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Journal articles on the topic 'Macrophages M2-Like'

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Published: 20 April 2024

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1

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 (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.

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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 eosi

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Lalor, Richard, та Sandra O’Neill. "Bovine κ-Casein Fragment Induces Hypo-Responsive M2-Like Macrophage Phenotype". Nutrients 11, № 7 (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

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Lyu, Qingkang, Edwin J. A. Veldhuizen, Irene S. Ludwig, et al. "Characterization of polarization states of canine monocyte derived macrophages." PLOS ONE 18, no. 11 (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 featur

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Sánchez-Reyes, Karina, Alejandro Bravo-Cuellar, Georgina Hernández-Flores, et al. "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.Res

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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 (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 inde

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Strizova, Zuzana, Iva Benesova, Robin Bartolini, et al. "M1/M2 macrophages and their overlaps – myth or reality?" Clinical Science 137, no. 15 (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

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Li, Dezhi, Min Yan, Fengfei Sun, et al. "miR-498 inhibits autophagy and M2-like polarization of tumor-associated macrophages in esophageal cancer via MDM2/ATF3." Epigenomics 13, no. 13 (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 pol

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Ronaghan, Natalie J., Mandy Soo, Uriel Pena, et al. "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 (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

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Di Martile, Marta, Valentina Farini, Francesca Maria Consonni, et al. "Melanoma-specific bcl-2 promotes a protumoral M2-like phenotype by tumor-associated macrophages." Journal for ImmunoTherapy of Cancer 8, no. 1 (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

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Shao, Xia, Boting Wu, Pu Chen, et al. "The Role of M2 Macrophage in Primary Immune Thrombocytopenia." Blood 134, Supplement_1 (2019): 2355. http://dx.doi.org/10.1182/blood-2019-129667.

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Background: Primary immune thrombocytopenia (ITP) is an acquired autoimmune hemorrhagic disorder, characterized by immune-mediated platelet destruction and impaired megakaryocyte maturation. Although impaired T cells have been implicated to participate in the pathogenesis of ITP, another immune cell signified as M2 macrophages has not been investigated properly in ITP patients. This study aimed to investigate the role of M2 macrophage subsets in primary immune thrombocytopenia (ITP). Methods: Peripheral blood mononuclear cells (PBMC) from newly diagnosed ITP patients and healthy controls (HC)

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Vicenzi, Silvia, Trung Tran, Lara Avsharian, Joshua Hartman, Anna Rapp, and Leslie Crews. "Tuning the Innate Immune Multiple Myeloma Microenvironment By Modulating IRF4." Blood 142, Supplement 1 (2023): 6604. http://dx.doi.org/10.1182/blood-2023-187814.

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The tumor microenvironment (TME) has emerged as a key contributor to cancer progression in numerous solid tumors as well as blood cancers that evolve in the bone marrow (BM). In the context of multiple myeloma (MM), survival of malignant plasma cells is supported by interactions with the BM microenvironment, which is comprised of various components including cells, extracellular matrix, and soluble factors. Therefore, the development of strategies that specifically target the MM BM microenvironment is crucial for improving current disease prognosis. Within the BM niche, M2-like myeloma-associa

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Laskar, Amit, Jonas Eilertsen, Wei Li, and Xi-Ming Yuan. "SPION primes THP1 derived M2 macrophages towards M1-like macrophages." Biochemical and Biophysical Research Communications 441, no. 4 (2013): 737–42. http://dx.doi.org/10.1016/j.bbrc.2013.10.115.

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Kumar, Sudhir, Sonam Mittal, Prachi Gupta, Mona Singh, Pradeep Chaluvally-Raghavan, and Sunila Pradeep. "Metabolic Reprogramming in Tumor-Associated Macrophages in the Ovarian Tumor Microenvironment." Cancers 14, no. 21 (2022): 5224. http://dx.doi.org/10.3390/cancers14215224.

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The interaction between tumor cells and macrophages in the tumor microenvironment plays an essential role in metabolic changes in macrophages and reprograms them towards a pro-tumorigenic phenotype. Increasing evidence indicates that macrophage metabolism is a highly complex process and may not be as simple as previously thought. Pro-inflammatory stimuli switch macrophages towards an M1-like phenotype and rely mainly on aerobic glycolysis and fatty acid synthesis, whereas anti-inflammatory stimuli switch macrophages towards an M2-like phenotype. M2-like macrophages depend more on oxidative pho

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Gong, Xiaocheng, Yunfei Liu, Keying Liang, et al. "Cucurbitacin I Reverses Tumor-Associated Macrophage Polarization to Affect Cancer Cell Metastasis." International Journal of Molecular Sciences 24, no. 21 (2023): 15920. http://dx.doi.org/10.3390/ijms242115920.

