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Relevant bibliographies by topics / Macrophage heterogeneity

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Academic literature on the topic 'Macrophage heterogeneity'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "Macrophage heterogeneity"

1

Gordon, Siamon. "Macrophage Heterogeneity." Arteriosclerosis, Thrombosis, and Vascular Biology 32, no. 6 (June 2012): 1339–42. http://dx.doi.org/10.1161/atvbaha.111.238139.

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Nolte, Anna, Johannes Junginger, Berit Baum, and Marion Hewicker-Trautwein. "Heterogeneity of macrophages in canine histiocytic ulcerative colitis." Innate Immunity 23, no. 3 (January 18, 2017): 228–39. http://dx.doi.org/10.1177/1753425916686170.

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Histiocytic ulcerative colitis (HUC) is a chronic enteropathy which most notably occurs in Boxer dogs and French bulldogs. The inflamed mucosa is hallmarked by large, foamy, periodic acid–Schiff (PAS)-positive macrophages infiltrating the colonic mucosa. As little is known about their origin and phenotype, an immunohistochemical study was performed using different macrophage markers. Generally, canine colonic macrophages showed high expression of ionised calcium-binding adaptor molecule 1 and MHC class II. In canine HUC, macrophages revealed up-regulation of lysozyme and L1 Ag but decreased CD163 expression compared with controls, suggesting them to be pro-inflammatory cells, whereas the healthy colonic mucosa was characterised by an anti-inflammatory macrophage phenotype. In addition, PAS reaction was used to discriminate macrophage subpopulations. PAS– macrophages displayed higher expression of L1 Ag and CD64, whereas PAS+ cells, which were only present in HUC patients, were characterised by increased expression of lysozyme, inducible nitric oxide synthase and CD204. This indicates PAS+ cells to be mature macrophages contributing to the inflammatory process, which are most likely maintained by differentiation of immature PAS– macrophages continuously recruited from blood monocytes. In summary, macrophage heterogeneity in canine HUC probably illustrates their different maturation states and functions compared with the healthy animals.

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Boorsma, Carian E., Christina Draijer, and Barbro N. Melgert. "Macrophage Heterogeneity in Respiratory Diseases." Mediators of Inflammation 2013 (2013): 1–19. http://dx.doi.org/10.1155/2013/769214.

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Macrophages are among the most abundant cells in the respiratory tract, and they can have strikingly different phenotypes within this environment. Our knowledge of the different phenotypes and their functions in the lung is sketchy at best, but they appear to be linked to the protection of gas exchange against microbial threats and excessive tissue responses. Phenotypical changes of macrophages within the lung are found in many respiratory diseases including asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis. This paper will give an overview of what macrophage phenotypes have been described, what their known functions are, what is known about their presence in the different obstructive and restrictive respiratory diseases (asthma, COPD, pulmonary fibrosis), and how they are thought to contribute to the etiology and resolution of these diseases.

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OLIVER, A. M. "Macrophage heterogeneity in human fetal tissue. Fetal macrophages." Clinical & Experimental Immunology 80, no. 3 (June 28, 2008): 454–59. http://dx.doi.org/10.1111/j.1365-2249.1990.tb03309.x.

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Stremmel, Christopher, Konstantin Stark, and Christian Schulz. "Heterogeneity of Macrophages in Atherosclerosis." Thrombosis and Haemostasis 119, no. 08 (June 26, 2019): 1237–46. http://dx.doi.org/10.1055/s-0039-1692665.

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AbstractAtherosclerosis is a prevalent inflammatory condition and a frequent cause of morbidity and mortality worldwide. Macrophages are among the key immune cells driving lesion formation in the arterial wall. They have therefore evolved as potential targets for therapeutic strategies. Understanding of the different macrophage phenotypes and functions seems to be of pivotal importance for the development of treatments to target these immune cells. This review highlights the complexity of the mononuclear phagocyte system and summarizes important features of macrophage biology contributing to atherosclerosis.

