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Добірка наукової літератури з теми "Macrophages M2-Like"

Автор: Grafiati

Опубліковано: 20 квітня 2024

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Статті в журналах з теми "Macrophages M2-Like"

Wen, Zhifa, Hongxiang Liu, Meng Zhou, and Li-xin Wang. "Tumor released autophagosomes regulate M2-like macrophage polarization (TUM6P.974)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 141.22. http://dx.doi.org/10.4049/jimmunol.194.supp.141.22.

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Abstract Tumor cells secrete mediators that modulate macrophage activation and polarization into M2 type tumor associated macrophages (TAMs), which contribute to tumor progression. However, the mechanisms that regulate the polarization are poorly defined. We have previously reported that the enrichment of autophagosomes in tumor cell conditioned medium and malignant ascites from patients. The present study investigated the hypothesis that tumor released autophagosomes promoted M2 polarization. Here we isolated autophagosomes released from murine liver cancer cells using affinity purification. In vivo mouse experiments demonstrated that intraperitoneal injected autophagosomes were efficiently internalized by peritoneal macrophages, which correlated with upregulation of M2 markers. In vitro, coculture of autophagosomes with bone marrow-derived macrophages (BMDMs) also induced macrophage polarization into a M2-like phenotype. Furthmore, this effect of autophagosomes was largely abolished in BMDMs from MyD88 KO mice. Taken together, our findings suggest that, under stress conditions, tumor released autophagosomes may promote tumor progression via regulation of TAMs in tumor microenvironment, providing new insight into TAMs polarization. Keywords: Tumor released autophagosomes, Macrophage, Polarization, MyD88.

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Draijer, Christina, Patricia Robbe, Carian E. Boorsma, Machteld N. Hylkema, and Barbro N. Melgert. "Characterization of Macrophage Phenotypes in Three Murine Models of House-Dust-Mite-Induced Asthma." Mediators of Inflammation 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/632049.

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In asthma, an important role for innate immunity is increasingly being recognized. Key innate immune cells in the lungs are macrophages. Depending on the signals they receive, macrophages can at least have an M1, M2, or M2-like phenotype. It is unknown how these macrophage phenotypes behave with regard to (the severity of) asthma. We have quantified the phenotypes in three models of house dust mite (HDM-)induced asthma (14, 21, and 24 days). M1, M2, and M2-like phenotypes were identified by interferon regulatory factor 5 (IRF5), YM1, and IL-10, respectively. We found higher percentages of eosinophils in HDM-exposed mice compared to control but no differences between HDM models. T cell numbers were higher after HDM exposure and were the highest in the 24-day HDM protocol. Higher numbers of M2 macrophages after HDM correlated with higher eosinophil numbers. In mice with less severe asthma, M1 macrophage numbers were higher and correlated negatively with M2 macrophages numbers. Lower numbers of M2-like macrophages were found after HDM exposure and these correlated negatively with M2 macrophages. The balance between macrophage phenotypes changes as the severity of allergic airway inflammation increases. Influencing this imbalanced relationship could be a novel approach to treat asthma.

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Lalor, Richard, та Sandra O’Neill. "Bovine κ-Casein Fragment Induces Hypo-Responsive M2-Like Macrophage Phenotype". Nutrients 11, № 7 (23 липня 2019): 1688. http://dx.doi.org/10.3390/nu11071688.

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Immunomodulatory nutraceuticals have garnered special attention due to their therapeutic potential for the amelioration of many chronic inflammatory conditions. Macrophages are key players in the induction, propagation and resolution of inflammation, actively contributing to the pathogenesis and resolution of inflammatory disorders. As such, this study aimed to investigate the possible therapeutic effects bovine casein derived nutraceuticals exert on macrophage immunological function. Initial studies demonstrated that sodium caseinate induced a M2-like macrophage phenotype that was attributed to the kappa-casein subunit. Kappa-casein primed macrophages acquired a M2-like phenotype that expressed CD206, CD54, OX40L, CD40 on the cell surface and gene expression of Arg-1, RELM-α and YM1, archetypical M2 markers. Macrophages stimulated with kappa-casein secreted significantly reduced TNF-α and IL-10 in response to TLR stimulation through a mechanism that targeted the nuclear factor-κB signal transduction pathway. Macrophage proteolytic processing of kappa-casein was required to elicit these suppressive effects, indicating that a fragment other than C-terminal fragment, glycomacropeptide, induced these modulatory effects. Kappa-casein treated macrophages also impaired T-cell responses. Given the powerful immuno-modulatory effects exhibited by kappa-casein and our understanding of immunopathology associated with inflammatory diseases, this fragment has the potential as an oral nutraceutical and therefore warrants further investigation.

