International immunology最新文献_第2页

PP2A negatively regulates NK cell T-bet expression and anti-tumor effector function. PP2A 负向调节 NK 细胞 T-bet 的表达和抗肿瘤效应功能。

IF 4.8 4区医学

International immunology Pub Date : 2024-12-26 DOI: 10.1093/intimm/dxae057

Yui Shinzawa, Daisuke Hara, Yuki Shinguryo, Satoru Yokoyama, Manabu Kawada, Yoshihiro Hayakawa

{"title":"PP2A negatively regulates NK cell T-bet expression and anti-tumor effector function.","authors":"Yui Shinzawa, Daisuke Hara, Yuki Shinguryo, Satoru Yokoyama, Manabu Kawada, Yoshihiro Hayakawa","doi":"10.1093/intimm/dxae057","DOIUrl":"10.1093/intimm/dxae057","url":null,"abstract":"The transcription factor T-bet is essential for the anti-tumor effector function of natural killer (NK) cells, but the mechanism regulating its expression in NK cells remains unclear. In this study, we aimed to identify an NK cell-intrinsic regulator that controls T-bet expression. Using T-bet-luciferase reporter assay screening, we identified a protein phosphatase inhibitor as a potential activator of T-bet expression. A series of protein phosphatase 2A (PP2A)-specific inhibitors (PP2Ai) or PP2A siRNA induced the expression of T-bet. In PP2Ai-treated mice, the expression of T-bet and its downstream effector molecules, granzyme B and IFN-γ, was also upregulated in NK cells. Mechanistically, PP2Ai increased the phosphorylation of mTOR and ribosomal protein S6 in NK cells, and mTOR inhibitor canceled the effects of PP2Ai in NK cells. Importantly, NK cells isolated from PP2Ai-treated mice showed higher cytotoxicity and IFN-γ production; therefore, they increased the anti-tumor effector function of NK cells. Accordingly, PP2Ai treatment inhibited lung metastasis of B16 melanoma by NK cell- and mTOR-dependent mechanisms. These results suggest that PP2A negatively regulates NK cell T-bet expression and effector function by an mTOR-dependent mechanism.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"97-107"},"PeriodicalIF":4.8,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A splice of life: the discovery, function, and clinical implications of FOXP3 isoforms in autoimmune disease. "生命的剪接：FOXP3 同工酶在自身免疫性疾病中的发现、功能和临床意义"。

IF 4.8 4区医学

International immunology Pub Date : 2024-12-26 DOI: 10.1093/intimm/dxae049

Kristin N Weinstein, Phillip P Domeier, Steven F Ziegler

{"title":"A splice of life: the discovery, function, and clinical implications of FOXP3 isoforms in autoimmune disease.","authors":"Kristin N Weinstein, Phillip P Domeier, Steven F Ziegler","doi":"10.1093/intimm/dxae049","DOIUrl":"10.1093/intimm/dxae049","url":null,"abstract":"Regulatory T cells (Tregs) are a specialized subset of CD4+ T cells essential for the maintenance of immune homeostasis and prevention of autoimmunity. Treg lineage and functions are programmed by the X-chromosome encoded transcription factor forkhead box P3 (FOXP3). In humans, multiple FOXP3 isoforms are generated through alternative splicing. A full-length isoform containing all coding exons (FOXP3-FL) and a version lacking the second exon (FOXP3-ΔE2) are the predominant FOXP3 isoforms. Additionally, there are two minor isoforms lacking either exon 7 (FOXP3-ΔE7) and both exons 2 and 7 (FOXP3-ΔE2ΔE7). Although healthy humans express approximately equal levels of the FOXP3-FL and FOXP3-ΔE2 isoforms, sole expression of FOXP3-ΔE2 results in the development of a systemic autoimmune disease that resembles immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome. These clinical observations strongly suggest functional defects in suppression by Tregs programmed by the FOXP3-ΔE2 isoform. Work from the past two decades has provided phenotypic and functional evidence of differences between Tregs programmed by the FOXP3-FL, FOXP3-ΔE2, and FOXP3-ΔE7 isoforms. In this review, we discuss the discovery of the FOXP3 isoforms, differences in the phenotype and function of Tregs programmed by different FOXP3 isoforms, and the role that these isoforms are known to play in autoimmunity.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"83-90"},"PeriodicalIF":4.8,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141971053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Spatial diversity of in vivo tissue immunity. 体内组织免疫的空间多样性。