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Seu, Katie Giger, Julien Papoin, Rose Fessler, Jimmy Hom, Gang Huang, Narla Mohandas, Lionel Blanc, and Theodosia A. Kalfa. "Unravelling Macrophage Heterogeneity in Erythroblastic Islands Between Species." Blood 128, no. 22 (December 2, 2016): 2436. http://dx.doi.org/10.1182/blood.v128.22.2436.2436.

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Abstract Erythroblastic islands (EBIs) are a hallmark of mammalian erythropoiesis consisting of a central macrophage surrounded by and interacting closely with maturing erythroblasts. While it is generally accepted that the island macrophages play an important role in erythropoiesis, the inability to identify and isolate this macrophage subpopulation has limited our understanding of their functional involvement. Previous studies have relied on immunohistochemistry/immunofluorescence in situ or in vitro. More recently, flow cytometry was used to characterize EBI formation and the immunophenotype of the central macrophages in murine erythroblastic islands. These approaches provide either morphological/structural information or high-throughput quantification, but not both, and often carry the expectation that all EBI macrophages have similar phenotype (F4/80+/CD169+/VCAM1+ for example), and thus potentially overlook critical information about the nature and biology of the islands and the central macrophages. We have developed a novel method for analysis and characterization of EBI macrophages from hematopoietic tissues using multispectral imaging flow cytometry, which combines the high-throughput advantage of flow cytometry with the morphology and fluorescence details obtained from microscopy. This method allows automated, non-biased evaluation of the EBIs recovered from a sample, their number, mean size, as well as structural and morphological details of the central macrophages and associated erythroblasts. Most importantly, the images, combined with the fluorescence similarity feature, enables the evaluation of co-expression of any phenotypic markers that may be used to identify the macrophages which is crucial since some antigens used to identify macrophages (e.g. CD45, CD11b) may also be expressed on non-erythroid cells associated with the islands instead of, or in addition to, the central macrophage itself. We used this method to confirm the expression of various markers previously reported to be expressed on the erythroblastic island macrophages by flow, including CD11b, VCAM1, F4/80, CD169, and CD163, in mouse, rat, and human bone marrow. Indeed, while a large number of studies have focused on murine erythropoiesis, the identity and role of the EBIs in other species is much less known. We confirmed expression of CD169 and VCAM1 on the F4/80+ central macrophages of murine EBIs and also identified a population of VCAM+/F4/80- central cells associated with developing erythroblasts. CD11b is abundantly expressed by non-erythroid, non-macrophage cells associated with the islands, but is not expressed significantly on the central macrophages (Figure 1). CD163, a marker of EBI macrophages in rat and human, was not detected in the murine EBIs by imaging flow cytometry, but this may be due to limitation of the antibodies tested. In contrast, anti-CD163 stained well rat and human EBI macrophages but CD11b or VCAM1 were not detected in EBIs from rat and human bone marrow respectively, raising the question of a species-specificity regarding the macrophage heterogeneity and satellite cells present within erythroblastic islands. In summary, the data presented herein demonstrate the effectiveness of this method for the analysis and characterization of EBIs and establish a new tool for future investigations of EBIs and their central macrophages in the nurturing of erythropoiesis. Figure 1 Representative image of an erythroblastic island harvested from murine bone marrow stained with F4/80-AF488 (green), CD11b-PE (blue), and CD71-BV421 (red) and analyzed by imaging flow cytometry. Figure 1. Representative image of an erythroblastic island harvested from murine bone marrow stained with F4/80-AF488 (green), CD11b-PE (blue), and CD71-BV421 (red) and analyzed by imaging flow cytometry. Disclosures No relevant conflicts of interest to declare.

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Mori, M., Y. Sadahira, S. Kawasaki, T. Hayashi, and M. Awai. "Macrophage heterogeneity in bone marrow culture in vitro." Journal of Cell Science 95, no. 3 (March 1, 1990): 481–85. http://dx.doi.org/10.1242/jcs.95.3.481.