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The tumor microenvironment plays a critical role in tumor progression and immune regulation. As one of the most important components of the tumor microenvironment, macrophages have become a new therapeutic target for inhibiting tumor progression. Despite the well-documented anticancer activity of cucurbitacin I, its effect on macrophages remains unclear. In this study, we established a coculture system of macrophages and cancer cells under hypoxic conditions to simulate the tumor-promoting environment mediated by M2-like macrophages. We determined whether cucurbitacin I modulates M2-like polar

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Kuo, Chan-Yen, Tzu-Hsien Yang, Pei-Fang Tsai, and Chun-Hsien Yu. "Role of the Inflammatory Response of RAW 264.7 Cells in the Metastasis of Novel Cancer Stem-Like Cells." Medicina 57, no. 8 (2021): 778. http://dx.doi.org/10.3390/medicina57080778.

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Background and objectives: Tumor progression and the immune response are intricately linked. Additionally, the presence of macrophages in the microenvironment is essential for carcinogenesis, but regulation of the polarization of M1- and M2-like macrophages and their role in metastasis remain unclear. Based on previous studies, both reactive oxygen species (ROS) and the endoplasmic reticulum (ER) are emerging as key players in macrophage polarization. While it is known that cancers alter macrophage inflammatory responses to promote tumor progression, there is limited knowledge regarding how th

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Myers, Kayla V., Amber E. de Groot, Anna L. Gonye, Luke V. Loftus, Sarah R. Amend, and Kenneth J. Pienta. "Abstract 2546: Targeting MerTK-mediated efferocytosis in the prostate cancer TME." Cancer Research 82, no. 12_Supplement (2022): 2546. http://dx.doi.org/10.1158/1538-7445.am2022-2546.

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Abstract The prostate cancer tumor microenvironment (TME) is comprised of many different components and cell types that influence tumor progression and patient outcome. Macrophages are highly abundant immune cells in the prostate cancer TME. Macrophage phenotypes can be modeled on a continuous spectrum of M1-like (anti-tumor macrophages) to M2-like (pro-tumor macrophages) and most macrophages in the prostate cancer TME are M2-like. Efferocytosis, the phagocytosis of apoptotic cells, is a pro-tumor function of M2-like macrophages. We have developed a flow cytometry assay to quantify efferocytos

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Gunes, Emine Gulsen, Sung Hee Kil, Xiwei Wu та ін. "Tnfα Promotes an Immunosuppressive Microenvironment in Cutaneous T Cell Lymphoma and Regulates PD-L1 Expression". Blood 136, Supplement 1 (2020): 33–34. http://dx.doi.org/10.1182/blood-2020-141070.

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Background: Tumor-associated macrophages (TAMs) play a key role in cutaneous T cell lymphoma (CTCL) growth and neoplastic T cells escape immune surveillance via PD1-PD-L1 axis (Querfeld, C., et al., Blood 2019; Khodadoust, M.S., et al., J Clin Oncol, 2020). There remains a lack of knowledge about how cytokines regulate the mechanisms controlling tumor-growth and polarize the tumor microenvironment (TME). Methods and Results: To investigate PD-L1 and PD1 expression on TAMs and T cells in mycosis fungoides (MF) and the leukemic variant Sézary syndrome (SS) patients, we performed multiplex immuno

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Schnellhardt, Sören, Ramona Erber, Maike Büttner-Herold, et al. "Accelerated Partial Breast Irradiation: Macrophage Polarisation Shift Classification Identifies High-Risk Tumours in Early Hormone Receptor-Positive Breast Cancer." Cancers 12, no. 2 (2020): 446. http://dx.doi.org/10.3390/cancers12020446.

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Studies have demonstrated correlations between accumulations of tumour-associated macrophages (TAMs), especially of M2-like phenotype, and increased mortality in advanced breast cancer. We investigated the prognostic potential of both main macrophage phenotypes in early hormone receptor-positive (HR+) breast cancer. The studied cohort of 136 patients participated in an institutional APBI phase II trial. Patient selection was characterized by HR+, small tumour size and no metastasis. Tissue microarrays from pre-RT resection samples were double stained for CD68/CD163 using immunohistochemistry.

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Yang, Jing, Chengxian Xu, Joseph Lechner, Haley Walls, and Kai Yang. "LKB1 regulates macrophage metabolism and functional polarization in immunomodulation." Journal of Immunology 210, no. 1_Supplement (2023): 168.14. http://dx.doi.org/10.4049/jimmunol.210.supp.168.14.