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Lyu, Qingkang, Edwin J. A. Veldhuizen, Irene S. Ludwig, Victor P. M. G. Rutten, Willem van Eden, Alice J. A. M. Sijts, and Femke Broere. "Characterization of polarization states of canine monocyte derived macrophages." PLOS ONE 18, no. 11 (November 8, 2023): e0292757. http://dx.doi.org/10.1371/journal.pone.0292757.

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Macrophages can reversibly polarize into multiple functional subsets depending on their micro-environment. Identification and understanding the functionality of these subsets is relevant for the study of immune‑related diseases. However, knowledge about canine macrophage polarization is still in its infancy. In this study, we polarized canine monocytes using GM-CSF/IFN- γ and LPS towards M1 macrophages or M-CSF and IL-4 towards M2 macrophages and compared them to undifferentiated monocytes (M0). Polarized M1 and M2 macrophages were thoroughly characterized for morphology, surface marker features, gene profiles and functional properties. Our results showed that canine M1-polarized macrophages obtained a characteristic large, roundish, or amoeboid shape, while M2-polarized macrophages were smaller and adopted an elongated spindle-like morphology. Phenotypically, all macrophage subsets expressed the pan-macrophage markers CD14 and CD11b. M1-polarized macrophages expressed increased levels of CD40, CD80 CD86 and MHC II, while a significant increase in the expression levels of CD206, CD209, and CD163 was observed in M2-polarized macrophages. RNAseq of the three macrophage subsets showed distinct gene expression profiles, which are closely associated with immune responsiveness, cell differentiation and phagocytosis. However, the complexity of the gene expression patterns makes it difficult to assign clear new polarization markers. Functionally, undifferentiated -monocytes, and M1- and M2- like subsets of canine macrophages can all phagocytose latex beads. M2-polarized macrophages exhibited the strongest phagocytic capacity compared to undifferentiated monocytes- and M1-polarized cells. Taken together, this study showed that canine M1 and M2-like macrophages have distinct features largely in parallel to those of well-studied species, such as human, mouse and pig. These findings enable future use of monocyte derived polarized macrophages particularly in studies of immune related diseases in dogs.

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Sánchez-Reyes, Karina, Alejandro Bravo-Cuellar, Georgina Hernández-Flores, José Manuel Lerma-Díaz, Luis Felipe Jave-Suárez, Paulina Gómez-Lomelí, Ruth de Celis, Adriana Aguilar-Lemarroy, Jorge Ramiro Domínguez-Rodríguez, and Pablo Cesar Ortiz-Lazareno. "Cervical Cancer Cell Supernatants Induce a Phenotypic Switch from U937-Derived Macrophage-Activated M1 State into M2-Like Suppressor Phenotype with Change in Toll-Like Receptor Profile." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/683068.

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Cervical cancer (CC) is the second most common cancer among women worldwide. Infection with human papillomavirus (HPV) is the main risk factor for developing CC. Macrophages are important immune effector cells; they can be differentiated into two phenotypes, identified as M1 (classically activated) and M2 (alternatively activated). Macrophage polarization exerts profound effects on the Toll-like receptor (TLR) profile. In this study, we evaluated whether the supernatant of human CC cells HeLa, SiHa, and C-33A induces a shift of M1 macrophage toward M2 macrophage in U937-derived macrophages.Results. The results showed that soluble factors secreted by CC cells induce a change in the immunophenotype of macrophages from macrophage M1 into macrophage M2. U937-derived macrophages M1 released proinflammatory cytokines and nitric oxide; however, when these cells were treated with the supernatant of CC cell lines, we observed a turnover of M1 toward M2. These cells increased CD163 and IL-10 expression. The expression of TLR-3, -7, and -9 is increased when the macrophages were treated with the supernatant of CC cells.Conclusions. Our result strongly suggests that CC cells may, through the secretion of soluble factors, induce a change of immunophenotype M1 into M2 macrophages.

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Zhu, Wenya, Qianqian Chen, Yi Li, Jun Wan, Jia Li та Shuai Tang. "HIF-1α-Overexpressing Mesenchymal Stem Cells Attenuate Colitis by Regulating M1-like Macrophages Polarization toward M2-like Macrophages". Biomedicines 11, № 3 (8 березня 2023): 825. http://dx.doi.org/10.3390/biomedicines11030825.

