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Cancer ego-system in glioma: an iron-replenishing niche network systemically self-organized by cancer stem cells. 胶质瘤中的癌症自我系统:一个由癌症干细胞系统自组织的补铁生态位网络。
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-11-30 DOI: 10.1186/s41232-022-00240-8
Kouichi Tabu, Tetsuya Taga

For all living organisms, the adaptation to outside environments is an essential determinant to survive natural and artificial selections and to sustain the whole ecosystem intact with functional biodiversity. Likewise, cancer cells have similar characteristics that evade not only stresses from the host-internal innate and adaptive immune systems but also those from host-externally administered therapeutic interventions. Such selfish characteristics of cancer cells lead to the formation of cancerous ecosystem with a wide variety of phenotypic heterogeneity, which should be called cancer "egosystem" from the host point of view. Recently increasing evidence demonstrates that cancer stem cells (CSCs) are responsible for this cancer egosystem by effectively exploiting host inflammatory and hematopoietic cells and thereby reconstructing their own advantageous niches, which may well be a driving force in cancer recurrence. CSCs are further likely to render multiple niches mutually interconnected and cooperating as a network to support back CSCs themselves. Here, we summarize a recently identified iron-replenishing niche network self-organized by glioma CSCs (GSCs) through remote regulation of host myeloid and erythroid lineage cells. GSCs recruit bone marrow (BM)-derived inflammatory monocytes into tumor parenchyma, facilitate their differentiation into macrophages (Mφs) and skew their polarization into pro-tumoral phenotype, i.e., tumor-associated Mφs (TAMs). Meanwhile, GSCs distantly enhance erythropoiesis in host hematopoietic organs like BM and spleen potentially by secreting some soluble mediators that maintain continuous supply of erythrocytes within tumors. In addition, as normal red pulp Mφs (RPMs) under steady state conditions in spleen recycle iron by phagocytosing the aged or damaged erythrocytes (a/dECs) and release it in time of need, TAMs at least in gliomas phagocytose the hemorrhaged erythrocytes within tumors and potentially serve as a source of iron, an important nutrient indispensable to GSC survival and glioma progression. Taken together, these studies provide the substantial evidence that CSCs have a unique strategy to orchestrate multiple niches as an ecosystem that threatens the host living, which in this sense must be an egosystem. Targeting such an adaptive subpopulation of CSCs could achieve drastic disturbance of the CSC niches and subsequent extinction of malignant neoplasms.

对于所有生物来说,适应外部环境是生存于自然和人为选择以及维持整个生态系统完整和功能性生物多样性的基本决定因素。同样,癌细胞也具有类似的特征,不仅可以逃避宿主内部固有免疫系统和适应性免疫系统的压力,还可以逃避宿主外部给予的治疗干预。癌细胞的这种自私自利的特性导致形成了具有多种表型异质性的癌变生态系统,从宿主的角度来看,这应该被称为癌症的“自我系统”。最近越来越多的证据表明,癌症干细胞(CSCs)通过有效地利用宿主的炎症细胞和造血细胞,从而重建自己的优势生态位,从而负责这种癌症自我系统,这很可能是癌症复发的驱动力。csc进一步有可能使多个利基相互联系并作为一个网络合作,以支持csc本身。在这里,我们总结了最近发现的一个由胶质瘤CSCs (GSCs)通过远程调节宿主髓系和红系细胞自我组织的补铁生态位网络。GSCs将骨髓(BM)来源的炎症单核细胞招募到肿瘤实质,促进其分化为巨噬细胞(m - φs),并使其极化为肿瘤前表型,即肿瘤相关的m - φs (tam)。同时,GSCs通过分泌一些可溶性介质,维持肿瘤内红细胞的持续供应,潜在地远距离促进宿主造血器官如骨髓和脾脏的红细胞生成。此外,在稳态条件下,正常的红浆Mφs (rpm)通过吞噬老化或受损的红细胞(a/dECs)在脾脏循环铁,并在需要时释放出来,tam至少在胶质瘤中吞噬肿瘤内的出血红细胞,并可能作为铁的来源,铁是GSC存活和胶质瘤进展所不可缺少的重要营养物质。综上所述,这些研究提供了大量证据,证明csc有一种独特的策略来协调多个生态位,作为一个威胁宿主生活的生态系统,从这个意义上说,宿主必须是一个自我系统。针对这样一个适应性的CSC亚群可以实现CSC生态位的剧烈干扰和随后的恶性肿瘤的灭绝。
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引用次数: 3
Next-generation proteomics of serum extracellular vesicles combined with single-cell RNA sequencing identifies MACROH2A1 associated with refractory COVID-19. 新一代血清细胞外囊泡蛋白质组学结合单细胞RNA测序鉴定出与难治性COVID-19相关的MACROH2A1
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-11-30 DOI: 10.1186/s41232-022-00243-5
Takahiro Kawasaki, Yoshito Takeda, Ryuya Edahiro, Yuya Shirai, Mari Nogami-Itoh, Takanori Matsuki, Hiroshi Kida, Takatoshi Enomoto, Reina Hara, Yoshimi Noda, Yuichi Adachi, Takayuki Niitsu, Saori Amiya, Yuta Yamaguchi, Teruaki Murakami, Yasuhiro Kato, Takayoshi Morita, Hanako Yoshimura, Makoto Yamamoto, Daisuke Nakatsubo, Kotaro Miyake, Takayuki Shiroyama, Haruhiko Hirata, Jun Adachi, Yukinori Okada, Atsushi Kumanogoh