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Abstract Macrophages play critical roles in maintaining tissue homeostasis and modulating immune responses. In response to microenvironmental cytokines, macrophages coordinate cellular signaling networks and diverse transcriptional programs to dictate their phenotypical and functional heterogeneity. For instance, LPS/IFNγ and IL-4 induce classically (M1) and alternatively (M2) activated macrophages, respectively. Remodeling cellular metabolism has been highlighted a key process underlying macrophage functional polarization. However, the precise mechanisms coordinating macrophage metabolism and

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Janss, Thibaut J., Simon Lefevre, Martijn Vlaming, Johan Arnold, Ellen Boelen, and Sofie Pattijn. "Abstract 2120: In vitro suppressive bioassays using macrophages for the evaluation of immuno-oncology drug." Cancer Research 82, no. 12_Supplement (2022): 2120. http://dx.doi.org/10.1158/1538-7445.am2022-2120.

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Abstract Targeted activation of tumor infiltrating lymphocytes in the tumor microenvironment (TME) with so-called immune checkpoint inhibitors (ICIs) has resulted in the development of revolutionizing therapeutic anti-tumor strategies. A deepening understanding of the TME has followed in the ability to see beyond current immune checkpoint strategies. It becomes clear that players like Tumor Associated Macrophages (TAM) and Myeloid Derived Suppressor Cells (MDSC) play a significant role by downregulating anti-tumor responses. Their presence and roles in the TME open novel possibilities for modu

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Chen, Li-Mei, Hong-Yu Tseng, Yen-An Chen, Aushia Tanzih Al Haq, Pai-An Hwang, and Hsin-Ling Hsu. "Oligo-Fucoidan Prevents M2 Macrophage Differentiation and HCT116 Tumor Progression." Cancers 12, no. 2 (2020): 421. http://dx.doi.org/10.3390/cancers12020421.

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Reactive oxygen species (ROS) produced during intracellular metabolism or triggered by extrinsic factors can promote neoplastic transformation and malignant microenvironment that mediate tumor development. Oligo-Fucoidan is a sulfated polysaccharide isolated from the brown seaweed. Using human THP-1 monocytes and murine Raw264.7 macrophages as well as human HCT116 colorectal cancer cells, primary C6P2-L1 colorectal cancer cells and human MDA-MB231 breast cancer cells, we investigated the effect of Oligo-Fucoidan on inhibiting M2 macrophage differentiation and its therapeutic potential as a sup

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Jo, Wol Soon, Sohi Kang, Soo Kyung Jeong, et al. "Low Dose Rate Radiation Regulates M2-like Macrophages in an Allergic Airway Inflammation Mouse Model." Dose-Response 20, no. 3 (2022): 155932582211173. http://dx.doi.org/10.1177/15593258221117349.

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We investigated the effects of low dose rate radiation (LDR) on M1 and M2 macrophages in an ovalbumin-induced mouse model of allergic airway inflammation and asthma. After exposure to LDR (1 Gy, 1.818 mGy/h) for 24 days, mice were euthanized and the changes in the number of M1 and M2 macrophages in the bronchoalveolar lavage fluid and lung, and M2-associated cytokine levels, were assessed. LDR treatment not only restored the M2-rich microenvironment but also ameliorated asthma-related progression in a macrophage-dependent manner. In an ovalbumin-induced mouse model, LDR treatment significantly

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Mazzoni, Mara, Giuseppe Mauro, Lucia Minoli, et al. "Senescent Thyrocytes, Similarly to Thyroid Tumor Cells, Elicit M2-like Macrophage Polarization In Vivo." Biology 10, no. 10 (2021): 985. http://dx.doi.org/10.3390/biology10100985.

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Inflammation plays a critical role in thyroid cancer onset and progression. We previously characterized the in vitro interplay between macrophages and senescent human thyrocytes and thyroid tumor-derived cell lines, modeling the early and the late thyroid tumor phases, respectively. We reported that both models are able to induce pro-tumoral M2-like macrophage polarization, through the activation of the COX2-PGE2 axis. Here, we investigated the presence of macrophage infiltrating cells in mouse xenografts derived from the above described cells models. We showed that subcutaneous injection in i

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Warmink, Kelly, Michiel Siebelt, Philip S. Low, et al. "Folate Receptor Expression by Human Monocyte–Derived Macrophage Subtypes and Effects of Corticosteroids." CARTILAGE 13, no. 1 (2022): 194760352210814. http://dx.doi.org/10.1177/19476035221081469.