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Macrophages in mouse bone marrow cultures were investigated with macrophage-specific monoclonal antibody F4/80 and anti-Forssman glycosphingolipid (GSL) antibody, which was specific for macrophages in hematopoietic foci. Antibody F4/80 stained two types of cells, small macrophages and large flat macrophages associated with hematopoietic cells. The cytochemical and phagocytotic characteristics were similar between these two types of cells, but Forssman GSL was positive only for the large flat macrophages associated with hematopoietic cells. The data suggest that Forssman GSL positive macrophages, derived from resident bone marrow macrophages, play an important role in hematopoiesis and are clearly distinguished from small macrophages in vitro.

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Gordon, Siamon, and Philip R. Taylor. "Monocyte and macrophage heterogeneity." Nature Reviews Immunology 5, no. 12 (December 2005): 953–64. http://dx.doi.org/10.1038/nri1733.

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Gombozhapova, A. E., Yu V. Rogovskaya, M. S. Rebenkova, J. G. Kzhyshkowska, and V. V. Ryabov. "PHENOTYPIC HETEROGENEITY OF CARDIAC MACROPHAGES DURING WOUND HEALING FOLLOWING MYOCARDIAL INFARCTION: PERSPECTIVES IN CLINICAL RESEARCH." Siberian Medical Journal 33, no. 2 (July 14, 2018): 70–76. http://dx.doi.org/10.29001/2073-8552-2018-33-2-70-76.

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Purpose. Myocardial regeneration is one of the most ambitious goals in prevention of adverse cardiac remodeling. Macrophages play a key role in transition from inflammatory to regenerative phase during wound healing following myocardial infarction (MI). We have accumulated data on macrophage properties ex vivo and in cell culture. However, there is no clear information about phenotypic heterogeneity of cardiac macrophages in patients with MI. The purpose of the project was to assess cardiac macrophage infiltration during wound healing following myocardial infarction in clinical settings taking into consideration experimental knowledge.Material and Methods. The study included 41 patients with fatal MI type 1. In addition to routine analysis, macrophages infiltration was assessed by immunohistochemistry. We used CD68 as a marker for the cells of the macrophage lineage, while CD163, CD206, and stabilin-1 were considered as M2 macrophage biomarkers. Nine patients who died from noncardiovascular causes comprised the control group.Results. The intensity of cardiac macrophage infiltration was higher during the regenerative phase than during the inflammatory phase. Results of immunohistochemical analysis demonstrated the presence of phenotypic heterogeneity of cardiac macrophages in patients with MI. We noticed that numbers of CD68+, CD163+, CD206+, and stabilin-1+ macrophages depended on MI phase.Conclusion. Our study supports prospects for implementation of macrophage phenotyping in clinic practice. Improved understanding of phenotypic heterogeneity might become the basis of a method to predict adverse cardiac remodeling and the first step in developing myocardial regeneration target therapy.

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Rojas, Joselyn, Juan Salazar, María Sofía Martínez, Jim Palmar, Jordan Bautista, Mervin Chávez-Castillo, Alexis Gómez, and Valmore Bermúdez. "Macrophage Heterogeneity and Plasticity: Impact of Macrophage Biomarkers on Atherosclerosis." Scientifica 2015 (2015): 1–17. http://dx.doi.org/10.1155/2015/851252.

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Cardiovascular disease (CVD) is a global epidemic, currently representing the worldwide leading cause of morbidity and mortality. Atherosclerosis is the fundamental pathophysiologic component of CVD, where the immune system plays an essential role. Monocytes and macrophages are key mediators in this aspect: due to their heterogeneity and plasticity, these cells may act as either pro- or anti-inflammatory mediators. Indeed, monocytes may develop heterogeneous functional phenotypes depending on the predominating pro- or anti-inflammatory microenvironment within the lesion, resulting in classic, intermediate, and non-classic monocytes, each with strikingly differing features. Similarly, macrophages may also adopt heterogeneous profiles being mainly M1 and M2, the former showing a proinflammatory profile while the latter demonstrates anti-inflammatory traits; they are further subdivided in several subtypes with more specialized functions. Furthermore, macrophages may display plasticity by dynamically shifting between phenotypes in response to specific signals. Each of these distinct cell profiles is associated with diverse biomarkers which may be exploited for therapeutic intervention, including IL-10, IL-13, PPAR-γ, LXR, NLRP3 inflammasomes, and microRNAs. Direct modulation of the molecular pathways concerning these potential macrophage-related targets represents a promising field for new therapeutic alternatives in atherosclerosis and CVD.