IF 4.8 4区医学

International immunology Pub Date : 2024-12-26 DOI: 10.1093/intimm/dxae051

Yu Miyamoto, Masaru Ishii

引用次数: 0

Intra-tumoral delivery of 5'ppp-dsRNA induces a robust antitumor response via RIG-I activation and Bcl-2 gene downregulation in a murine model of prostate cancer. 在小鼠前列腺癌模型中，5'ppp-dsRNA 的瘤内给药通过 RIG-I 激活和 Bcl-2 基因下调诱导强有力的抗肿瘤反应。

IF 4.8 4区医学

International immunology Pub Date : 2024-12-26 DOI: 10.1093/intimm/dxae061

Kasturi Ganguly, Siddhanath M Metkari, Barnali Biswas, Rambhadur Subedi, Taruna Madan

{"title":"Intra-tumoral delivery of 5'ppp-dsRNA induces a robust antitumor response via RIG-I activation and Bcl-2 gene downregulation in a murine model of prostate cancer.","authors":"Kasturi Ganguly, Siddhanath M Metkari, Barnali Biswas, Rambhadur Subedi, Taruna Madan","doi":"10.1093/intimm/dxae061","DOIUrl":"10.1093/intimm/dxae061","url":null,"abstract":"Onco-immunotherapy via blocking checkpoint inhibitors has revolutionized the treatment-landscape of several malignancies, though not in the metastatic castration-resistant prostate cancer (PCa) owing to an immunosuppressive and poorly immunogenic \"cold\" tumor microenvironment (TME). Turning up the heat of such a cold TME via triggering innate immunity is now of increasing interest to restore immune-surveillance. Retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) are cytosolic innate-sensors that can detect exogenous RNAs and induce type-I interferons and other pro-inflammatory signaling. RIG-I activation is suggested to be a valuable addition to the treatment approaches for several cancers. However, the knowledge about RIG-I signaling in PCa remains elusive. The present study evaluated the expression of two important RLRs, RIG-I and melanoma differentiation-associated protein 5 (MDA5), along with their downstream partners, mitochondrial antiviral-signaling protein (MAVS) and ERA G-protein-like 1 (ERAL1), during PCa progression in the transgenic adenocarcinoma of mouse prostate (TRAMP) model. The early stage of PCa revealed a significant increment in the expression of RLRs but not MAVS. However, the advanced stage showed downregulated RLR signaling. Further, the therapeutic implication of 5'ppp-dsRNA, a synthetic RIG-I agonist and Bcl2 gene silencer, has been investigated in vitro and in vivo. Intra-tumoral delivery of 5'ppp-dsRNA regressed tumor growth via triggering tumor cell apoptosis, immunomodulation, and inducing phagocytic \"eat me\" signals. These findings highlight that, for the first time, RIG-I activation and Bcl-2 silencing with 5'ppp-dsRNA can serve as a potent tumor-suppressor strategy in PCa and has a significant clinical implication in transforming a \"cold\" TME into an immunogenic \"hot\" TME of PCa.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"109-129"},"PeriodicalIF":4.8,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Analysis of antigen specificity of Treg cell clonotypes expanded upon SARS-CoV-2 infection. SARS-CoV-2感染扩增的Treg细胞克隆型抗原特异性分析。

IF 4.8 4区医学

International immunology Pub Date : 2024-12-12 DOI: 10.1093/intimm/dxae072

Yukiko Takeuchi, Eri Ishikawa, Takashi Sato, Masaharu Shinkai, Yoshimasa Takahashi, Xiuyuan Lu, Sho Yamasaki