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Objective Folate receptor beta (FR-β) has been used as a clinical marker and target in multiple inflammatory diseases, including osteoarthritis (OA) and rheumatoid arthritis (RA). However, the conditions under which FR-β+ macrophages arise remain unclear and could be affected by corticosteroids. Therefore, we studied FR-β expression in vitro in macrophage subtypes and determined their response to triamcinolone acetonide (TA), a clinically often-used corticosteroid. Design Human monocyte–derived macrophages were differentiated to the known M0, M1, or M2 macrophage phenotypes. The phenotype and

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Hult, Elissa M., Stephen J. Gurczynski, and Bethany B. Moore. "M2 macrophages have unique transcriptomes but conditioned media does not promote profibrotic responses in lung fibroblasts or alveolar epithelial cells in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 321, no. 3 (2021): L518—L532. http://dx.doi.org/10.1152/ajplung.00107.2021.

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Macrophages are critical regulators of pulmonary fibrosis. Their plasticity, proximity, and ability to cross talk with structural cells of the lung make them a key cell type of interest in the regulation of lung fibrosis. Macrophages can express a variety of phenotypes, which have been historically represented through an “M1-like” to “M2-like” delineation. In this classification, M1-like macrophages are proinflammatory and have increased phagocytic capacity compared with alternatively activated M2-like macrophages that are profibrotic and are associated with wound healing. Extensive evidence i

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Rabani, Razieh, Allen Volchuk, Mirjana Jerkic, et al. "Mesenchymal stem cells enhance NOX2-dependent reactive oxygen species production and bacterial killing in macrophages during sepsis." European Respiratory Journal 51, no. 4 (2018): 1702021. http://dx.doi.org/10.1183/13993003.02021-2017.

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Human mesenchymal stem/stromal cells (MSCs) have been reported to produce an M2-like, alternatively activated phenotype in macrophages. In addition, MSCs mediate effective bacterial clearance in pre-clinical sepsis models. Thus, MSCs have a paradoxical antimicrobial and anti-inflammatory response that is not understood.Here, we studied the phenotypic and functional response of monocyte-derived human macrophages to MSC exposure in vitro.MSCs induced two distinct, coexistent phenotypes: M2-like macrophages (generally elongated morphology, CD163+, acute phagosomal acidification, low NOX2 expressi

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Liu, Peng, Yahui Liu, Lanying Chen, Zeping Fan, Yingying Luo, and Yaru Cui. "Anemoside A3 Inhibits Macrophage M2-Like Polarization to Prevent Triple-Negative Breast Cancer Metastasis." Molecules 28, no. 4 (2023): 1611. http://dx.doi.org/10.3390/molecules28041611.

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Triple negative breast cancer (TNBC) exhibits the characteristics of strong metastatic ability and a high recurrence rate, and M2-type macrophages play an important role in this process. Previous research data suggested that Anemoside A3 (A3), a monomeric component of Pulsatilla Chinensis, could prevent and treat TNBC by converting M0 macrophages into M1 immunogen phenotypes. This study showed that A3 significantly restrained the lung metastases of 4 T1-Luc cells with bioluminescence imaging in vivo and Hematoxylin and Eosin (H&E) staining. Meanwhile, the percentage of M2-type macrophages

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Kallemeijn, Wouter W., Sarah Spear, Josephine Walton, et al. "Abstract 439: From foe to friend: In vivo reprogramming of tumor-associated macrophages to an anti-cancer phenotype by modulating N-myristoyltransferase activity." Cancer Research 83, no. 7_Supplement (2023): 439. http://dx.doi.org/10.1158/1538-7445.am2023-439.

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Abstract Tumor-associated macrophages (TAMs) play a central role in cancer by driving tumor growth, metastasis, therapy failure and cancer recurrence. Macrophage plasticity and diversity allows classification along a M1-M2 polarization axis, where TAMs have a M2-like polarization, associated with a pro-tumoral phenotype, whereas M1 macrophages exhibit anti-tumor functions. Reprogramming TAMs to a M1-like anti-cancer phenotype is an increasingly coveted therapeutic strategy in oncology. Here, we report TAMs can be favorably reprogrammed by modulating N-myristoyltransferase (NMT) activity using

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Horuluoglu, Begum Han, Defne Bayik, Neslihan Kayraklioglu, et al. "PAM3 supports the generation of M2-like macrophages from lupus patient monocytes and improves disease outcome in murine lupus." Journal of Immunology 202, no. 1_Supplement (2019): 182.21. http://dx.doi.org/10.4049/jimmunol.202.supp.182.21.

