suboptimal with mismatched donors. Gene therapy aims to correct autologous hematopoietic stem and progenitor cells (HSPC) and is emerging as an alternative to allogeneic HSCT. Gene therapy based on viral gene addition exploits viral vectors to add a correct copy of a mutated gene into the genome of HSPCs. Only recently, after a prolonged phase of development, viral gene addition has been approved for clinical testing in RAG1-SCID patients. In the meantime, a new technology, CRISPR/Cas9, has made its debut to compete with viral gene addition. Gene editing based on CRISPR/Cas9 allows to perform targeted genomic integrations of a correct copy of a mutated gene, circumventing the risk of virus-mediated insertional mutagenesis. In this review, we present the biology of the RAG genes, the challenges faced during the development of viral gene addition for RAG1-SCID, and the current status of gene therapy for RAG1 deficiency. In particular, we highlight the latest advances and challenges in CRISPR/Cas9 gene editing and their potential for the future of gene therapy.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286177","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 alpha2-adrenoceptor agonist clonidine protects against hypoxic-ischemic brain damage in neonatal mice through the Nrf2/NF-κB signaling pathway.","authors":"Daojing Su, Huan Gao, Min He, Hu Hao, Heng Liao, Su Zheng","doi":"10.1016/j.imlet.2024.106928","DOIUrl":"https://doi.org/10.1016/j.imlet.2024.106928","url":null,"abstract":"<p><p>Neonatal hypoxic-ischemic brain damage (HIBD) is a severe condition closely associated with neuroinflammation and oxidative stress. Clonidine, a selective α2-adrenergic receptor agonist, is known for its anti-inflammatory and antioxidant properties. Despite these recognized therapeutic benefits, the exact mechanisms by which clonidine exerts its effects in the context of HIBD are not fully understood. This study was designed to thoroughly investigate the impact of clonidine on HIBD-induced neuronal injury and to clarify its underlying mechanism of action. We employed a neonatal mouse model of HIBD to meticulously assess the effects of clonidine on neuronal injury, apoptosis, inflammation, and oxidative stress markers. In addition, we conducted extensive in vitro studies to evaluate the neuroprotective effects of clonidine on primary hippocampal neuronal cells, utilizing advanced techniques such as the Cell Counting Kit-8 (CCK-8), flow cytometry, enzyme-linked immunosorbent assay (ELISA), immunofluorescence assay, and western blotting. Furthermore, we explored the regulatory effects of clonidine on the nuclear factor erythroid 2-related factor (Nrf2)/nuclear factor-κB (NF-κB) signaling pathway through a combination of in vivo and in vitro experiments. The results showed that clonidine significantly reduced cerebral infarction, neuronal damage, and apoptosis in HIBD mice. It also alleviated neuroinflammation and oxidative stress, improved cell viability, and reduced neuronal injury following oxygen-glucose deprivation/reoxygenation (OGD/R). The neuroprotective effects of clonidine were linked to the activation of the Nrf2/heme oxygenase-1 (HO-1) pathway and the inhibition of the NF-κB pathway. Overall, clonidine exhibited neuroprotective properties in HIBD by reducing neuroinflammation and oxidative stress, likely through the modulation of the Nrf2/NF-κB signaling pathway.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286179","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":"IL-21 drives skin and lung inflammation and fibrosis in a model for systemic sclerosis","authors":"","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":null,"pages":null},"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":"","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":null,"pages":null},"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":"","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":null,"pages":null},"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":"","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":null,"pages":null},"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":"","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":null,"pages":null},"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":"","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":null,"pages":null},"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}