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A modified mesenchymal stem cell (MSC) transplantation is a highly effective and precise treatment for inflammatory bowel disease (IBD), with a significant curative effect. Thus, we aim to examine the efficacy of hypoxia-inducible factor (HIF)–1α-overexpressing MSC (HIF-MSC) transplantation in experimental colitis and investigate the immunity regulation mechanisms of HIF-MSC through macrophages. A chronic experimental colitis mouse model was established using 2,4,6-trinitrobenzene sulfonic acid. HIF-MSC transplantation significantly attenuated colitis in weight loss rate, disease activity index (DAI), colon length, and pathology score and effectively rebuilt the local and systemic immune balance. Macrophage depletion significantly impaired the benefits of HIF-MSCs on mice with colitis. Immunofluorescence analysis revealed that HIF-MSCs significantly decreased the number of M1-like macrophages and increased the number of M2-like macrophages in colon tissues. In vitro, co-culturing with HIF-MSCs significantly decreased the expression of pro-inflammatory factors, C-C chemokine receptor 7 (CCR-7), and inducible nitric oxide synthase (INOS) and increased the expression of anti-inflammatory factors and arginase I (Arg-1) in induced M1-like macrophages. Flow cytometry revealed that co-culturing with HIF-MSCs led to a decrease in the proportions of M1-like macrophages and an increase in that of M2-like macrophages. HIF-MSCs treatment notably upregulated the expression of downstream molecular targets of phosphatidylinositol 3-kinase-γ (PI3K-γ), including HIF-1α and p-AKT/AKT in the colon tissue. A selected PI3K-γ inhibitor, IPI549, attenuated these effects, as well as the effect on M2-like macrophage polarization and inflammatory cytokines in colitis mice. In vitro, HIF-MSCs notably upregulated the expression of C/EBPβ and AKT1/AKT2, and PI3K-γ inhibition blocked this effect. Modified MSCs stably overexpressed HIF-1α, which effectively regulated macrophage polarization through PI3K-γ. HIF-MSC transplantation may be a potentially effective precision therapy for IBD.

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Strizova, Zuzana, Iva Benesova, Robin Bartolini, Rene Novysedlak, Eva Cecrdlova, Lily Koumbas Foley, and Ilja Striz. "M1/M2 macrophages and their overlaps – myth or reality?" Clinical Science 137, no. 15 (August 2023): 1067–93. http://dx.doi.org/10.1042/cs20220531.

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Abstract Macrophages represent heterogeneous cell population with important roles in defence mechanisms and in homoeostasis. Tissue macrophages from diverse anatomical locations adopt distinct activation states. M1 and M2 macrophages are two polarized forms of mononuclear phagocyte in vitro differentiation with distinct phenotypic patterns and functional properties, but in vivo, there is a wide range of different macrophage phenotypes in between depending on the microenvironment and natural signals they receive. In human infections, pathogens use different strategies to combat macrophages and these strategies include shaping the macrophage polarization towards one or another phenotype. Macrophages infiltrating the tumours can affect the patient’s prognosis. M2 macrophages have been shown to promote tumour growth, while M1 macrophages provide both tumour-promoting and anti-tumour properties. In autoimmune diseases, both prolonged M1 activation, as well as altered M2 function can contribute to their onset and activity. In human atherosclerotic lesions, macrophages expressing both M1 and M2 profiles have been detected as one of the potential factors affecting occurrence of cardiovascular diseases. In allergic inflammation, T2 cytokines drive macrophage polarization towards M2 profiles, which promote airway inflammation and remodelling. M1 macrophages in transplantations seem to contribute to acute rejection, while M2 macrophages promote the fibrosis of the graft. The view of pro-inflammatory M1 macrophages and M2 macrophages suppressing inflammation seems to be an oversimplification because these cells exploit very high level of plasticity and represent a large scale of different immunophenotypes with overlapping properties. In this respect, it would be more precise to describe macrophages as M1-like and M2-like.

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Li, Dezhi, Min Yan, Fengfei Sun, Junmei Song, Xingsheng Hu, Sijia Yu, Lina Tang, and Shishan Deng. "miR-498 inhibits autophagy and M2-like polarization of tumor-associated macrophages in esophageal cancer via MDM2/ATF3." Epigenomics 13, no. 13 (July 2021): 1013–30. http://dx.doi.org/10.2217/epi-2020-0341.

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Structured abstract Aim: To elucidate the effect of miRNA (miR)-498 on autophagy and M2-like macrophage polarization in esophageal cancer. Methods: Autophagy was evaluated in esophageal cancer. Macrophage markers specific for M1- or M2-like phenotype were determined. The binding relationships between miR-498 and MDM2, MDM2 and ATF3 were analyzed. Results: miR-498 was downregulated in esophageal cancer and was associated with disease-free and overall patient survival. Enhanced miR-498 reduced LC3I conversion to LC3II and increased p62 accumulation in KYSE-150 cells, and increased macrophage polarization to M2-like phenotype in KYSE-150 and TAM co-culture. miR-498 inhibited MDM2-mediated ATF3 degradation, thus suppressing autophagy and M2-like polarization of macrophages in esophageal cancer. Conclusion: miR-498 may inhibit autophagy and M2-like polarization of macrophages to suppress esophageal cancer via MDM2/ATF3.

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Ronaghan, Natalie J., Mandy Soo, Uriel Pena, Marisa Tellis, Wenming Duan, Nooshin Tabatabaei-Zavareh, Philipp Kramer, Juan Hou, and Theo J. Moraes. "M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion." PLOS ONE 17, no. 10 (October 13, 2022): e0276013. http://dx.doi.org/10.1371/journal.pone.0276013.