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Abstract Systematic Lupus Erythematosus (SLE) is an autoimmune syndrome of unclear etiology. While T and B cell abnormalities contribute to disease pathogenesis, recent work suggests that inflammatory M1-like macrophages also play a role. Previous work showed that the TLR2/1 agonist PAM3CSK4 (PAM3) could stimulate normal human monocytes to preferentially differentiate into immunosuppressive M2-like rather than inflammatory M1-like macrophages. This raised the possibility of PAM3 being used to normalize the M1:M2 ratio in SLE. Consistent with that possibility, monocytes from lupus patients diff

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Zhang, Cong, Sisi Wei, Suli Dai, et al. "The NR_109/FUBP1/c-Myc axis regulates TAM polarization and remodels the tumor microenvironment to promote cancer development." Journal for ImmunoTherapy of Cancer 11, no. 5 (2023): e006230. http://dx.doi.org/10.1136/jitc-2022-006230.

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BackgroundTumor-associated macrophages (TAMs) are a major component of the tumor microenvironment (TME) and exert an important role in tumor progression. Due to the heterogeneity and plasticity of TAMs, modulating the polarization states of TAMs is considered as a potential therapeutic strategy for tumors. Long noncoding RNAs (lncRNAs) have been implicated in various physiological and pathological processes, yet the underlying mechanism on how lncRNAs manipulate the polarization states of TAMs is still unclear and remains to be further investigated.MethodsMicroarray analyses were employed to c

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Niu, Xiao-Ling, Dan Feng, Sheng Hao, et al. "The significance of M1/M2 macrophage-like monocytes in children with systemic lupus erythematosus." European Journal of Inflammation 17 (January 2019): 205873921882446. http://dx.doi.org/10.1177/2058739218824463.

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Monocytes/macrophages are important in the development of systemic lupus erythematosus. To research M1 and M2 macrophage-like monocytes in the peripheral blood of children with systemic lupus erythematosus and explore the clinical significance, M1 and M2 macrophage-like monocytes, tumor necrosis factor-α, interleukin-1, interleukin-6, interleukin-10, and interleukin-18 are tested in the peripheral blood of children with systemic lupus erythematosus by flow cytometry. A correlation analysis is made between M1 and M2 macrophage-like monocytes and erythrocyte sedimentation rate and C-reactive pro

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Yun, Kun, Reona Sakemura, Truc Huynh, et al. "Abstract 6813: Immunosuppressive monocytes suppress CART19 functions through modulation of the IL-1 pathway." Cancer Research 84, no. 6_Supplement (2024): 6813. http://dx.doi.org/10.1158/1538-7445.am2024-6813.

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Abstract CD19-directed chimeric antigen receptor T (CART19) cell therapy has shown remarkable outcomes in B cell malignancies and was FDA approved in multiple indications, but durable remissions are limited to ~40%. Inhibitory myeloid cells in the tumor microenvironment have been found to suppress T cell expansion and contribute to CART19 failure. Here, we studied interactions between monocytes, CART19, and tumor cells to understand the impact of monocytes on CART19 effector functions. First, CD28-costimulated CART19 (CART19-28ζ) generated in the lab from healthy donors were cocultured with Je

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Lu, Yufei, Leiming Guo, and Gaofeng Ding. "PD1+ tumor associated macrophages predict poor prognosis of locally advanced esophageal squamous cell carcinoma." Future Oncology 15, no. 35 (2019): 4019–30. http://dx.doi.org/10.2217/fon-2019-0519.

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Aim: Tumor associated macrophages are the most abundant cancer immune cells. However, little was known about the identity of CD68+PD1+ macrophages as well as the contributions in the prognosis of esophageal squamous cell carcinoma (ESCC). Methods & methods: Immunofluorescence, flowcytometry and RT-PCR were used to analysis PD1+ macrophages in ESCC. Results: CD68+PD1+ macrophages which can express higher M2 markers in cancer tissues, increased about 4.2-times compared with para-cancer tissues. Additionally, PD1high macrophages were significantly correlated with more malignant phenotypes and

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Lu, Chih-Hao, Chao-Yang Lai, Da-Wei Yeh, et al. "Involvement of M1 Macrophage Polarization in Endosomal Toll-Like Receptors Activated Psoriatic Inflammation." Mediators of Inflammation 2018 (December 16, 2018): 1–14. http://dx.doi.org/10.1155/2018/3523642.