Background: The coronavirus disease 2019 (COVID-19) pandemic is widespread; however, accurate predictors of refractory cases have not yet been established. Circulating extracellular vesicles, involved in many pathological processes, are ideal resources for biomarker exploration.

Methods: To identify potential serum biomarkers and examine the proteins associated with the pathogenesis of refractory COVID-19, we conducted high-coverage proteomics on serum extracellular vesicles collected from 12 patients with COVID-19 at different disease severity levels and 4 healthy controls. Furthermore, single-cell RNA sequencing of peripheral blood mononuclear cells collected from 10 patients with COVID-19 and 5 healthy controls was performed.

Results: Among the 3046 extracellular vesicle proteins that were identified, expression of MACROH2A1 was significantly elevated in refractory cases compared to non-refractory cases; moreover, its expression was increased according to disease severity. In single-cell RNA sequencing of peripheral blood mononuclear cells, the expression of MACROH2A1 was localized to monocytes and elevated in critical cases. Consistently, single-nucleus RNA sequencing of lung tissues revealed that MACROH2A1 was highly expressed in monocytes and macrophages and was significantly elevated in fatal COVID-19. Moreover, molecular network analysis showed that pathways such as "estrogen signaling pathway," "p160 steroid receptor coactivator (SRC) signaling pathway," and "transcriptional regulation by STAT" were enriched in the transcriptome of monocytes in the peripheral blood mononuclear cells and lungs, and they were also commonly enriched in extracellular vesicle proteomics.

Conclusions: Our findings highlight that MACROH2A1 in extracellular vesicles is a potential biomarker of refractory COVID-19 and may reflect the pathogenesis of COVID-19 in monocytes.

背景:2019冠状病毒病(COVID-19)大流行广泛存在;然而,对难治性病例的准确预测尚未建立。循环细胞外囊泡参与了许多病理过程,是探索生物标志物的理想资源。方法:为了鉴定难治性COVID-19的潜在血清生物标志物并检测与发病机制相关的蛋白质,我们对12例不同疾病严重程度的COVID-19患者和4名健康对照者的血清细胞外囊泡进行了高覆盖率的蛋白质组学分析。此外,对10例COVID-19患者和5名健康对照者的外周血单个核细胞进行单细胞RNA测序。结果:在鉴定的3046个细胞外囊泡蛋白中,与非难治性病例相比,难治性病例中MACROH2A1的表达显著升高;其表达随疾病严重程度的增加而增加。在外周血单核细胞的单细胞RNA测序中,MACROH2A1的表达定位于单核细胞,在危重病例中表达升高。与此一致,肺组织单核RNA测序结果显示,MACROH2A1在单核细胞和巨噬细胞中高表达,在致死性COVID-19中显著升高。此外,分子网络分析显示,外周血单核细胞和肺的转录组中富集了“雌激素信号通路”、“p160类固醇受体共激活因子(SRC)信号通路”和“STAT转录调控”等通路,细胞外囊泡蛋白质组学中也普遍富集。结论:我们的研究结果表明,细胞外囊泡中的MACROH2A1是难治性COVID-19的潜在生物标志物,可能反映了COVID-19在单核细胞中的发病机制。
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引用次数: 0
Current understanding of T cell immunity against SARS-CoV-2. 目前对SARS-CoV-2的T细胞免疫的认识。
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-11-29 DOI: 10.1186/s41232-022-00242-6
Xiuyuan Lu, Sho Yamasaki