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Dissertations / Theses on the topic "Macrophage heterogeneity"

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McCarthy, Sean Patrick. "Studies on human macrophage heterogeneity." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238184.

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Luk, Sheung Fung Simon. "Alveolar macrophage heterogeneity in idiopathic pulmonary fibrosis." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/29433.

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Idiopathic Pulmonary Fibrosis (IPF) involves excess extracellular matrix (ECM) deposition within the lung interstitium, caused by non-resolving chronic inflammation and dysregulated repair. Alveolar macrophage (AMφ) may contribute to IPF through releasing various mediators by different subsets, investigated here in vitro, and ex vivo using a mouse model of bleomycin (BLM)-induced pulmonary fibrosis. The role of foamy AMφ in the reported increased susceptibility of Hermansky Pudlak Syndrome (HPS) 1 mice to BLM-induced pulmonary fibrosis was also assessed. Novel characterisation studies revealed that terminally differentiated AMφ are inducible into M1-like [nitric oxide synthase 2 (NOS2)hi interleukin (IL)-1βhi IL-12 p40 (total)hi major histocompatibility protein (MHC)-IIhi mannose receptor C, type 1 (MRC1)-] or M2-like [Arginase 1 (Arg1)hi Fibronectinhi IGF-1hi MHC-IIlo MRC1-/+] phenotypes following IFN-γ or IL-13 priming respectively. Lipopolysccharide (LPS) altered these AMφ subset phenotypes. AMφ heterogeneity in a novel multiple oropharyngeal dose, BLM-induced pulmonary fibrosis was evaluated from days 7 to 21. Accumulation of M1-like AMφ at day 7, and M1/M2-hybrid AMφ [Arg1hi IL-12 p40 (total)hi fibronectinhi MHC-IIlo MRC1-/+] from days 7 to 21, may promote inflammation and fibrosis respectively. Toll-like Receptor (TLR) 9 messenger ribonucleic acid (mRNA) and TLR2 surface protein, and both TLRs2 and 9 ex vivo activities were increased in BLM-challenged mice from days 7 to 21, suggesting their roles in inflammation and fibrosis. Foamy AMφ accumulated in BLM-induced pulmonary fibrosis, and their potential role in the reported increased susceptibility to BLM-induced pulmonary fibrosis of HPS1 mice was evaluated. BLM-challenged HPS1 mice (days 7-21) had increased weight loss indicating reduced BLM tolerance from days 7 to 11, but little/no difference in collagen accumulation, suggesting that reduced BLM tolerance is not correlated with increased pulmonary fibrosis. In conclusion AMφ alter their phenotype in response to their environment that contributes to different stages of BLM-induced pulmonary fibrosis. Reduced BLM tolerance in HPS1 mice is not correlated with increased pulmonary fibrosis.

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Rabinowitz, S. S. "Macrophage membrane glycoproteins defined by wheat germ agglutinin." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235087.

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Liao, Chia-Te. "The study of macrophage heterogeneity in the peritoneal cavity." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/76762/.