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Psoriasis is a chronic inflammatory skin disorder that affects ~2%–3% of the worldwide population. Inappropriate and excessive activation of endosomal Toll-like receptors 7, 8, and 9 (TLRs 7–9) at the psoriatic site has been shown to play a pathogenic role in the onset of psoriasis. Macrophage is a major inflammatory cell type that can be differentiated into phenotypes M1 and M2. M1 macrophages produce proinflammatory cytokines, and M2 macrophages produce anti-inflammatory cytokines. The balance between these two types of macrophages determines the progression of various inflammatory diseases;

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Teo, Kristeen Ye Wen, Shipin Zhang, Jia Tong Loh, et al. "Mesenchymal Stromal Cell Exosomes Mediate M2-like Macrophage Polarization through CD73/Ecto-5′-Nucleotidase Activity." Pharmaceutics 15, no. 5 (2023): 1489. http://dx.doi.org/10.3390/pharmaceutics15051489.

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Mesenchymal stem/stromal cell (MSC) exosomes have been shown to alleviate immune dysfunction and inflammation in preclinical animal models. This therapeutic effect is attributed, in part, to their ability to promote the polarization of anti-inflammatory M2-like macrophages. One polarization mechanism has been shown to involve the activation of the MyD88-mediated toll-like receptor (TLR) signaling pathway by the presence of extra domain A-fibronectin (EDA-FN) within the MSC exosomes. Here, we uncovered an additional mechanism where MSC exosomes mediate M2-like macrophage polarization through ex

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Chae, Wook-Jin, Eun-Ah Sung, Brian Hur, and Min Hee Park. "The Wnt antagonist Dickkopf1(DKK1) promotes pulmonary fibrosis via M2-like macrophage polarization." Journal of Immunology 206, no. 1_Supplement (2021): 13.01. http://dx.doi.org/10.4049/jimmunol.206.supp.13.01.

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Abstract Tissue fibrosis is a progressive pathological process induced by repeated tissue injury and inflammation resulting in excessive collagen deposition. The Wnt signaling pathway regulates cell proliferation and differentiation for tissue repair processes. Dickkopf1 (DKK1) is a quintessential inhibitory ligand of the Wnt pathway. M2-like macrophages, induced by type 2 cytokines such as IL-13, play a central role in tissue fibrosis. We found that DKK1 protein expression markedly increased in both lung tissues of human idiopathic pulmonary fibrosis (IPF) and lungs from the murine bleomycin

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Chen, Peiwen, Hao Zuo, Hu Xiong, et al. "Gpr132 sensing of lactate mediates tumor–macrophage interplay to promote breast cancer metastasis." Proceedings of the National Academy of Sciences 114, no. 3 (2017): 580–85. http://dx.doi.org/10.1073/pnas.1614035114.

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Macrophages are prominent immune cells in the tumor microenvironment that exert potent effects on cancer metastasis. However, the signals and receivers for the tumor–macrophage communication remain enigmatic. Here, we show that G protein-coupled receptor 132 (Gpr132) functions as a key macrophage sensor of the rising lactate in the acidic tumor milieu to mediate the reciprocal interaction between cancer cells and macrophages during breast cancer metastasis. Lactate activates macrophage Gpr132 to promote the alternatively activated macrophage (M2)-like phenotype, which, in turn, facilitates can

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Li, Feng, Yongsheng Yang, Xiaohua Zhu, Lan Huang, and Jinhua Xu. "Macrophage Polarization Modulates Development of Systemic Lupus Erythematosus." Cellular Physiology and Biochemistry 37, no. 4 (2015): 1279–88. http://dx.doi.org/10.1159/000430251.

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Background/Aims: Macrophages have recently been shown to play a critical role in the pathogenesis of systemic lupus erythematosus (SLE). However, the underlying mechanisms remain unclear. Methods: Here, we used an activated lymphocyte-derived DNA (ALD-DNA) method to induce SLE in mice. We used a macrophage-specific eliminator clodronate to selectively deplete macrophages in mice. We isolated macrophages from bone marrow of the mice and used cytokines to differentiate M1 and M2 macrophages, respectively. Adoptive transplantation of M1 or M2 macrophages was performed in clodronate-treated mice.

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Mohr, Annika, Manuela Besser, Sonja Broichhausen, et al. "The Influence of Apremilast-Induced Macrophage Polarization on Intestinal Wound Healing." Journal of Clinical Medicine 12, no. 10 (2023): 3359. http://dx.doi.org/10.3390/jcm12103359.

