Polarization Toward(两极分化)研究综述
Polarization Toward 两极分化 - Overall, humoral and cellular immune response data suggested the induction of both Th1 and Th2 immunity with polarization towards an antiviral Th1 response. [1] Their activation and polarization toward a proinflammatory phenotype are associated with injury and disease. [2] Sema7A orchestrated MΦ chemotaxis and chemokinesis, activated MΦ differentiation and polarization toward the proresolving M2 phenotype, and promoted leukocyte clearance. [3] Moreover, the combination therapy remodeled the tumor microenvironment and enhanced anti-tumor immunity by further increasing the infiltration and improving the function of T cells, decreasing the percentage of tumor-associated macrophages (TAMs) and inhibiting their polarization toward the M2 phenotype. [4] 7 cells promoted their polarization toward the M2 phenotype and upregulated their marker expression levels (P<0. [5] Together with the in vivo tracking of mCherry+ macrophages in zebrafish models, we confirmed that M6T treatment accelerated blood-borne macrophage infiltration and polarization toward a subset of tissue repair macrophages that expressed similar genes as microglia for neuroprotection, angiogenesis and cell migration. [6] Exposure of Treg cells to EVs results in faster proliferation, augmented production of IL-10, and polarization toward an intermediate FOXP3+RORγt+ phenotype. [7] Ex vivo primary FL-FDC co-cultures (n = 19) and in vivo mouse co-xenografts demonstrated that FL-FDC crosstalk favors tumor growth and, via the secretion of CCL2 and CSF-1, promotes monocyte recruitment, differentiation, and polarization towards an M2-like protumoral phenotype. [8] Single-cell sequencing of pressure-overloaded hearts from these mice revealed that miR-21 in macrophages is essential for their polarization toward a M1-like phenotype. [9] Single-cell RNA sequencing further revealed monocytes/macrophages with polarization toward a pro-inflammatory M1-like phenotype and increased effector function, including antiviral immunity, phagocytosis, respiratory burst, and antibody-dependent cellular cytotoxicity. [10] Even if PFC-labeling of monocytes/macrophages has been largely investigated and used, information is lacking about the impact of these agents over the polarization towards one of their cell subsets and on the best way to image them. [11] Colony-Stimulating Factor 1 (CSF1)/Colony-Stimulating Factor Receptor 1 (CSF1R) signaling orchestrates tumor-associated macrophage (TAM) recruitment and polarization towards a pro-tumor M2 phenotype, the dominant phenotype of TAMs infiltrating mesothelioma tumors. [12] Analysis of the effects of the interaction between WT cells and monocytes revealed their polarization towards alternatively activated macrophages (M2) that, in turn, further impaired NK cell functions. [13] We and others have described how matrix molecules commonly upregulated within the tumor stroma, such as tenascin-C, fibronectin and collagen, exert a complex influence over macrophage behavior, for example restricting or enhancing their infiltration into the tumor, and driving their polarization towards or away from a pro-tumoral phenotype, and how in turn macrophages can modify matrix production in the tumor to favor tumor growth and metastasis. [14]总体而言，体液和细胞免疫反应数据表明 Th1 和 Th2 免疫的诱导与抗病毒 Th1 反应的极化。 [1] 它们的激活和向促炎表型的极化与损伤和疾病有关。 [2] Sema7A 协调 MΦ 趋化性和趋化作用，激活 MΦ 分化和极化向促分解 M2 表型，并促进白细胞清除。 [3] 此外，联合疗法通过进一步增加浸润和改善 T 细胞的功能、降低肿瘤相关巨噬细胞 (TAM) 的百分比并抑制其向 M2 表型的极化来重塑肿瘤微环境并增强抗肿瘤免疫。 [4] 7个细胞促进了它们向M2表型的极化并上调了它们的标志物表达水平（P<0. [5] 结合斑马鱼模型中 mCherry+ 巨噬细胞的体内追踪，我们证实 M6T 治疗加速了血源性巨噬细胞的浸润和极化，这些巨噬细胞表达了与小胶质细胞类似的基因，用于神经保护、血管生成和细胞迁移。 [6] 将 Treg 细胞暴露于 EV 会导致更快的增殖、增加的 IL-10 的产生以及向中间 FOXP3+RORγt+ 表型的极化。 [7] 体外原代 FL-FDC 共培养 (n = 19) 和体内小鼠共异种移植物证明 FL-FDC 串扰有利于肿瘤生长，并通过分泌 CCL2 和 CSF-1 促进单核细胞募集、分化和极化朝向 M2 样前肿瘤表型。 [8] 对这些小鼠压力超负荷心脏的单细胞测序表明，巨噬细胞中的 miR-21 对于它们向 M1 样表型的极化至关重要。 [9] 单细胞 RNA 测序进一步揭示了单核细胞/巨噬细胞具有向促炎性 M1 样表型极化和增强的效应功能，包括抗病毒免疫、吞噬作用、呼吸爆发和抗体依赖性细胞毒性。 [10] 即使单核细胞/巨噬细胞的 PFC 标记已被广泛研究和使用，但仍缺乏关于这些试剂对其细胞亚群之一极化的影响以及对它们进行成像的最佳方式的信息。 [11] 集落刺激因子 1 (CSF1)/集落刺激因子受体 1 (CSF1R) 信号传导协调肿瘤相关巨噬细胞 (TAM) 的募集和向促肿瘤 M2 表型的极化，这是 TAM 浸润间皮瘤的主要表型。 [12] 对 WT 细胞和单核细胞之间相互作用的影响的分析揭示了它们向交替激活的巨噬细胞 (M2) 的极化，这反过来又进一步损害了 NK 细胞的功能。 [13] 我们和其他人已经描述了通常在肿瘤基质中上调的基质分子，如生腱蛋白-C、纤连蛋白和胶原蛋白，如何对巨噬细胞行为产生复杂的影响，例如限制或增强它们对肿瘤的浸润，并推动它们的极化朝向或远离促肿瘤表型，以及巨噬细胞如何反过来改变肿瘤中的基质产生以促进肿瘤生长和转移。 [14]
pro inflammatory phenotype 促炎表型
The process of microglia polarization towards pro-inflammatory phenotype often occurs during neuroinflammation. [1] The damaged hepatocytes then activate the mtDNA/STING pathway in KCs and trigger KCs polarization towards pro-inflammatory phenotype. [2] 1 macrophages and do not induce polarization towards the M1 pro-inflammatory phenotype. [3] Assessment of the transcriptome and proteome of CD14+-derived macrophages with further bioinformatic analysis identified the most significant differences after polarization towards the pro-inflammatory phenotype. [4] The ratio of free versus conjugated ISG15 driven by the papain-like protease (PLpro) enzyme of SARS-CoV-2 correlates with macrophage polarization toward a pro-inflammatory phenotype and attenuated antigen presentation. [5] Neutrophil infiltration and microglia/macrophage polarization toward the pro-inflammatory phenotype increased after ICH. [6]小胶质细胞向促炎表型极化的过程通常发生在神经炎症期间。 [1] 受损的肝细胞随后激活 KCs 中的 mtDNA/STING 通路，并触发 KCs 向促炎表型极化。 [2] 1 巨噬细胞并且不诱导向 M1 促炎表型极化。 [3] nan [4] nan [5] nan [6]
anti inflammatory phenotype 抗炎表型
Improved gross wound resolution observed with dHACA was accompanied by increased granulation tissue formation, proliferation and vascular ingrowth observed in the wound bed, early macrophage polarization towards anti-inflammatory phenotypes, and downregulation of pro-fibrotic gene expression. [1] Notably, the presence of platelet-T reg cell aggregates in the lung was also required for macrophage transcriptional reprogramming, polarization toward an anti-inflammatory phenotype, and effective resolution of pulmonary inflammation. [2] Taken together, these data suggest that FAAH inhibition promotes cytoskeleton reorganization, regulates phagocytosis and cell migration processes, thus driving microglial polarization towards an anti-inflammatory phenotype. [3] The chelated Mg2+ can not only activate macrophage polarization towards the anti-inflammatory phenotype but also directly stimulate the osteogenic differentiation of bone marrow-derived stem cells (BMSCs). [4] GEN treatment also regulated microglia polarization towards anti-inflammatory phenotype M2 and inhibited the production of pro-inflammatory cytokines IL-6 and TNF-α. [5]用 dHACA 观察到的改善的总伤口分辨率伴随着伤口床中观察到的肉芽组织形成、增殖和血管向内生长、早期巨噬细胞极化向抗炎表型以及促纤维化基因表达的下调。 [1] 值得注意的是，肺中存在血小板-T reg 细胞聚集体也是巨噬细胞转录重编程、抗炎表型极化和肺部炎症有效消退所必需的。 [2] nan [3] nan [4] nan [5]
bone marrow derived 骨髓来源
Here, we report that macrophage-specific deletion of the SUMO-specific protease SENP3 promotes macrophage polarization towards M2 in bone-marrow-derived macrophage (BMDM) induced by IL4/IL13 and in an ex vivo model (murine Py8119 cell line), as well as in a mouse orthotopic tumor model. [1] We showed that bone marrow-derived macrophages from huCETP mice reduce polarization toward the M1 phenotype, but with increased IL-10. [2] In vitro co-culture experiments showed that EOS shifted bone marrow-derived macrophage polarization towards the CD206+ phenotypes. [3] In isolated mouse bone marrow-derived macrophages, pretreatment with riclinoctaose promoted the macrophage polarization toward M2-like phenotype. [4]在这里，我们报告在由 IL4/IL13 和离体模型（鼠 Py8119 细胞系）诱导的骨髓衍生巨噬细胞 (BMDM) 中，巨噬细胞特异性缺失 SUMO 特异性蛋白酶 SENP3 促进巨噬细胞向 M2 极化，如以及在小鼠原位肿瘤模型中。 [1] 我们发现来自 huCETP 小鼠的骨髓来源的巨噬细胞减少了向 M1 表型的极化，但增加了 IL-10。 [2] nan [3] nan [4]