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Respiratory syncytial virus (RSV) is a common childhood infection that in young infants can progress into severe bronchiolitis and pneumonia. Disease pathogenesis results from both viral mediated and host immune processes of which alveolar macrophages play an important part. Here, we investigated the role of different types of alveolar macrophages on RSV infection using an in vitro co-culture model involving primary tissue-derived human bronchial epithelial cells (HBECs) and human blood monocyte-derived M0-like, M1-like, or M2-like macrophages. It was hypothesized that the in vitro model would recapitulate previous in vivo findings of a protective effect of macrophages against RSV infection. It was found that macrophages maintained their phenotype for the 72-hour co-culture time period and the bronchial epithelial cells were unaffected by the macrophage media. HBEC infection with RSV was decreased by M1-like macrophages but enhanced by M0- or M2-like macrophages. The medium used during the co-culture also impacted the outcome of the infection. This work demonstrates that alveolar macrophage phenotypes may have differential roles during epithelial RSV infection, and demonstrates that an in vitro co-culture model could be used to further investigate the roles of macrophages during bronchial viral infection.

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Di Martile, Marta, Valentina Farini, Francesca Maria Consonni, Daniela Trisciuoglio, Marianna Desideri, Elisabetta Valentini, Simona D'Aguanno, et al. "Melanoma-specific bcl-2 promotes a protumoral M2-like phenotype by tumor-associated macrophages." Journal for ImmunoTherapy of Cancer 8, no. 1 (April 2020): e000489. http://dx.doi.org/10.1136/jitc-2019-000489.

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BackgroundA bidirectional crosstalk between tumor cells and the surrounding microenvironment contributes to tumor progression and response to therapy. Our previous studies have demonstrated that bcl-2 affects melanoma progression and regulates the tumor microenvironment. The aim of this study was to evaluate whether bcl-2 expression in melanoma cells could influence tumor-promoting functions of tumor-associated macrophages, a major constituent of the tumor microenvironment that affects anticancer immunity favoring tumor progression.MethodsTHP-1 monocytic cells, monocyte-derived macrophages and melanoma cells expressing different levels of bcl-2 protein were used. ELISA, qRT-PCR and Western blot analyses were used to evaluate macrophage polarization markers and protein expression levels. Chromatin immunoprecipitation assay was performed to evaluate transcription factor recruitment at specific promoters. Boyden chamber was used for migration experiments. Cytofluorimetric and immunohistochemical analyses were carried out to evaluate infiltrating macrophages and T cells in melanoma specimens from patients or mice.ResultsHigher production of tumor-promoting and chemotactic factors, and M2-polarized activation was observed when macrophages were exposed to culture media from melanoma cells overexpressing bcl-2, while bcl-2 silencing in melanoma cells inhibited the M2 macrophage polarization. In agreement, the number of melanoma-infiltrating macrophages in vivo was increased, in parallel with a greater expression of bcl-2 in tumor cells. Tumor-derived interleukin-1β has been identified as the effector cytokine of bcl-2-dependent macrophage reprogramming, according to reduced tumor growth, decreased number of M2-polarized tumor-associated macrophages and increased number of infiltrating CD4+IFNγ+and CD8+IFNγ+effector T lymphocytes, which we observed in response to in vivo treatment with the IL-1 receptor antagonist kineret. Finally, in tumor specimens from patients with melanoma, high bcl-2 expression correlated with increased infiltration of M2-polarized CD163+macrophages, hence supporting the clinical relevance of the crosstalk between tumor cells and microenvironment.ConclusionsTaken together, our results show that melanoma-specific bcl-2 controls an IL-1β-driven axis of macrophage diversion that establishes tumor microenvironmental conditions favoring melanoma development. Interfering with this pathway might provide novel therapeutic strategies.

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Більше джерел

Дисертації з теми "Macrophages M2-Like"

Eisel, David [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "Reprogramming of M2-like macrophages by CD4+ T cells, transcription factor knockdown and miRNA transfection / David Eisel ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1213029317/34.

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Abdulhadi, Fatma Husien S. "DIFFERENTIATION OF U-937 MONOCYTES TO MACROPHAGE-LIKE CELLS POLARIZED INTO M1 OR M2 PHENOTYPES ACCORDING TO THEIR SPECIFIC ENVIRONMENT: A STUDY OF MORPHOLOGY, CELL VIABILITY, AND CD MARKERS OF AN IN VITRO MODEL OF HUMAN MACROPHAGES." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1401357388.

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Bouchard, Alexanne. "La protéine de stress du réticulum endoplasmique GRP94 dans le cancer du sein triple négatif, intérêt diagnostique et thérapeutique." Electronic Thesis or Diss., Bourgogne Franche-Comté, 2023. https://nuxeo.u-bourgogne.fr/nuxeo/site/esupversions/8b1b931d-83a7-49fd-9779-012ad3949e79.