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There is compelling evidence suggesting a pivotal role played by macrophages in orchestrating intestinal wound healing. Since macrophages display significant plasticity and heterogeneity, exhibiting an either classically activated (M1-like) or alternatively activated (M2-like) phenotype, they can aggravate or attenuate intestinal wound healing. Growing evidence also demonstrates a causal link between impaired mucosal healing in inflammatory bowel disease (IBD) and defects in the polarization of pro-resolving macrophages. By targeting the switch from M1 to M2 macrophages, the phosphodiesterase-

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Ni, Ping, Yue-Qin Liu, Jin-Yu Man, et al. "C16, a novel sinomenine derivatives, promoted macrophage reprogramming toward M2-like phenotype and protected mice from endotoxemia." International Journal of Immunopathology and Pharmacology 35 (January 2021): 205873842110267. http://dx.doi.org/10.1177/20587384211026786.

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Macrophage plays a critical part in host defense, tissue repair, and anti-inflammation; Macrophage reprogramming is responsible for disease development or regression. We aimed to clarify the effect of sinomenine-4-hydroxy-palmitate (C16), on macrophage reprogramming and anti-inflammatory in endotoxemia model. According to a structure modification of SIN (Sinomenine), C16 was found. Then, based on the endotoxin model, the mice liver and kidney toxicity was evaluated and serum cytokines level of IL-6 (Interleukin-6), TNF-α (Tumor necrosis factor-α), and IL-1β (Interleukin-1β) were measured by EL

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Liu, Shuangqing, Huilei Zhang, Yanan Li та ін. "S100A4 enhances protumor macrophage polarization by control of PPAR-γ-dependent induction of fatty acid oxidation". Journal for ImmunoTherapy of Cancer 9, № 6 (2021): e002548. http://dx.doi.org/10.1136/jitc-2021-002548.

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BackgroundThe peroxisome proliferator-activated receptor γ (PPAR-γ)-dependent upregulation of fatty acid oxidation (FAO) mediates protumor (also known as M2-like) polarization of tumor-associated macrophages (TAMs). However, upstream factors determining PPAR-γ upregulation in TAM protumor polarization are not fully identified. S100A4 plays crucial roles in promotion of cancer malignancy and mitochondrial metabolism. The fact that macrophage-derived S100A4 is major source of extracellular S100A4 suggests that macrophages contain a high abundance of intracellular S100A4. However, whether intrace

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Rajput, Charu, Megan P. Walsh, Breanna N. Eder, Ediri E. Metitiri, Antonia P. Popova, and Marc B. Hershenson. "Rhinovirus infection induces distinct transcriptome profiles in polarized human macrophages." Physiological Genomics 50, no. 5 (2018): 299–312. http://dx.doi.org/10.1152/physiolgenomics.00122.2017.

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Infections with rhinovirus (RV) cause asthma exacerbations. Recent studies suggest that macrophages play a role in asthmatic airway inflammation and the innate immune response to RV infection. Macrophages exhibit phenotypes based on surface markers and gene expression. We hypothesized that macrophage polarization state alters gene expression in response to RV infection. Cells were derived from human peripheral blood derived monocytes. M1 and M2 polarization was carried out by using IFN-γ and IL-4, respectively, and RNA was extracted for Affymetrix Human Gene ST2.1 exon arrays. Selected genes w

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Meiliana, Anna, and Andi Wijaya. "Macrophage Polarization in Metabolism and Metabolic Disease." Indonesian Biomedical Journal 5, no. 2 (2013): 81. http://dx.doi.org/10.18585/inabj.v5i2.56.

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BACKGROUND: Obesity is now recognized as the main cause of the worldwide epidemic of type 2 diabetes. Obesity-associated chronic inflammation is a contributing key factor for type 2 diabetes and cardiovascular disease. Numbers of studies have clearly demonstrated that the immune system and metabolism are highly integrated.CONTENT: Macrophages are an essential component of innate immunity and play a central role in inflammation and host defense. Moreover, these cells have homeostatic functions beyond defense, including tissue remodeling in ontogenesis and orchestration of metabolic functions. D

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Loureiro, J. Pedro, Mariana S. Cruz, Ana P. Cardoso, Maria J. Oliveira, and M. Fátima Macedo. "Human iNKT Cells Modulate Macrophage Survival and Phenotype." Biomedicines 10, no. 7 (2022): 1723. http://dx.doi.org/10.3390/biomedicines10071723.