Macrophage Polarization Toward 巨噬细胞极化
In the mouse model, we then found that Ac2-26 administered at the start of reperfusion shifted microglia/macrophage polarization toward anti-inflammatory M2-phenotype in ischemic penumbra, thus alleviating blood–brain barrier leakage and neuronal apoptosis and improving outcomes at 3 days post-tMCAO/R. [1] LPS-induced SMAR1 expression decreases STAT3 expression and also skews the macrophage polarization towards M1 phenotype. [2] Moreover, specifically designed scaffolds used within the present thesis showed auspicious design criteria positively influencing the macrophage polarization towards the anti-inflammatory, pro-healing type and might be adaptable to other biomaterials in future approaches. [3] CRC exosomes-derived circ_0125473 drived macrophages polarization towards M2 through miR-5787/Wnt1/β-catenin signaling pathway. [4] GDNF treatment could facilitate the macrophages polarization towards the M2-like phenotype in DSS-treated mice and LPS-stimulated RAW264. [5] There was no difference on monocyte derived macrophage polarization towards pro-inflammatory M1 or anti-inflammatory M2 on PEEUm and PEEUm + E. [6] Results: A significant shift of macrophage polarization towards M1 was observed in skin, spleen and lung tissue of animals, with and without surgical trauma, treated with BP when compared to those without BP application. [7] A total of 81 cyclic sulfur compounds were screened, and their effects on macrophage polarization toward an M2-like phenotype were tested using human monocyte-derived macrophages (HMDMs). [8] We screened and identified an anti-ChemR23 mAb which induces RvE1-like Akt and ERK signaling in mouse and human macrophages and favors macrophage polarization towards a pro-resolutive phenotype. [9] Results ADM2 treatment reversed AGE-induced M1 macrophage polarization towards the M2 phenotype, which was partially achieved by the peroxisome proliferator-activated receptor γ (PPARγ)-mediated inhibition of NF-κB signaling. [10] Following IRI, old kidney showed increased macrophage polarization toward M1 inflammatory phenotype, cytokine upregulation, endothelial-mesenchymal transition, and fibrosis compared to young kidney. [11] Macrophage polarization toward M1 phenotype (pro-inflammation) is closely associated with the destructive phase of periodontal inflammation. [12] Results show that chitosan-ending capsules, as well as the presence of MSCs, favor the balance of macrophage polarization toward a more regenerative profile, through the up-regulation of anti-inflammatory markers, and the release of pro-regenerative cytokines. [13] Here, we report that macrophage-specific deletion of the SUMO-specific protease SENP3 promotes macrophage polarization towards M2 in bone-marrow-derived macrophage (BMDM) induced by IL4/IL13 and in an ex vivo model (murine Py8119 cell line), as well as in a mouse orthotopic tumor model. [14] In addition, an in vitro study discovered that bFGF-HDC@Fe3O4 could promote macrophage polarization toward an anti-inflammatory (pro-healing) M2 phenotype especially under eMF. [15] IRF5 promoted macrophage polarization towards M1-phenotype and secretion of inflammatory factors. [16] The specific deletion of Sema3A in keratinocytes alleviated Ni allergy and regulated the macrophage polarization towards an anti-inflammatory direction. [17] Macrophage polarization toward M1 and M2 subtypes mediate pro-inflammatory and anti-inflammatory responses, respectively, which are crucial for bone repairing