As an important part of adaptive immunity, T cells are indispensable in the defense against pathogens including viruses. SARS-CoV-2 is a new human coronavirus that occurred at the end of 2019 and has caused the COVID-19 pandemic. Nevertheless, most of the infected patients recovered without any antiviral therapies, suggesting an effective immunity developed in the bodies. T cell immunity responds upon SARS-CoV-2 infection or vaccination and plays crucial roles in eliminating the viruses and generating T cell memory. Specifically, a subpopulation of CD4+ T cells could support the production of anti-SARS-CoV-2 antibodies, and cytotoxic CD8+ T cells are also protective against the infection. SARS-CoV-2-recognizing T cells could be detected in SARS-CoV-2-unexposed donors, but the role of these cross-reactive T cells is still in debate. T cell responses could be diverse across individuals, mainly due to the polymorphism of HLAs. Thus, compared to antibodies, T cell responses are generally less affected by the mutations of SARS-CoV-2 variants. Up to now, a huge number of studies on SARS-CoV-2-responsive T cells have been published. In this review, we introduced some major findings addressing the questions in the main aspects about T cell responses elicited by SARS-CoV-2, to summarize the current understanding of COVID-19.

T细胞作为适应性免疫的重要组成部分,在抵御包括病毒在内的病原体方面发挥着不可缺少的作用。SARS-CoV-2是一种新的人类冠状病毒,于2019年底发生,并引起了COVID-19大流行。然而,大多数受感染的患者在没有任何抗病毒治疗的情况下康复,这表明体内形成了有效的免疫力。T细胞免疫对SARS-CoV-2感染或疫苗接种作出反应,并在消除病毒和产生T细胞记忆方面发挥关键作用。具体来说,CD4+ T细胞亚群可以支持抗sars - cov -2抗体的产生,细胞毒性CD8+ T细胞也可以防止感染。在未暴露于sars - cov -2的供体中可以检测到识别sars - cov -2的T细胞,但这些交叉反应性T细胞的作用仍存在争议。不同个体的T细胞反应可能不同,这主要是由于hla的多态性。因此,与抗体相比,T细胞反应通常受SARS-CoV-2变体突变的影响较小。到目前为止,已经发表了大量关于sars - cov -2反应性T细胞的研究。本文综述了SARS-CoV-2诱导T细胞应答的主要方面的一些主要发现,以总结目前对COVID-19的认识。
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引用次数: 10
Collagen type I-mediated mechanotransduction controls epithelial cell fate conversion during intestinal inflammation. i型胶原介导的机械转导控制肠道炎症期间上皮细胞命运的转化。
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-11-28 DOI: 10.1186/s41232-022-00237-3
Sakurako Kobayashi, Nobuhiko Ogasawara, Satoshi Watanabe, Yosuke Yoneyama, Sakura Kirino, Yui Hiraguri, Masami Inoue, Sayaka Nagata, Yoshimi Okamoto-Uchida, Satoshi Kofuji, Hiromichi Shimizu, Go Ito, Tomohiro Mizutani, Shinichi Yamauchi, Yusuke Kinugasa, Yoshihito Kano, Yasuhiro Nemoto, Mamoru Watanabe, Kiichiro Tsuchiya, Hiroshi Nishina, Ryuichi Okamoto, Shiro Yui

Background: The emerging concepts of fetal-like reprogramming following tissue injury have been well recognized as an important cue for resolving regenerative mechanisms of intestinal epithelium during inflammation. We previously revealed that the remodeling of mesenchyme with collagen fibril induces YAP/TAZ-dependent fate conversion of intestinal/colonic epithelial cells covering the wound bed towards fetal-like progenitors. To fully elucidate the mechanisms underlying the link between extracellular matrix (ECM) remodeling of mesenchyme and fetal-like reprogramming of epithelial cells, it is critical to understand how collagen type I influence the phenotype of epithelial cells. In this study, we utilize collagen sphere, which is the epithelial organoids cultured in purified collagen type I, to understand the mechanisms of the inflammatory associated reprogramming. Resolving the entire landscape of regulatory networks of the collagen sphere is useful to dissect the reprogrammed signature of the intestinal epithelium.