{"title":"Analysis of antigen specificity of Treg cell clonotypes expanded upon SARS-CoV-2 infection.","authors":"Yukiko Takeuchi, Eri Ishikawa, Takashi Sato, Masaharu Shinkai, Yoshimasa Takahashi, Xiuyuan Lu, Sho Yamasaki","doi":"10.1093/intimm/dxae072","DOIUrl":"https://doi.org/10.1093/intimm/dxae072","url":null,"abstract":"The pandemic outbreak of SARS-CoV-2 has threatened human health worldwide. Among protective immune reactions, T cell responses are diverse among individuals, which is related to the differences in severity. A T cell subset, regulatory T (Treg) cells, is crucial for limiting excessive immune responses. If SARS-CoV-2-specific Tregs are developed during infection, they may counteract anti-viral immunity and cause severe symptom. To address this possibility, we conducted single-cell TCR-RNA-sequencing of PBMCs from convalescent COVID-19 patients. Among thirteen donors, one with severe symptom had substantially more FOXP3-expressing Treg clonotypes activated in the presence of SARS-CoV-2 virion or other major antigen proteins. To define the reactivity of these Treg clonotypes, fifteen highly expanded Treg clonotypes were reconstituted into reporter cells and stimulated with 27 distinct peptide pools that cover all SARS-CoV-2 proteins. However, none of these clonotypes react to any SARS-CoV-2 antigens. Instead, the reporter cells expressing one TCR clonotype (23599) were activated in the presence of EBV-transformed B cells without adding exogenous antigens. Furthermore, 23599 TCR-expressing cells were activated by non-transformed naïve syngenic B cells in DQA1*03:03-DQB1*04:01-dependent manner, suggesting that clonotype 23599 may be autoreactive. This Treg clonotype, 23599, was also detected in a public TCR database, and significantly expanded in COVID-19 patients compared to healthy donors. These results suggest that SARS-CoV-2 is not the dominant antigen inducing Treg during infection.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IL-5-producing group 2 innate lymphoid cells promote T cell-independent IgA production in cooperation with eosinophils. 产生 IL-5 的第 2 组先天性淋巴细胞与嗜酸性粒细胞合作，促进不依赖 T 细胞的 IgA 生成。

IF 4.8 4区医学

International immunology Pub Date : 2024-12-04 DOI: 10.1093/intimm/dxae070

Tsutomu Yanagibashi, Masashi Ikutani, Terumi Nagai, Makoto Arita, Yasuharu Watanabe, Yoshinori Nagai, Kiyoshi Takatsu

{"title":"IL-5-producing group 2 innate lymphoid cells promote T cell-independent IgA production in cooperation with eosinophils.","authors":"Tsutomu Yanagibashi, Masashi Ikutani, Terumi Nagai, Makoto Arita, Yasuharu Watanabe, Yoshinori Nagai, Kiyoshi Takatsu","doi":"10.1093/intimm/dxae070","DOIUrl":"https://doi.org/10.1093/intimm/dxae070","url":null,"abstract":"Intestinal bacteria play a critical role in the regulation of the host immune system and an imbalance in intestinal bacterial composition induces various host diseases. Therefore, maintaining a balance in the intestinal bacterial composition is crucial for health. Immunoglobulin A (IgA), produced through T cell-dependent and T cell-independent (TI) pathways, is essential for host defense against pathogen invasion and maintaining the balance of intestinal symbiotic bacteria. Interleukin (IL)-5 is constitutively produced by group 2 innate lymphoid cells (ILC2s) and plays a critical role in the survival and proliferation of B cells and eosinophils. Here, we show that the role of IL-5-producing ILC2s in intestinal TI IgA production at steady state using TCRα deficient mice. In this mouse model, ILC2s increased fecal TI IgA levels in a non-inflammatory state in an IL-5-dependent manner. The administration of recombinant IL-33 (rIL-33) increased the amount of TI IgA production, accompanied by an increase in the number of IL-5-producing ILC2s in the large intestine. In addition, rIL-33 treatment increased IL-5-dependent IgA+ cells in isolated lymphoid follicles, the site of TI IgA production. Furthermore, eosinophils recruited by ILC2s were required for the maximal production of IgA in the TI pathway. Moreover, IL-5 increased the frequency of TI IgA-binding intestinal bacteria and was involved in the maintenance of intestinal bacterial composition. These findings indicate that IL-5-producing ILC2s together with eosinophils contribute to TI IgA production. In addition to their role in TI IgA production, IL-5-producing ILC2s may contribute to the homeostasis of intestinal commensal bacteria.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A complex of NLRP3 with caspase-4 is essential for inflammasome activation by Tannerella forsythia infection. NLRP3与caspase-4的复合物对于连翘Tannerella感染的炎性体激活至关重要。