at different stages. [18] We found that H/SD reduced BMSC viability and migration, increased BMSC apoptosis, and induced macrophage polarization toward the M1 phenotype. [19] Mesenchymal stem cells (MSCs) have been widely studied as a versatile cell source for tissue regeneration and remodeling due to their potent bioactivity, which includes modulation of inflammation response, macrophage polarization toward proregenerative lineage, promotion of angiogenesis, and reduction in fibrosis. [20] Moreover, IRF4 knockout driven the macrophage polarization toward M1phenotype at 8 h after stroke. [21] Improved gross wound resolution observed with dHACA was accompanied by increased granulation tissue formation, proliferation and vascular ingrowth observed in the wound bed, early macrophage polarization towards anti-inflammatory phenotypes, and downregulation of pro-fibrotic gene expression. [22] These effects of reduced calpain expression or activity were associated with prevention of macrophage polarization toward M1 phenotype and consequent reduced production of pro-inflammatory cytokines including TNF-α, IL-12 and IL-23 in lung tissues of Capns1-ko mice with SSc. [23] ST8Sia6 expression on tumors also altered macrophage polarization toward M2, including upregulation of the immune modulator arginase, which also required Siglec-E. [24] In vitro co-culture experiments showed that ADRCs induced macrophage polarization toward M2. [25] In vitro co-culture experiments showed that EOS shifted bone marrow-derived macrophage polarization towards the CD206+ phenotypes. [26] In vivo results showed increased macrophage polarization toward the M2 phenotype, IL-10 expression, regenerated bone and fibrocartilage at the patella-patellar tendon interface of animals received MSCS modified ATS implantation. [27] Results We observed macrophage polarization towards the M2 phenotype in the peripheral blood of HSP rats. [28] CONCLUSIONS In DIOS, macrophage polarization toward the M2 alternative phenotype is impaired but not associated with a pro-inflammatory profile. [29] Furthermore, we discuss therapeutic strategies which utilize macrophage polarization towards an anti-inflammatory or reparative phenotype for the treatment of myocardial infarction. [30] These results indicate that NK-4 drives macrophage polarization toward an inflammatory M1-like phenotype with increased phagocytic activity. [31] Probiotic V and Met also promoted macrophage polarization towards the M2 phenotype in ethanol-exposed RAW 264. [32] Results: The macrophage polarization toward the M2 phenotype was observed inperipheral blood from HSP rats. [33] MSCs and miR-466 promoted macrophage polarization toward Type 2 phenotype through TIRAP-MyD88-NFκB axis. [34] We previously demonstrated that PGE2 leads to macrophage polarization toward the M1 phenotype and stimulates inflammasome activation in infected macrophages. [35] Finally, secreted MIF from autophagy deficient 66 cl4 cells induced macrophage polarization towards the M1 subtype. [36] In particular, we provide examples of the most recent biomimetic platforms proposed to accomplish this goal, with an emphasis on those able to induce macrophage polarization towards a pro-regenerative phenotype. [37] Heme oxygenase-1 (HO-1) plays a crucial role in macrophage polarization toward M2 phenotype, but its prognosis significance in NPC has been rarely determined. [38] In vitro experiment with primary macrophages demonstrated that deletion of the TF cytoplasmic domain inhibited macrophage polarization toward the M1 phenotype. [39] PRRSV infection skews macrophage polarization toward an M2 phenotype, followed by T-cells inactivation. [40] AGEs in diabetes accelerate atherosclerotic plaque initiation and