Methods: We performed microarray, RNA-seq, and ATAC-seq analyses of the murine collagen sphere in comparison with Matrigel organoid and fetal enterosphere (FEnS). We subsequently cultured human colon epithelium in collagen type I and performed RNA-seq analysis. The enriched genes were validated by gene expression comparison between published gene sets and immunofluorescence in pathological specimens of ulcerative colitis (UC).

Results: The murine collagen sphere was confirmed to have inflammatory and regenerative signatures from RNA-seq analysis. ATAC-seq analysis confirmed that the YAP/TAZ-TEAD axis plays a central role in the induction of the distinctive signature. Among them, TAZ has implied its relevant role in the process of reprogramming and the ATAC-based motif analysis demonstrated not only Tead proteins, but also Fra1 and Runx2, which are highly enriched in the collagen sphere. Additionally, the human collagen sphere also showed a highly significant enrichment of both inflammatory and fetal-like signatures. Immunofluorescence staining confirmed that the representative genes in the human collagen sphere were highly expressed in the inflammatory region of ulcerative colitis.

Conclusions: Collagen type I showed a significant influence in the acquisition of the reprogrammed inflammatory signature in both mice and humans. Dissection of the cell fate conversion and its mechanisms shown in this study can enhance our understanding of how the epithelial signature of inflammation is influenced by the ECM niche.