IF 4.8 4区医学

International immunology Pub Date : 2024-12-03 DOI: 10.1093/intimm/dxae071

Chen Wei Hsu, Tokuju Okano, Yuiko Niinuma, Anongwee Leewananthawet, Tamako Iida, Poramed Onsoi, Kotchakorn Boonyaleka, Hiroshi Ashida, Toshihiko Suzuki

{"title":"A complex of NLRP3 with caspase-4 is essential for inflammasome activation by Tannerella forsythia infection.","authors":"Chen Wei Hsu, Tokuju Okano, Yuiko Niinuma, Anongwee Leewananthawet, Tamako Iida, Poramed Onsoi, Kotchakorn Boonyaleka, Hiroshi Ashida, Toshihiko Suzuki","doi":"10.1093/intimm/dxae071","DOIUrl":"https://doi.org/10.1093/intimm/dxae071","url":null,"abstract":"Periodontitis, a chronic inflammatory disease of periodontal tissue, is often associated with a group of pathogenic bacteria known as the \"red complex,\" including Tannerella forsythia (T. forsythia). Previous papers showed that T. forsythia induces many kinds of inflammatory cytokines including IL-1β regulated by inflammasome activation. However, the physiological function for periodontitis and mechanism to induce inflammasome activation by T. forsythia infection are poorly understood. In this study, we demonstrate that NLRP3 and caspase-4 are essential for inflammasome activation by T. forsythia infection, playing a crucial role in IL-1β maturation in THP-1 cells. We also showed that knockout of ASC or GSDMD suppress the pyroptotic cell death. Moreover, co-immunoprecipitation assays confirmed the formation of a complex involving caspase-4, NLRP3, and ASC following T. forsythia infection. Additionally, reactive oxygen species (ROS) production was identified as a key factor in caspase-4-mediated NLRP3 inflammasome activation by T. forsythia infection. These results enhance our understanding of inflammasome activation in response to T. forsythia infection and provide new insights into the pathogenic mechanisms of periodontitis.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The immune memory of innate immune systems. 先天性免疫系统的免疫记忆。

IF 4.8 4区医学

International immunology Pub Date : 2024-11-26 DOI: 10.1093/intimm/dxae067

Yasuhiro Kato, Atsushi Kumanogoh

引用次数: 0

CCR2-dependent placental migration of inflammatory monocytes suppresses abnormal pregnancies caused by Toxoplasma gondii infection. 依赖 CCR2 的炎性单核细胞胎盘迁移可抑制弓形虫感染引起的异常妊娠。

IF 4.8 4区医学

International immunology Pub Date : 2024-11-25 DOI: 10.1093/intimm/dxae046

Naganori Kamiyama, Mai Ueno, Yuma Sasaki, Thanyakorn Chalalai, Nozomi Sachi, Sotaro Ozaka, Yasuhiro Soga, Yomei Kagoshima, Supanuch Ekronarongchai, Masaaki Okamoto, Masahiro Yamamoto, Takashi Kobayashi