progression via promoting macrophages polarization towards pro-inflammatory state. [41] This puts into context our observation that estrogens (E2) working through the estrogen receptor (ERα) stimulate melanoma growth in murine models by skewing macrophage polarization towards an immune-suppressive state that promotes CD8+ T cell dysfunction/exhaustion and ICB resistance. [42] The ratio of free versus conjugated ISG15 driven by the papain-like protease (PLpro) enzyme of SARS-CoV-2 correlates with macrophage polarization toward a pro-inflammatory phenotype and attenuated antigen presentation. [43] Thus, rocaglates represent a novel class of immunomodulators that can direct macrophage polarization toward the M1-like phenotype in complex microenvironments associated with hypofunction of type 1 and/or hyperactivation of type 2 immunity, e. [44] Furthermore, ZT01 significantly inhibited T cell differentiation into Th1 and/or Th17 cell subsets and macrophage polarization towards into an inflammatory phenotype via regulating the JAK-STAT signaling pathway. [45] The signaling mechanisms that promote M2-like macrophage polarization toward CaOx nephrocalcinosis, include the NLRP3, PPARγ-miR-23-Irf1/Pknox1, miR-93-TLR4/IRF1, and miR-185-5p/CSF1 pathways. [46] HR treatment induced macrophage polarization towards the M1 phenotype, which mediated CM pyroptosis through exosomal miR-29a transfer by targeting MCL-1. [47] Finally, the implantation of an LNEM hydrogel in a mouse volumetric muscle loss model facilitates the recruitment of host macrophages to the site of injury and enhances macrophage polarization toward the M2 phenotype for tissue healing in vivo. [48] CGF extract also promoted THP-1 macrophage polarization toward the M2 phenotype with upregulated CD163 expression, as detected by cell morphology and surface marker expression. [49] Overexpression of KLF6 recused miR-200b-induced macrophage polarization toward M2, and the inhibitory effect of miR-200b on M1 polarization. [50]在小鼠模型中，我们随后发现在再灌注开始时给予 Ac2-26 将小胶质细胞/巨噬细胞极化转变为缺血半暗带中的抗炎 M2 表型，从而减轻血脑屏障渗漏和神经元凋亡并改善 3 天的结果后 tMCAO/R。 [1] LPS 诱导的 SMAR1 表达降低了 STAT3 的表达，并且还使巨噬细胞极化向 M1 表型倾斜。 [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] 在这里，我们报告在由 IL4/IL13 和离体模型（鼠 Py8119 细胞系）诱导的骨髓衍生巨噬细胞 (BMDM) 中，巨噬细胞特异性缺失 SUMO 特异性蛋白酶 SENP3 促进巨噬细胞向 M2 极化，如以及在小鼠原位肿瘤模型中。 [14] nan [15] nan [16] nan [17] nan [18] nan [19] nan [20] nan [21] 用 dHACA 观察到的改善的总伤口分辨率伴随着伤口床中观察到的肉芽组织形成、增殖和血管向内生长、早期巨噬细胞极化向抗炎表型以及促纤维化基因表达的下调。 [22] nan [23] 肿瘤上的 ST8Sia6 表达也改变了巨噬细胞向 M2 的极化，包括免疫调节剂精氨酸酶的上调，这也需要 Siglec-E。 [24] nan [25] nan [26] nan [27] nan [28] nan [29] nan [30] nan [31] nan [32] nan [33] nan [34] nan [35] nan [36] nan [37] nan [38] nan [39] nan [40] nan [41] nan [42] nan [43] nan [44] nan [45] nan [46] nan [47] nan [48] nan [49] nan [50]
Microglial Polarization Toward 小胶质细胞极化
The immune tolerance state was evident by microglial polarization towards non-reactive M2 state, lower astrocyte activation, epigenetic reprogramming, and decreased neurodegeneration. [1] Furthermore, JWH133 drove microglial polarization toward the protective M2 phenotype and modulated the redistribution of microglia in the striatum. [2] Furthermore, JWH133 drove microglial polarization toward the protective M2 phenotype and modulated the redistribution of microglia in the striatum. [3] Mechanistically, CBR1 decreased the levels of 4-HNE in the brain after stroke; it also modulated microglial polarization toward the M2 phenotype, which was well-known to confer neuroprotection after ischemic injury. [4] Therefore, ways to promote microglial polarization toward M2 phenotype after stroke have become the focus of attention in recent years. [5] Taken together, these data suggest that FAAH inhibition promotes cytoskeleton