背景:组织损伤后胎儿样重编程的新概念已被公认为解决炎症期间肠上皮再生机制的重要线索。我们之前揭示了胶原原纤维间质重塑诱导覆盖在伤口床上的肠/结肠上皮细胞向胎儿样祖细胞的YAP/ taz依赖性命运转化。为了充分阐明间质细胞外基质(ECM)重塑与上皮细胞胎儿样重编程之间联系的机制,了解I型胶原如何影响上皮细胞的表型至关重要。在本研究中,我们利用胶原球,即纯化型胶原中培养的上皮类器官,来了解炎症相关重编程的机制。解决胶原球调控网络的整个景观有助于解剖肠上皮的重编程特征。方法:我们对小鼠胶原球进行微阵列、RNA-seq和ATAC-seq分析,并与Matrigel类器官和胎儿肠球(FEnS)进行比较。随后,我们用I型胶原培养人结肠上皮,并进行RNA-seq分析。通过已发表的基因集和溃疡性结肠炎(UC)病理标本的免疫荧光基因表达比较,证实了富集基因的有效性。结果:通过RNA-seq分析证实小鼠胶原球具有炎症和再生特征。ATAC-seq分析证实,YAP/TAZ-TEAD轴在诱导独特特征中起核心作用。其中,TAZ暗示了其在重编程过程中的相关作用,基于atac的基序分析不仅发现了Tead蛋白,还发现了在胶原球中高度富集的Fra1和Runx2蛋白。此外,人胶原球也显示出高度显著的炎症和胎儿样特征的富集。免疫荧光染色证实,人胶原球的代表性基因在溃疡性结肠炎炎症区高度表达。结论:I型胶原蛋白对小鼠和人类重编程炎症特征的获得有显著影响。本研究中对细胞命运转化及其机制的解剖可以增强我们对炎症的上皮特征如何受到ECM生态位的影响的理解。
{"title":"Collagen type I-mediated mechanotransduction controls epithelial cell fate conversion during intestinal inflammation.","authors":"Sakurako Kobayashi,&nbsp;Nobuhiko Ogasawara,&nbsp;Satoshi Watanabe,&nbsp;Yosuke Yoneyama,&nbsp;Sakura Kirino,&nbsp;Yui Hiraguri,&nbsp;Masami Inoue,&nbsp;Sayaka Nagata,&nbsp;Yoshimi Okamoto-Uchida,&nbsp;Satoshi Kofuji,&nbsp;Hiromichi Shimizu,&nbsp;Go Ito,&nbsp;Tomohiro Mizutani,&nbsp;Shinichi Yamauchi,&nbsp;Yusuke Kinugasa,&nbsp;Yoshihito Kano,&nbsp;Yasuhiro Nemoto,&nbsp;Mamoru Watanabe,&nbsp;Kiichiro Tsuchiya,&nbsp;Hiroshi Nishina,&nbsp;Ryuichi Okamoto,&nbsp;Shiro Yui","doi":"10.1186/s41232-022-00237-3","DOIUrl":"https://doi.org/10.1186/s41232-022-00237-3","url":null,"abstract":"<p><strong>Background: </strong>The emerging concepts of fetal-like reprogramming following tissue injury have been well recognized as an important cue for resolving regenerative mechanisms of intestinal epithelium during inflammation. We previously revealed that the remodeling of mesenchyme with collagen fibril induces YAP/TAZ-dependent fate conversion of intestinal/colonic epithelial cells covering the wound bed towards fetal-like progenitors. To fully elucidate the mechanisms underlying the link between extracellular matrix (ECM) remodeling of mesenchyme and fetal-like reprogramming of epithelial cells, it is critical to understand how collagen type I influence the phenotype of epithelial cells. In this study, we utilize collagen sphere, which is the epithelial organoids cultured in purified collagen type I, to understand the mechanisms of the inflammatory associated reprogramming. Resolving the entire landscape of regulatory networks of the collagen sphere is useful to dissect the reprogrammed signature of the intestinal epithelium.</p><p><strong>Methods: </strong>We performed microarray, RNA-seq, and ATAC-seq analyses of the murine collagen sphere in comparison with Matrigel organoid and fetal enterosphere (FEnS). We subsequently cultured human colon epithelium in collagen type I and performed RNA-seq analysis. The enriched genes were validated by gene expression comparison between published gene sets and immunofluorescence in pathological specimens of ulcerative colitis (UC).</p><p><strong>Results: </strong>The murine collagen sphere was confirmed to have inflammatory and regenerative signatures from RNA-seq analysis. ATAC-seq analysis confirmed that the YAP/TAZ-TEAD axis plays a central role in the induction of the distinctive signature. Among them, TAZ has implied its relevant role in the process of reprogramming and the ATAC-based motif analysis demonstrated not only Tead proteins, but also Fra1 and Runx2, which are highly enriched in the collagen sphere. Additionally, the human collagen sphere also showed a highly significant enrichment of both inflammatory and fetal-like signatures. Immunofluorescence staining confirmed that the representative genes in the human collagen sphere were highly expressed in the inflammatory region of ulcerative colitis.</p><p><strong>Conclusions: </strong>Collagen type I showed a significant influence in the acquisition of the reprogrammed inflammatory signature in both mice and humans. Dissection of the cell fate conversion and its mechanisms shown in this study can enhance our understanding of how the epithelial signature of inflammation is influenced by the ECM niche.</p>","PeriodicalId":13588,"journal":{"name":"Inflammation and Regeneration","volume":"42 1","pages":"49"},"PeriodicalIF":8.1,"publicationDate":"2022-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9703763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10388668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 2
Marine-derived microbes and molecules for drug discovery 用于药物发现的海洋微生物和分子
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-06-03 DOI: 10.1186/s41232-022-00207-9
Yoshimasa Tanaka, M. Nishikawa, Kaho Kamisaki, Saki Hachiya, Moeka Nakamura, Takahiro Kuwazuru, S. Tanimura, K. Soyano, K. Takeda
