Macrophage最新文献

Autophagy in inflammation: the p38α MAPK-ULK1 axis 炎症中的自噬：p38αMAPK-ULK1轴

Macrophage Pub Date : 2018-03-09 DOI: 10.14800/MACROPHAGE.1629

H. She, Yingli He, Ying‐ren Zhao, Zixu Mao

引用次数: 4

Autophagy in inflammation: the p38α MAPK-ULK1 axis. 炎症中的自噬：p38α MAPK-ULK1 轴。

Macrophage Pub Date : 2018-01-01 Epub Date: 2018-03-09

Hua She, Yingli He, Yingren Zhao, Zixu Mao

引用次数: 0

Myeloid cell neuropilin 1 ameliorates high-fat diet-induced insulin resistance via suppression of Nlrp3 inflammasome. 髓系细胞neuropilin 1通过抑制Nlrp3炎性体改善高脂肪饮食诱导的胰岛素抵抗。

Macrophage Pub Date : 2017-09-18 DOI: 10.14800/MACROPHAGE.1594

X. Dai, I. Okon, M. Zou

引用次数: 2

Myeloid cell neuropilin 1 ameliorates high-fat diet-induced insulin resistance via suppression of Nlrp3 inflammasome. 髓系细胞neuropilin 1通过抑制Nlrp3炎性体改善高脂肪饮食诱导的胰岛素抵抗。

Macrophage Pub Date : 2017-01-01 Epub Date: 2017-09-19

Xiaoyan Dai, Imoh Okon, Ming-Hui Zou

引用次数: 0

Mammary epithelial polarity and macrophage infiltration. 乳腺上皮极性与巨噬细胞浸润。

Macrophage Pub Date : 2017-01-01 Epub Date: 2017-03-13 DOI: 10.14800/Macrophage.1521

Ren Xu

引用次数: 1

The role of Siglec-1 in HIV-1/macrophage interaction. siglec1在HIV-1/巨噬细胞相互作用中的作用。

Macrophage Pub Date : 2016-10-17 DOI: 10.14800/MACROPHAGE.1435

O. Jobe, Jiae Kim, M. Rao

引用次数: 7

Coordinated expression of tyro3, axl, and mer receptors in macrophage ontogeny 巨噬细胞个体发生中tyro3、axl和mer受体的协调表达

Macrophage Pub Date : 2016-04-22 DOI: 10.14800/MACROPHAGE.1261

Anna Malawista, Xiaomei Wang, M. Trentalange, H. Allore, Ruth R. Montgomery

{"title":"Coordinated expression of tyro3, axl, and mer receptors in macrophage ontogeny","authors":"Anna Malawista, Xiaomei Wang, M. Trentalange, H. Allore, Ruth R. Montgomery","doi":"10.14800/MACROPHAGE.1261","DOIUrl":"https://doi.org/10.14800/MACROPHAGE.1261","url":null,"abstract":"The TAM receptors (Tyro3, Axl, and Mer) are a family of homologous receptor-tyrosine kinases that inhibit Toll-like receptor signaling to regulate downstream pathways and restore homeostasis. TAM triple mutant mice (Tyro3−/−, Axl−/−, Mer−/−) have elevated levels of pro-inflammatory cytokines and are prone to developing lymphoproliferative disorders and autoimmunity. Understanding differential expression of TAM receptors among human subjects is critical to harnessing this pathway for therapeutic interventions. We have quantified changes in TAM expression during the ontogeny of human macrophages using paired samples of monocytes and macrophages to take advantage of characteristic expression within an individual. No significant differences in levels of Tyro3 were found between monocytes and macrophages (flow cytometry: p=0.652, immunoblot: p=0.231, qPCR: p=0.389). Protein levels of Axl were reduced (flow cytometry: p=0.049, immunoblot: p<0.001) when monocytes matured to macrophages. No significant differences in the levels of Axl mRNA transcripts were found (qPCR: p=0.082), however, Tyro3 and Axl were proportionate. The most striking difference was upregulation of expression of Mer with both protein and mRNA being significantly increased when monocytes developed into macrophages (flow cytometry: p<0.001, immunoblot: p<0.001, qPCR: p=0.004). A fuller characterization of TAM receptor expression in macrophage ontogeny informs our understanding of their function and potential therapeutic interventions.","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66657062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

MK2: an unrecognized regulator of tumor promoting macrophages in colorectal cancer? MK2:结直肠癌中促瘤巨噬细胞未被识别的调节因子?