reorganization, regulates phagocytosis and cell migration processes, thus driving microglial polarization towards an anti-inflammatory phenotype. [6] Thus, manipulating microglial polarization towards the M2 phenotype is a promising therapeutic approach for CNS repair and regeneration. [7] CONCLUSIONS Our findings demonstrate that HLYND mitigates cognitive impairment after chronic cerebral hypoperfusion in rats through mechanisms involving increased neuronal plasticity and white matter remyelination, with a subtile modulation of macrophage/microglial polarization toward the M2 phenotype. [8] PBM reduced reactive gliosis and inflammation, and shifted microglial polarization toward an antiinflammatory phenotype, all the while preventing mitochondrial dysfunction. [9]免疫耐受状态通过小胶质细胞极化向非反应性 M2 状态、较低的星形胶质细胞活化、表观遗传重编程和减少的神经退行性变明显。 [1] 此外，JWH133 驱动小胶质细胞向保护性 M2 表型极化，并调节小胶质细胞在纹状体中的重新分布。 [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9]
Cell Polarization Toward 细胞极化
In NAFLD progression, MIF contributes to liver fibrogenesis skewing NKT cell polarization toward a pro-fibrotic phenotype highlighting the complex, context-dependent role of MIF during chronic liver injury. [1] Background Phorbol 12-myristate 13-acetate (PMA)-induced differentiation of human monocytic THP-1 cells is an experimental model for preparing resting macrophages (M0) for cell polarization toward the different functional specializations of macrophages. [2] In vitro maturation confirmed that the collagen and ELR provided a favorable environment for the HDFn viability, while histology revealed the wavy and homogenous morphology of the ELR and collagen layer respectively, the cell polarization towards the cell-attachment sites encoded on the ELR, and the enhanced expression of glycosaminoglycan-rich extracellular matrix and differentiation of the embedded HDFn into myofibroblasts. [3] We found that TIMP1 and TIMP2 were effective in interfering with TGFβ induced NK cell polarization towards a decidual-like-phenotype. [4] Exogenous 14-3-3ζ promoted PBMC proliferation and T cell polarization toward Th1 and Th17 populations. [5] In contrast, GPBAR1 agonism rescued wild-type mice from acute liver damage and redirects the NKT cells polarization toward a NKT10, a regulatory, IL-10 secreting, type I NKT cell subset. [6]在 NAFLD 进展中，MIF 有助于肝纤维化，使 NKT 细胞极化向促纤维化表型倾斜，突出了 MIF 在慢性肝损伤过程中复杂的、依赖于环境的作用。 [1] 背景佛波醇 12-肉豆蔻酸酯 13-乙酸 (PMA) 诱导的人单核细胞 THP-1 细胞分化是一种实验模型，用于制备静息巨噬细胞 (M0) 以使细胞极化朝向巨噬细胞的不同功能特化。 [2] nan [3] nan [4] nan [5] nan [6]
Microglium Polarization Toward 小胶质细胞极化
However, both compounds contributed to the microglia polarization towards the M2-phenotype. [1] The process of microglia polarization towards pro-inflammatory phenotype often occurs during neuroinflammation. [2] Intraperitoneal administration of the NK1R selective antagonist, Aprepitant, significantly improved neurobehavior, reduced hematoma volume and hemoglobin levels after ICH, and promoted microglia polarization towards M2 phenotype. [3] Moreover, the detailed mechanism of ischemic stroke therapy via MPBzyme@NCM uptake by microglia was further studied, including microglia polarization toward M2, reduced recruitment of neutrophils, decreased apoptosis of neurons, and proliferation of neural stem cells, neuronal precursors, and neurons. [4] GEN treatment also regulated microglia polarization towards anti-inflammatory phenotype M2 and inhibited the production of pro-inflammatory cytokines IL-6 and TNF-α. [5]然而，这两种化合物都有助于小胶质细胞向 M2 表型极化。 [1] 小胶质细胞向促炎表型极化的过程通常发生在神经炎症期间。 [2] nan [3] nan [4] nan [5]
Monocyte Polarization Toward 单核细胞极化