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Le cancer du sein triple négatif (CSTN) est caractérisé par l’absence sur les cellules tumorales de récepteurs aux œstrogènes, à la progestérone ainsi que de HER2. Il s’agit du sous-type de cancer du sein le plus agressif et il est associé à un risque plus élevé de métastases. Il représente 15 à 20% de tous les cancers du sein. En raison du manque de cibles spécifiques, l'hormonothérapie et les médicaments ciblant HER2 sont inefficaces. Les CSTN représentent en fait un sous-groupe de tumeurs hétérogènes pouvant être classées en fonction de leurs caractéristiques moléculaires. Une meilleure compréhension des mécanismes moléculaires, notamment ceux impliqués dans la modulation de la réponse immunitaire, est nécessaire dans le but d’optimiser la prise en charge de ce cancer. Dans ce contexte, l'imagerie moléculaire peut représenter un outil intéressant : elle permet en effet l’identification non invasive et la visualisation in vivo de cibles spécifiques de la tumeur ou du microenvironnement tumoral (MET) grâce à des sondes moléculaires sélectives pouvant être utilisées à des fins diagnostiques et/ou thérapeutiques. Dans ce travail de thèse, deux cibles spécifiques du MET ont été étudiées à l’aide de telles sondes : les macrophages M2-like et la protéine GARP, un récepteur d’ancrage du TGF-β. Les macrophages de type M2-like sont reconnus comme ayant un rôle pro-tumoral majeur. Les résultats obtenus nous ont permis de mettre en évidence la présence de macrophages M2-like CD206+ dans notre modèle de CSTN grâce à l’imagerie multimodale in vivo. Au cours de cette étude, nous avons validé l’efficacité du 99mTc-Tilmanocept en SPECT/CT en tant que sonde pour imager les macrophages M2-like du MET de notre modèle de CSTN. Nous avons également montré une co-expression de ces macrophages M2-like CD206+ avec la protéine GRP94, un chaperon important impliqué dans les réponses immunitaires. Enfin, l'inhibition de GRP94 à l'aide d’un inhibiteur spécifique, le PU-WS13, a significativement diminué le nombre de macrophages M2-like ainsi que la croissance tumorale dans notre modèle de CSTN. Ainsi, l'imagerie SPECT avec le 99mTc-Tilmanocept pourrait représenter une méthode innovante pour l'imagerie des macrophages M2-like CD206+ en tant que biomarqueur potentiel pour le pronostic, la prédiction thérapeutique et/ou la surveillance des tumeurs solides. La seconde cible étudiée, la protéine GARP, est exprimée à la membrane des Tregs et des cellules tumorales et joue un rôle clé dans l’activation du TGF-β, une cytokine immunosuppressive majeure dans le développement du cancer. Le développement d'une approche théranostique ciblant GARP combinant l'imagerie (111In-DOTAGA-GARP) et la radiothérapie interne vectorisée (RIV) (177Lu-DOTAGA-GARP) a été réalisé. Nous avons montré dans notre modèle préclinique de CSTN que l'expression de GARP était augmentée après radiothérapie externe, une stratégie thérapeutique classique, et pouvait être spécifiquement détectée et quantifiée dans le MET en utilisant l'imagerie SPECT/CT in vivo avec la sonde 111In-DOTAGA-GARP. De plus, son utilisation sous sa forme thérapeutique (177Lu-DOTAGA-GARP) limitait la croissance tumorale. Cette stratégie théranostique pourrait permettre la personnalisation des traitements anticancéreux par l'identification et le traitement des patients susceptibles de répondre à une thérapie ciblant les Tregs via la RIV
Triple-negative breast cancer (TNBC) is characterized by the absence of estrogen and progesterone receptors, as well as HER2, on tumor cells. It is the most aggressive subtype of breast cancer and is associated with a higher risk of metastasis. It accounts for 15-20% of all breast cancers. Due to the lack of specific targets, hormone therapy and HER2-targeted drugs are ineffective. TNBC represents a subgroup of heterogeneous tumors that can be classified according to their molecular characteristics. A better understanding of molecular mechanisms, particularly those involved in modulating the immune response, is needed to optimize the management of this cancer. In this context, molecular imaging can represent an interesting tool: it enables the non-invasive identification and in vivo visualization of specific targets in the tumor or tumor microenvironment (TME), thanks to selective molecular probes that can be used for diagnostic and/or therapeutic purposes. In this thesis work, two specific TME targets were studied using such probes: M2-like macrophages and GARP protein, a TGF-β anchoring receptor. M2-like macrophages are recognized as having a major pro-tumoral role. The results obtained enabled us to demonstrate the presence of CD206+ M2-like macrophages in our CSTN model using in vivo multimodal imaging. In this study, we validated the efficacy of 99mTc-Tilmanocept in SPECT/CT as a probe for imaging M2-like macrophages in the TME of our TNBC model. We also demonstrated co-expression of these CD206+ M2-like macrophages with the GRP94 protein, an important chaperone involved in immune responses. Finally, inhibition of GRP94 with a specific inhibitor, PU-WS13, significantly decreased the number of M2-like macrophages as well as tumor growth in our TNBC model. Thus, SPECT imaging with 99mTc-Tilmanocept could represent an innovative method for imaging CD206+ M2-like macrophages as a potential biomarker for prognosis, therapeutic prediction and/or monitoring of solid tumors. The second target studied, the GARP protein, is expressed at the membrane of Tregs and tumor cells and plays a key role in the activation of TGF-β, a major immunosuppressive cytokine in cancer development. The development of a theranostic approach targeting GARP combining imaging (111In-DOTAGA-GARP) and targeted radionuclide therapy (TRT) (177Lu-DOTAGA-GARP) has been achieved. We showed in our preclinical TNBC model that GARP expression was increased after external radiotherapy, a classic therapeutic strategy, and could be specifically detected and quantified in the TME using in vivo SPECT/CT imaging with the 111In-DOTAGA-GARP probe. Moreover, its use in its therapeutic form (177Lu-DOTAGA-GARP) limited tumor growth. This theranostic strategy could enable the personalization of cancer treatments by identifying and treating patients likely to respond to therapy targeting Tregs via TRT