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Mononuclear phagocytes play a key role in tissue homeostasis and in host defense against pathogen invasion. However, the phenotypic identities and functional properties of this heterogeneous population within the peritoneal cavity remains poorly elucidated. In the context of peritoneal dialysis, it is hypothesized that the modification of macrophage/dendritic cell biology by the dialysis process would alter tissue homeostasis, host susceptibility to infection and local immunity, compromising long-term outcomes of the patients. The research work carried out in this thesis has tested this hypothesis by examination of the immunobiology (mainly phenotype and function) of human and murine peritoneal macrophage and dendritic cell subsets. Moreover, the potential link between the altered immunobiology of peritoneal mononuclear phagocytes and clinical outcomes of the dialysis patients has been investigated. Several key findings were generated during these studies: 1) multiple discrete peritoneal macrophage and dendritic cell subsets have been phenotypically identified in humans (from different clinical settings of peritoneal dialysis) and in mice (from naïve and inflamed conditions); 2) in humans, the phenotypes and the activation/maturation status of peritoneal macrophages and dendritic cells are modified throughout the dialysis course and also during acute peritonitis; some characteristic alterations are associated with adverse patient outcomes; 3) in mice, the distinctive kinetics of the respective peritoneal macrophage and dendritic cell subsets in clinically relevant acute peritonitis models have been characterized; 4) individual peritoneal macrophage and dendritic cell subsets (human and mice) display differences in their phagocytic capacity and the ability to process and present antigen.

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Fischer, Cornelius [Verfasser]. "Transcriptome-wide Single-cell Analysis of Human Macrophage Heterogeneity / Cornelius Fischer." Berlin : Freie Universität Berlin, 2018. http://d-nb.info/1156901510/34.

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Hassim, Muhamad Fairus Bin Noor. "Molecular characterisation and computational modelling of macrophage heterogeneity of major immediate early gene expression during a murine cytomegalovirus infection." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/11780.

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Human cytomegalovirus (HCMV) is a major cause of morbidity and mortality amongst immuno-compromised individuals and is the leading cause of congenital diseases amongst newborn infants. Mouse CMV (MCMV) infection of inbred mice has been extensively used as a model for HCMV pathogenesis and host-virus interaction. Macrophages are a key target cell type in the pathogenesis of human and mouse CMV infections. Macrophages are semi-permissive to CMV infection, however, the nature of this restrictive mechanism of infection is open for investigation. In this thesis, I hypothesized that macrophage permissivity is determined by the dynamic interplay of the innate response during the immediate-early (IE) period of infection. To test this hypothesis, I first developed and validated a flow cytometry based assay. In MCMV infected macrophages, I found heterogeneous expression from the major IE promoter (MIEP) leading to the development of a refractory subpopulation for IE expression. I further developed a computational modelling approach to help elucidate the dynamics of infection during this period. Modelling work revealed that the occurrence of refractory subpopulation could be caused by either 1) pre-existence of heterogeneous permissivity of macrophages prior to infection or 2) through an emergent process. Experimental testing of the models shows that the heterogeneous IE expression of homogeneously infected macrophages is caused by an emergent process. MCMV infection using type I interferon receptor and signal transducers and activator of transcription 1 (Stat1) knockout macrophages reveals that the emergence of refractory subpopulation is predominantly mediated by type I interferon through Stat1. Comparative molecular analysis between progressively infected and refractory subpopulations reveals that MCMV MIEP activation in the refractory subpopulation is stochastically inhibited by high expression of type I interferon induced antiviral components.

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Damen, Angela N. "In vivo Characterization Of Non-Myocyte Heterogeneity During The Postnatal Development Of The Cardiac Interstitium." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1415625809.

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Kisters, N. "Heterogeneity in human atherosclerotic gene expression profiles from man to macrophages." [Maastricht] : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=13932.

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Cassado, Alexandra dos Anjos. "Heterogeneidade dos macrófagos peritoneais." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-20032012-155547/.