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CD1d-restricted invariant Natural Killer T (iNKT) cells are unconventional innate-like T cells whose functions highly depend on the interactions they establish with other immune cells. Although extensive studies have been reported on the communication between iNKT cells and macrophages in mice, less data is available regarding the relevance of this crosstalk in humans. Here, we dove into the human macrophage-iNKT cell axis by exploring how iNKT cells impact the survival and polarization of pro-inflammatory M1-like and anti-inflammatory M2-like monocyte-derived macrophages. By performing in vit

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Courtney, Amy N., Gengwen Tian, Daofeng Liu, et al. "Cross-talk between NKT cells and tumor associated macrophages in the tumor microenvironment." Journal of Immunology 196, no. 1_Supplement (2016): 142.7. http://dx.doi.org/10.4049/jimmunol.196.supp.142.7.

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Abstract CD1d-reactive Va24-invariant NKT cells (NKTs) control tumor growth via yet poorly understood interactions with tumor-associated macrophages (TAMs) and other myeloid cells. TAMs comprise M1- and M2-like subsets, but only CD163high M2-like TAMs are associated with poor outcome in neuroblastoma (NB) and other tumors. Here, we demonstrate that NKTs selectively target M2-like TAMs via contact-dependent and independent mechanisms. Upon direct contact with antigen-pulsed M1 or M2 macrophages, NKTs selectively killed the latter. Although the killing was strictly CD1d-dependent, CD1d expressio

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Myers, Kayla V., Kenneth J. Pienta, and Sarah R. Amend. "Cancer Cells and M2 Macrophages: Cooperative Invasive Ecosystem Engineers." Cancer Control 27, no. 1 (2020): 107327482091105. http://dx.doi.org/10.1177/1073274820911058.

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Many aspects of cancer can be explained utilizing well-defined ecological principles. Applying these principles to cancer, cancer cells are an invasive species to a healthy organ ecosystem. In their capacity as ecosystem engineers, cancer cells release cytokines that recruit monocytes to the tumor and polarize them to M2-like protumor macrophages. Macrophages, recruited by the cancer cells, act as a secondary invasive species. The ecosystem engineering functions of M2-macrophages in turn support and stimulate cancer cell survival and proliferation. The cooperative ecosystem engineering of both

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Cornice, Jessica, Daniela Verzella, Paola Arboretto та ін. "NF-κB: Governing Macrophages in Cancer". Genes 15, № 2 (2024): 197. http://dx.doi.org/10.3390/genes15020197.

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Tumor-associated macrophages (TAMs) are the major component of the tumor microenvironment (TME), where they sustain tumor progression and or-tumor immunity. Due to their plasticity, macrophages can exhibit anti- or pro-tumor functions through the expression of different gene sets leading to distinct macrophage phenotypes: M1-like or pro-inflammatory and M2-like or anti-inflammatory. NF-κB transcription factors are central regulators of TAMs in cancers, where they often drive macrophage polarization toward an M2-like phenotype. Therefore, the NF-κB pathway is an attractive therapeutic target fo

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Han, Ik-Hwan, Chanmi Jeong, Juwon Yang, Seung-Hyeok Park, Deok-Sang Hwang, and Hyunsu Bae. "Therapeutic Effect of Melittin–dKLA Targeting Tumor-Associated Macrophages in Melanoma." International Journal of Molecular Sciences 23, no. 6 (2022): 3094. http://dx.doi.org/10.3390/ijms23063094.

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Melanoma is an immunogenic tumor and a serious type of skin cancer. Tumor-associated macrophages (TAMs) express an M2-like phenotype and are involved in all stages of melanomagenesis; it is hence a promising target for cancer immunotherapy. We herein investigated whether melittin–dKLA inhibits the growth of melanoma by inducing apoptosis of M2-like macrophages. For the in vitro study, a conditioned medium of macrophages was prepared from M0, M1, or M2-differentiated THP-1 cells with and without melittin–dKLA. The affinity of melittin for M2 macrophages was studied with FITC (fluorescein isothi

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Minopoli, Michele, Sabrina Sarno, Lucia Cannella, et al. "Crosstalk between Macrophages and Myxoid Liposarcoma Cells Increases Spreading and Invasiveness of Tumor Cells." Cancers 13, no. 13 (2021): 3298. http://dx.doi.org/10.3390/cancers13133298.

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Myxoid liposarcoma (MLPS) is the second most common subtype of liposarcoma and has tendency to metastasize to soft tissues. To date, the mechanisms of invasion and metastasis of MLPS remain unclear, and new therapeutic strategies that improve patients’ outcomes are expected. In this study, we analyzed by immunohistochemistry the immune cellular components and microvessel density in tumor tissues from patients affected by MLPS. In order to evaluate the effects of primary human MLPS cells on macrophage polarization and, in turn, the ability of macrophages to influence invasiveness of MLPS cells,

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