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Sharp, Bradley M. "Conversion of the U937 Monocyte into “Macrophage-like&amp;#x201d; Populations Exhibiting M1 or M2 Characteristics." Wright State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=wright1368748415.

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Almeida, Cátia Alexandra Rebelo de. "Bevacizumab: more than an anti-angiogenic drug." Master's thesis, 2018. http://hdl.handle.net/10362/65518.

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Cancer cells interact with a variety of non-tumor cell types, participating cooperatively in cellular events during cancer development, as tumor-induced angiogenesis. Although Judah Folkman thought about blood vessels as sources of oxygen and nutrients essential for tumor growth, evidences suggest that tumor neovasculatures are structurally and functionally abnormal, leading to a microenvironment prompt to induce metastasis and tumor resistance to therapies. VEGF-A is the most potent pro-angiogenic factor and is upregulated in most tumors. To overcome it, therapies were developed to target VEGF family through the neutralization of VEGF-A ligand, as Bevacizumab, or the respective receptors. The main goal of this research project was to challenge zebrafish xenograft model to reveal differential tumor responses to Bevacizumab, so that it can, eventually, be used in the future to select the eligible patients for this therapy. For that, zebrafish xenografts were generated using cancer cell lines and several hallmarks of cancer were analyzed by confocal microscopy. Our data show that zebrafish xenografts are able to unveil different responses to Bevacizumab, allowing to infer localized tumor responses, but also the impact of the anti-angiogenic compound on metastatic potential, tumor- induced angiogenesis and modulation of immunity. In more detail: Bevacizumab can induce tumor size reduction; specifically interfere with different steps of invasion-metastatic cascade event; impair tumor-induced angiogenesis in sensitive and VEGF-A-dependent tumor-related blood vessels; normalize the remaining blood vessels and selectively act on innate immune cells. In particular, experiments in a triple negative breast cancer model revealed that Bevacizumab reduces tumor size by impairing the M2-like macrophage population, which seems to be crucial for breast tumor cells survival. Altogether, our data validate zebrafish larvae xenograft model as an in vivo platform for Bevacizumab screening. Moreover, highlight the importance of explore the impact of therapies on the immune landscape and how it can influence tumor responses.

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Dong-JerShiau and 蕭東哲. "NADPH oxidase regulates Toll-like receptor 2-dependent M2 tumor-associated macrophage polarization." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/02292645582092102396.

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碩士
國立成功大學
微生物及免疫學研究所
103
Tumor-associated macrophages (TAM) are considered to be a major cell population in the tumor microenvironment and can be differentiated into M2 phenotype supporting tumor existence. However, the switching mechanisms of polarized TAM by tumor cells are yet to be determined. We previously showed that unknown factors in the hepatoma microenvironment trigger Toll like receptor 2 (TLR2) signaling to induce the degradation of NF-κB p65 via ERK1/2 activation and autophagy promoting the polarization of M2 macrophages. The underlying mechanism is yet to be determined. In this study we found hepatoma conditioned medium stimulates reactive oxygen species (ROS) to trigger ERK1/2 activation, autophagy-mediated NF-κB degradation and M2 macrophage polarization. This ROS-mediated NF-κB p65 degradation was attenuated in NADPH oxidase 2 (NOX2)-deficient cells. In addition, TLR2 signaling was found to be involved in NOX2-regulated M2 macrophage polarization. An endogenous TLR2 ligand, high-mobility group protein B1 (HMGB1), was found to be secreted by hepatoma cells. HMGB1 suppression by RNA-silencing or neutralizing antibody reduces ROS generation, ERK1/2 activation, autophagy-mediated NF-κB p65 degradation and M2 macrophage polarization. Our findings suggest that soluble HMGB1 can trigger TLR2 -dependent autophagy-mediated NF-κB p65 degradation and M2 macrophage polarization. Furthermore, we demonstrated that HMGB1 regulates tumor nodule formation and M2 macrophage recruitment in an in situ mice hepatoma model. In conclusion, we found a novel function of HMGB1 to regulate-TLR2/NOX2 dependent M2 polarization and TAM recruitment in hepatoma.