Macrophage Pub Date : 2016-02-01 DOI: 10.14800/macrophage.1166

Eliseo F. Castillo, A. Ray, E. Beswick

{"title":"MK2: an unrecognized regulator of tumor promoting macrophages in colorectal cancer?","authors":"Eliseo F. Castillo, A. Ray, E. Beswick","doi":"10.14800/macrophage.1166","DOIUrl":"https://doi.org/10.14800/macrophage.1166","url":null,"abstract":"Colorectal cancer (CRC) is one of the most common malignancies and is associated closely with inflammation before and after development. Macrophages promote colitis and colitis-associated CRC. M1 macrophages contribute to colitis directly through the production of proinflammatory cytokines and through activation of proinflammatory immune cell phenotypes. In cancer, both M1 and M2 macrophages participate in tumor development and progression through cytokine production, changes in cell signaling and activation of T cells. We have identified the mitogen-activated protein kinase-activated protein kinase 2 (MK2) as a regulator of macrophages during colitis-associated CRC (CAC). MK2 is a proinflammatory kinase that promotes production of IL-1α, IL-1β, IL-6 and TNF-α. MK2−/− mice have decreases in macrophages, macrophage-associated chemokines, and proinflammatory cytokines. Most significantly, MK2−/− mice do not develop neoplasms in an inflammatory model of CRC. However, addition of MK2+/+ macrophages to MK2−/− mice increases production of proinflammatory cytokines. In wild type mice, both cytokines and tumor burdens increase upon addition of additional macrophages. These data support the importance of MK2 in macrophage regulation during inflammation-associated CRC.","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66657043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

The role of Siglec-1 in HIV-1/macrophage interaction. siglec1在HIV-1/巨噬细胞相互作用中的作用。

Macrophage Pub Date : 2016-01-01 Epub Date: 2016-09-17

Ousman Jobe, Jiae Kim, Mangala Rao

引用次数: 0

TRAF3: a novel tumor suppressor gene in macrophages. 巨噬细胞中一种新的肿瘤抑制基因TRAF3。

Macrophage Pub Date : 2015-09-30 DOI: 10.14800/MACROPHAGE.1009

Almin I. Lalani, Chang Luo, Yeming Han, P. Xie

{"title":"TRAF3: a novel tumor suppressor gene in macrophages.","authors":"Almin I. Lalani, Chang Luo, Yeming Han, P. Xie","doi":"10.14800/MACROPHAGE.1009","DOIUrl":"https://doi.org/10.14800/MACROPHAGE.1009","url":null,"abstract":"Tumor necrosis factor receptor-associated factor 3 (TRAF3), a member of the TRAF family of cytoplasmic adaptor proteins with E3 ligase activity, is ubiquitously expressed in various cell types of the immune system. It is shared for signaling by a variety of adaptive and innate immune receptors as well as cytokine receptors. Previous studies examining conditional TRAF3-deficient mouse models that have the Traf3 gene specifically deleted in B lymphocytes or T lymphocytes have revealed the diverse and critical in vivo functions of TRAF3 in adaptive immunity. Although in vitro evidence points to a pivotal and indispensable role for TRAF3 in type I interferon production induced by pattern recognition receptors in macrophages and dendritic cells, the in vivo functions of TRAF3 in the innate immune system had long remained unclear. Three laboratories have recently addressed this gap in knowledge by investigating myeloid cell-specific TRAF3-deficient (genotype: TRAF3flox/floxLysM+/Cre) mice. The new evidence together demonstrates that specific ablation of TRAF3 in myeloid cells leads to inflammatory diseases, altered progression of diabetes, and spontaneous development of different types of tumors and infections in mice. These new findings indicate that TRAF3 acts as an anti-inflammatory factor and is required for optimal innate immunity in myeloid cells. Strikingly, the new evidence also identifies TRAF3 as a novel tumor suppressor gene in macrophages and other myeloid cells. In this review, we discuss and summarize the new findings and current knowledge about the multi-faceted regulatory roles and complex signaling mechanisms of myeloid cell TRAF3 in inflammation, innate immunity, and tumor development.","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 1","pages":"e1009"},"PeriodicalIF":0.0,"publicationDate":"2015-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66656983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 25