This study provides new molecular insights into an evolutionary mismatch and uncovers new pathways through which Western diets alter monocyte polarization toward a proinflammatory phenotype. [1] In the tumor microenvironment, tumor-derived factors induce monocyte polarization towards a pro-tumor phenotype. [2]这项研究为进化错配提供了新的分子见解，并揭示了西方饮食改变单核细胞极化向促炎表型的新途径。 [1] 在肿瘤微环境中，肿瘤衍生因子诱导单核细胞极化朝向促肿瘤表型。 [2]
Centrosome Polarization Toward 中心体极化
We demonstrated that BBS1 allows for centrosome polarization towards the immune synapse. [1] We demonstrate that BBS1 allows for centrosome polarization towards the immune synapse. [2]我们证明了 BBS1 允许中心体极化向免疫突触。 [1] 我们证明 BBS1 允许中心体极化朝向免疫突触。 [2]
Induce Polarization Toward 诱导极化
1 macrophages and do not induce polarization towards the M1 pro-inflammatory phenotype. [1] During earlier studies we reported that LPA treatment of microglia induces polarization towards a neurotoxic phenotype. [2]1 巨噬细胞并且不诱导向 M1 促炎表型极化。 [1] 在早期的研究中，我们报道了 LPA 对小胶质细胞的治疗会导致极化向神经毒性表型。 [2]
polarization toward m1 向 M1 极化
Single-walled CNT (SWCNT), short-type multi-walled CNT (MWCNT), and long-type MWCNT exposure at dose of 50 µg/ml promote AMs polarization toward M1 phenotype at early stage, while promote AMs polarization toward M2 phenotype at late stage. [1] However, no polarization toward M1 or M2 was observed in macrophages exposed to EVs. [2] Macrophage infiltration and polarization toward M1-phenotype increases the risk of aneurysm rupture. [3] Following IRI, old kidney showed increased macrophage polarization toward M1 inflammatory phenotype, cytokine upregulation, endothelial-mesenchymal transition, and fibrosis compared to young kidney. [4] Macrophage polarization toward M1 phenotype (pro-inflammation) is closely associated with the destructive phase of periodontal inflammation. [5] Macrophage polarization toward M1 and M2 subtypes mediate pro-inflammatory and anti-inflammatory responses, respectively, which are crucial for bone repairing at different stages. [6] These effects of reduced calpain expression or activity were associated with prevention of macrophage polarization toward M1 phenotype and consequent reduced production of pro-inflammatory cytokines including TNF-α, IL-12 and IL-23 in lung tissues of Capns1-ko mice with SSc. [7] In particular, HANPs synergize with LPS to promote macrophage polarization toward M1 phenotype. [8] ELISA and confocal microscopy assay confirmed that baicalein significantly induced the production of TNF-α and the activation of NF-κB, while TNF-α neutralization inhibited baicalein-induced macrophage polarization toward M1, and NF-κB P65 knock-down suppressed baicalein-induced TNF-α production in THP-1-derived macrophages. [9] We found LPS-pretreated HPDLF induced macrophage polarization toward M1 phenotype. [10] IFN-γ and/or LPS was used to activate macrophages and M2 polarization toward M1 macrophages. [11] Bacillus Calmette-Guérin (BCG) immunotherapy increases macrophage polarization toward M1-type macrophages. [12] Taken together, we conclude that Cd activates the oxidative stress-mediated TLR4/NF-κB/NLRP3 inflammatory signal transduction, leading to porcine adrenal fibrosis by promoting macrophage polarization toward M1. [13] Conclusion: Monocytes subpopulation disequilibrium toward intermediate and nonclassic phenotypes and macrophage polarization toward M1 phenotype with increased proinflammatory cytokine release are more likely to be found in CD patients with depressive symptoms. [14] Taken together, these findings indicated that HDND-12 could prevent polarization toward M1-like macrophages, at least in part, through modulating JAK2/STAT3 pathway. [15]单壁碳纳米管 (SWCNT)、短型多壁碳纳米管 (MWCNT) 和长型多壁碳纳米管暴露在 50 μg/ml 的剂量下促进 AMs 极化在早期向 M1 表型，同时促进 AMs 向 M2 表型极化后期。 [1] 然而，在暴露于 EV 的巨噬细胞中没有观察到 M1 或 M2 的极化。 [2] 巨噬细胞浸润和向 M1 表型极化增加了动脉瘤破裂的风险。 [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] nan [14] nan [15]