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Книги з теми "Macrophages M2-Like"

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.

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Частини книг з теми "Macrophages M2-Like"

Multhoff, G., E. A. Repasky, and Peter Vaupel. "Mild Hyperthermia Induced by Water-Filtered Infrared A Irradiation: A Potent Strategy to Foster Immune Recognition and Anti-Tumor Immune Responses in Superficial Cancers?" In Water-filtered Infrared A (wIRA) Irradiation, 129–39. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_10.

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AbstractApart from a number of positive “physiological” effects such as an increase in local blood flow which results in an improved oxygen supply and a reversal of tumor hypoxia, a key hallmark of cancer growth which greatly impairs anti-tumor immune responses, hyperthermia (HT) also exerts beneficial effects on anti-cancer immunity. The water-filtered infrared A (wIRA) irradiation technique achieves tissue temperatures in the fever-range (tT = 39–41 °C) or mild hyperthermia levels (tT = 39–43 °C) up to tissue depths of ≈25 mm in tissues. At tissue temperatures of 39–43 °C, by fostering the reactivity of the “immunological” TME [e.g., the activity of CD8+ cytotoxic T cells, CD4+ helper T cells, dendritic cells (DC), M1 macrophages, natural killer (NK) cells, and NK-like T (NK-T) cells], while compromising immunosuppressive cells [e.g., tumor-associated M2 macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), regulatory T (Treg) cells]. Moreover, elevated temperatures resulting in mild hyperthermia induce the synthesis and release of heat-shock proteins (HSPs), and thereby augment tumor antigenicity.

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Zhu, Lingyan, Yu Xiao, Yao Xiao, Yinan Jiang, Maha Adama, and George K. Gittes. "Macrophages as a Target for Treating Diabetic Foot Ulcers." In Diabetic Foot - Recent Advances [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106613.

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In all stages of wound healing, macrophages play a pivotal role by coordinating the repair steps in a timely and accurate fashion. The successful completion of wound healing requires proper spatiotemporal presence and function of macrophages. Diabetes significantly alters the proliferation, polarization and functionality of macrophages, leading to a suboptimal but prolonged pro-inflammatory M1-like phenotype in wound macrophages and a failure of their late transition to a reparative M2-like phenotype. This defect in macrophage phenotype and the proper transition results in delayed or even failure of wound healing. Specifically in the diabetic foot ulcer (DFUs), this macrophage dysfunction results in chronic infection and potentially amputation. The abnormal macrophage phenotype in diabetes is not fully understood but is believed to mainly result from epigenetic changes in macrophages and altered interactions between macrophages and other cell types, such as fibroblasts, endothelial cells, neutrophils and T-cells. Recent research on DFUs has focused on developing strategies to improve diabetic wound repair through modulation of macrophage polarization. Treatment of DFUs will greatly benefit from a multi-modal therapy that includes controlling high blood glucose, topical support, prevention of secondary infection, resolution of sustained inflammation and application of cellular therapies targeting macrophages.

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Santa, Kazuki. "Macrophages: Phagocytosis, Antigen Presentation, and Activation of Immunity." In Phagocytosis - Main Key of Immune System [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.110832.

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Macrophages are phagocytes and one of the white blood cells discovered by Ilya I. Mechnikov in 1892. They engulf and digest foreign substances like pathogens and conduct antigen presentation, mature from haematopoietic stem cells in bone marrow, moving into blood vessels and become monocytes, and differentiate into macrophages in the tissue. Macrophages have intracellular granules called lysosome accumulating digestive enzymes. Their life span is several months and proliferates by cell division. There are three roles: First one is phagocytosis. Macrophages incorporate pathogens and work in natural immunity. In inflammation, macrophages aggregate after neutrophils recruitment and engulf pathogens into cellular phagosomes, fused with lysosomes and degrade. Second role is antigen presentation. Macrophages present fragment of digested foreign substances on cell surface MHC class II molecules and release cytokines. Dendritic cells and B cells are also APCs expressing MHC class II. CD4+ T cells recognize antigens presented on macrophages by using TCR. Only well-matched helper T cells via MHC class II-TCR interaction are activated. The third is activation of immunity. Cytokines produced by T cells activate macrophages and differentiate them into inflammatory M1 and wound-healing M2 macrophages.