{"title":"Marine-derived microbes and molecules for drug discovery","authors":"Yoshimasa Tanaka, M. Nishikawa, Kaho Kamisaki, Saki Hachiya, Moeka Nakamura, Takahiro Kuwazuru, S. Tanimura, K. Soyano, K. Takeda","doi":"10.1186/s41232-022-00207-9","DOIUrl":"https://doi.org/10.1186/s41232-022-00207-9","url":null,"abstract":"","PeriodicalId":13588,"journal":{"name":"Inflammation and Regeneration","volume":"42 1","pages":""},"PeriodicalIF":8.1,"publicationDate":"2022-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65781297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 2
Neuroplasticity related to chronic pain and its modulation by microglia 与慢性疼痛相关的神经可塑性及其小胶质细胞的调节
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-05-03 DOI: 10.1186/s41232-022-00199-6
Shin-ichiro Hiraga, T. Itokazu, Mariko Nishibe, T. Yamashita
{"title":"Neuroplasticity related to chronic pain and its modulation by microglia","authors":"Shin-ichiro Hiraga, T. Itokazu, Mariko Nishibe, T. Yamashita","doi":"10.1186/s41232-022-00199-6","DOIUrl":"https://doi.org/10.1186/s41232-022-00199-6","url":null,"abstract":"","PeriodicalId":13588,"journal":{"name":"Inflammation and Regeneration","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2022-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41555824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 18
The superficial zone of articular cartilage 关节软骨的浅层
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-05-02 DOI: 10.1186/s41232-022-00202-0
Taku Saito
{"title":"The superficial zone of articular cartilage","authors":"Taku Saito","doi":"10.1186/s41232-022-00202-0","DOIUrl":"https://doi.org/10.1186/s41232-022-00202-0","url":null,"abstract":"","PeriodicalId":13588,"journal":{"name":"Inflammation and Regeneration","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2022-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42522311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 12
Molecular mechanism of crosstalk between immune and metabolic systems in metabolic syndrome 代谢综合征免疫系统与代谢系统相互作用的分子机制
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-05-01 DOI: 10.1186/s41232-022-00198-7
R. Hachiya, Miyako Tanaka, Michiko Itoh, T. Suganami
{"title":"Molecular mechanism of crosstalk between immune and metabolic systems in metabolic syndrome","authors":"R. Hachiya, Miyako Tanaka, Michiko Itoh, T. Suganami","doi":"10.1186/s41232-022-00198-7","DOIUrl":"https://doi.org/10.1186/s41232-022-00198-7","url":null,"abstract":"","PeriodicalId":13588,"journal":{"name":"Inflammation and Regeneration","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46265661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 11
Immune-instructive copolymer scaffolds using plant-derived nanoparticles to promote bone regeneration 利用植物源纳米颗粒促进骨再生的免疫指导性共聚物支架
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-04-03 DOI: 10.1186/s41232-022-00196-9
Salwa Suliman, A. Mieszkowska, J. Folkert, Neha Rana, Samih Mohamed-Ahmed, Tiziana Fuoco, A. Finne‐Wistrand, K. Dirscherl, Bodil Jørgensen, K. Mustafa, Katarzyna Gurzawska-Comis
{"title":"Immune-instructive copolymer scaffolds using plant-derived nanoparticles to promote bone regeneration","authors":"Salwa Suliman, A. Mieszkowska, J. Folkert, Neha Rana, Samih Mohamed-Ahmed, Tiziana Fuoco, A. Finne‐Wistrand, K. Dirscherl, Bodil Jørgensen, K. Mustafa, Katarzyna Gurzawska-Comis","doi":"10.1186/s41232-022-00196-9","DOIUrl":"https://doi.org/10.1186/s41232-022-00196-9","url":null,"abstract":"","PeriodicalId":13588,"journal":{"name":"Inflammation and Regeneration","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2022-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47819573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 3
The roles and mechanisms of senescence-associated secretory phenotype (SASP): can it be controlled by senolysis? 衰老相关分泌表型(SASP)的作用和机制:是否可以通过senolysis来控制?
IF 8.1 3区 医学 Q2 IMMUNOLOGY Pub Date : 2022-04-02 DOI: 10.1186/s41232-022-00197-8
Naoko Ohtani
{"title":"The roles and mechanisms of senescence-associated secretory phenotype (SASP): can it be controlled by senolysis?","authors":"Naoko Ohtani","doi":"10.1186/s41232-022-00197-8","DOIUrl":"https://doi.org/10.1186/s41232-022-00197-8","url":null,"abstract":"","PeriodicalId":13588,"journal":{"name":"Inflammation and Regeneration","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2022-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43183417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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: 47
期刊
Inflammation and Regeneration
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