{"title":"CCR2-dependent placental migration of inflammatory monocytes suppresses abnormal pregnancies caused by Toxoplasma gondii infection.","authors":"Naganori Kamiyama, Mai Ueno, Yuma Sasaki, Thanyakorn Chalalai, Nozomi Sachi, Sotaro Ozaka, Yasuhiro Soga, Yomei Kagoshima, Supanuch Ekronarongchai, Masaaki Okamoto, Masahiro Yamamoto, Takashi Kobayashi","doi":"10.1093/intimm/dxae046","DOIUrl":"10.1093/intimm/dxae046","url":null,"abstract":"Toxoplasma gondii (T. gondii) is a zoonotic protozoan parasite that causes congenital toxoplasmosis, including fetal death, abortion, stillbirth, morphological abnormalities, and premature birth. Primary T. gondii infection in pregnant women results in congenital toxoplasmosis. C-C chemokine receptor (CCR) 2 is reportedly a critical host defense factor against T. gondii infection. However, details of the role of CCR2 in the host immune response to T. gondii in congenital toxoplasmosis remain unclear. Here, we infected pregnant CCR2-deficient mice with T. gondii, resulting in stillbirth, embryonic resorption, fetal morphological abnormalities, and preterm delivery at significantly higher rates than those in pregnant wild-type (WT) mice. Consistent with the severity of abnormal pregnancy, a large area of placental hemorrhage and a large number of T. gondii infections around the hemorrhagic area were observed in the placentas of CCR2-deficient mice. In addition, the accumulation of inflammatory monocytes in the placenta was reduced in CCR2-deficient mice during infection. We further confirmed that the adoptive transfer of inflammatory monocytes collected from WT mice into T. gondii-infected pregnant CCR2-deficient mice effectively suppressed placental damage and abnormal pregnancy. Collectively, CCR2 contributes to pregnancy maintenance by regulating the migration of inflammatory monocytes into the placenta of T. gondii-infected pregnant mice.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"39-52"},"PeriodicalIF":4.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11587896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The canonical Hippo pathway components modulate the differentiation of lamina propria regulatory T cells and T helper 17-like regulatory T cells in mouse colitis. 在小鼠结肠炎中，典型 Hippo 通路成分可调节固有膜调节性 T 细胞和 T 辅助 17 样调节性 T 细胞的分化。

IF 4.8 4区医学

International immunology Pub Date : 2024-11-25 DOI: 10.1093/intimm/dxae043

Liuqing Ge, Min Xu, Meifang Huang, Shaoping Liu, Zhidai Zhou, Ziqin Xia, Shouquan Dong, Qiu Zhao, Ruiping Zhu, Feng Zhou

{"title":"The canonical Hippo pathway components modulate the differentiation of lamina propria regulatory T cells and T helper 17-like regulatory T cells in mouse colitis.","authors":"Liuqing Ge, Min Xu, Meifang Huang, Shaoping Liu, Zhidai Zhou, Ziqin Xia, Shouquan Dong, Qiu Zhao, Ruiping Zhu, Feng Zhou","doi":"10.1093/intimm/dxae043","DOIUrl":"10.1093/intimm/dxae043","url":null,"abstract":"Regulatory T cells (Tregs) ameliorate inflammatory bowel diseases. However, their plasticity is not completely understood. In this study using a mouse colitis model, Tregs and T helper 17 (Th17)-like Tregs were detected and sorted using flow cytometry, followed by transcriptome sequencing, real-time reverse transcription polymerase chain reaction, and flow cytometry to analyze the mRNA profiles of these cells. Treg plasticity was evaluated by in vitro differentiation assays. The immunosuppressive activities of Tregs and Th17-like Tregs were assessed in an adoptive transfer assay. We found Treg-derived Th17-like Tregs in inflamed colonic lamina propria (LP). LP Th17-like Tregs expressed higher Th17-related cytokines and lower immunosuppressive cytokines compared with LP Tregs. Notably, Tregs expressed higher Yes-associated protein 1 (YAP1) but lower transcriptional coactivator with PDZ-binding motif (TAZ) than Th17-like Tregs. Verteporfin-mediated inhibition of YAP1 activity enhanced Th17-like Treg generation, whereas IBS008739-induced TAZ activation did not affect Th17-like Treg generation. Besides, verteporfin enhanced while IBS008739 suppressed the differentiation of Th17-like Tregs into Th17 cells. Furthermore, YAP1 activated STAT5 signaling in Tregs, whereas YAP1 and TAZ activated STAT3 and STAT5 signaling in Th17-like Tregs. Compared with Tregs, Th17-like Tregs were less efficacious in ameliorating colitis. Therefore, YAP1 suppressed Treg differentiation into Th17-like Tregs. Both YAP1 and TAZ inhibited the differentiation of Th17-like Tregs into Th17 cells. Therefore, YAP1 and TAZ probably maintain the immunosuppressive activities of Tregs and Th17-like Tregs in colitis.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"25-38"},"PeriodicalIF":4.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0