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Pedro Lapuente, Juan. "Immunomodulatory Effects of a M2-Conditioned Medium (PRS^® CK STORM): Theory on the Possible Complex Mechanism of Action through Anti-Inflammatory Modulation of the TLR System and the Purinergic System." In Purinergic System [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104486.

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Co-culture of primary or mesenchymal stem cells (MSC) with M2 macrophages produces a very special conditioned medium with a recognizable and stable cytokine pattern (PRS CK STORM), independent of the donor, with unique anti-inflammatory properties. This product can regulate certain pathways of inflammation in an anti-inflammatory manner, including TLR3, TLR4, the inflammasome, and the purinergic system. The anti-inflammatory action of PRS CK STORM is demonstrated both by its composition and by its action in in vitro and in vivo inflammatory models. The study of the mechanism of action showed changes in the pattern of toll-like receptors (TLR) and purinergic receptors, with an increase in the relative expression of mRNA encoding A2a and A3 receptors, together with a decrease in the relative expression of mRNA encoding P2X7 receptors. Second, it mitigated the adverse effects of a systemic inflammatory process in mice, especially in comparison with a known anti-inflammatory drug (Anakinra). Thus, due to its profile in terms of biosafety and efficacy, PRS CK STORM may be a strong candidate to treat inflammatory processes, such as cytokine storm associated with severe infectious processes, including COVID-19.

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Тези доповідей конференцій з теми "Macrophages M2-Like"

Eisel, David, Wolfram Osen, Krishna Das, Franziska Marie-Claire Hoerhold, Rainer König, and Stefan B. Eichmüller. "Abstract A067: Cognate interaction with CD4+ T-cells instructs M2-like macrophages to acquire M1-like phenotype." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a067.

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Sarkar, Sandipto, Prashant K. Thakkar, Heinz Lenz, Peter Enzinger, Andrew H. Ko, Allyson J. Ocean, Yao Lu, et al. "Abstract 2011: HER2 expression and M2-like tumor infiltrating macrophages associated with Cabazitaxel activity in gastric cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2011.

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Zhao, Hailan, Jing Xu, Jiaqi Wang, Haoming Xu, Wenqi Huang, Xue Guo, Yong Zhang, Yandi Liu, Hongli Huang, and Youlian Zhou. "IDDF2022-ABS-0079 Short-chain fatty acid-producing mixed bacteria improve experimental colitis via promoting M2-like macrophages polarization." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 2–4 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-iddf.44.

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El Kasmi, Karim C., Suzette R. Riddle, Aimee Anderson, Min Li, Amanda Flockton, Megan Noe, Adil Anwar, et al. "Activated Adventitial Pulmonary Artery Fibroblasts Drive Macrophages Toward A Distinct M2-Like Phenotype Through STAT3 Signaling In Pulmonary Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4745.

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Bruno, Antonino, Denisa Baci, Matteo Gallazzi, Annalisa Bosi, Angelo Naselli, Andrea Guarneri, Lorenzo Mortara, Douglas Noonan, and Adriana Albini. "Abstract 1581: Prostate tumor associated NK cells (PTANKs) acquire the decidual-like/pro-angiogenic phenotype and polarize macrophages towards the M2-like/TAM subset." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1581.

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Lee, Kim Yee, Siew Meng Chong, and Yaw Chyn Lim. "Abstract A10: L1236, a Hodgkin and Reed-Sternberg cell line, stimulates monocytes in vitro to differentiate into M2-like macrophages." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a10.

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Han, Zhen, Chingyu Su, Xiwei Wu, Hanjun Qin, Steven T. Rosen, and Christiane Querfeld. "Abstract 2759: Reprogramming of PD1+ M2-like tumor-associated macrophages with anti-PD-L1 and Lenalidomide in cutaneous T cell lymphoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2759.

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Sable, Rushikesh, Jesse Jaynes, Michael Ronzetti, Wendy Guzman, Zachary Knotts, Natalia de Val, Juan Morgan, Clayton Yates, Baljinnyam Bolormaa, and Udo Rudloff. "Abstract B49: Precision targeting of M2-like macrophages by the innate defense regulator RP-182 in pancreatic cancer and noncancerous diseases." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-b49.

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Dai, M.-S., H.-C. Lo, L.-C. Chen, A. Janckilla, and S.-F. Tseng. "Abstract P2-01-07: M2-like tumor-associated macrophages require Tartrate-resistant acid phosphatase as overall function to promote breast cancer metastasis." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p2-01-07.

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Albini, Adriana, Denisa Baci, Matteo Gallazzi, Federico Dehò, Angelo Naselli, Andrea Guernieri, Lorenzo Mortara, Douglas M. Noonan, and Antonino Bruno. "Abstract LT006: NK cells from prostate cancer patients acquire a pro-angiogenic phenotype and polarize macrophages towards a M2-like/TAM subset." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-lt006.

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