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Os macrófagos (MΦs) compõem uma população celular altamente heterogênea, e são extensivamente adotados como ferramenta experimental, em especial os MΦs peritoneais murinos. O objetivo desse trabalho foi revisitar o peritônio dando ênfase à heterogeneidade dos MΦs. Duas populações distintas compõem os MΦ peritoneais residentes: LPM (Large Peritoneal Macrophage) e SPM (Small Peritoneal Macrophage). Todas as condições proporcionadas in vivo resultam no desaparecimento de LPM, aumento de SPM e influxo de monócitos. Em paralelo, ocorre uma diminuição na marcação para b-galactosidase (marcador de senescência) e um aumento na produção de Óxido Nítrico (NO) e na frequência de células F4/80+IL-12+ após a subseqüente estimulação com LPS e IFN-g, que parece ser às custas da SPM. Além disso, parece haver uma especialização onde LPM assume um perfil M2 após inoculação de zimosan, e SPM um perfil M1 após reestimulo com LPS ou IFN-g.Esses dados sugerem que renovação celular que ocorre no peritônio após estimulação, parece ser benéfica para a resposta celular frente a estímulos infecciosos.
Macrophages (MΦ) are a heterogeneous population extensively adopted as experimental model, especially peritoneal MΦ. Then, the aim of this work was to revisit peritoneal cavity looking for MΦ heterogeneity. Peritoneal MΦ comprise two distinct subpopulations: LPM (Large Peritoneal Macrophage) and SPM (Small Peritoneal Macrophage). The different conditions proporcioned in vivo, resulted in the disappearance of LPM and the accumulation of SPM and monocytes. In parallel, adherent cells isolated from stimulated mice displayed reduced staining for b-galactosidase (senescence marker). Further, an increase in nitric oxide (NO) production and IL-12-producing cells frequency was observed in response to LPS/FN-g re-stimulation. In addition, there was a specialization of activation profile marked by a M2 activation profile after zymosan administered in vivo assumed by LPM, and SPM showed a bias to M1 after re-stimulation with LPS/IFN-g. Then, the substitution of LPM by a robust SPM and monocytes in response to infectious stimuli greatly improves peritoneal effector activity.

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Cassado, Alexandra dos Anjos. "Papel da flagelina e de lipopolissacarídeos bacterianos na ativação de populações heterogêneas de macrófagos." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-01112007-134739/.

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Os macrófagos (MO) são populações heterogêneas de células residentes em diversos tecidos, onde iniciam a resposta imune através do reconhecimento de padrões moleculares de patógenos. Para avaliar a modulação funcional dessas populações, MO peritoneais (PM) e alveolares (AM), com perfil M1 e M2, foram ativados in vivo por flagelina (FliCi) e lipopolissacarídeos bacterianos (LPS). Esse trabalho mostra que o microambiente parece influenciar a resposta diferencial das populações de MO, uma vez que a expressão de MHCII, CD80, CD86 e CD40 e produção de NO por PM são mais intensamente modulados por FliCi, enquanto os AM são mais sensíveis ao LPS. Porém, dentro da população de PM, encontramos duas subpopulações distintas, nomeadas F4/80hi e F4/80lo. A população F4/80hi parece adquirir um perfil M1 após estimulo com FliCi, com alta expressão de iNOS, enquanto a população F4/80sup>lo apresenta um perfil M2, com maior expressão basal de mTGF-ß, indicando que a heterogeneidade dos MO também pode estar expressa no mesmo microambiente.
Macrophages (MO) are a heterogeneous cell population that resides in distinct tissues, where they trigger the immune response through the recognition of pathogen-associated molecular patterns. To evaluate the functional modulation of these populations, peritoneal (PM) and alveolar (AM) MO, from M1 and M2 profile, were in vivo activated by flagellin (FliCi) and bacterial lipopolysaccharide (LPS). In this study we show that microenvironment seems to influence the differential responses of MO populations, since MHCII, CD80, CD86 e CD40 expression and NO production by PM are more intensely modulated by FliCi whereas AM are more sensitive to LPS. However, we found two distinct subpopulations within PM, named F4/80hi e F4/80lo. cells show a M1 profile after FliCi stimulation, with high iNOS expression of mTGF-ß, indicating that the MO heterogeneity can also be finding in the same microenvironment. NOS expression, and F4/80lo population presents a M2 profile, with higher basal expression of mTGF-ß, indicating that the MO heterogeneity can also be finding in the same microenvironment

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Books on the topic "Macrophage heterogeneity"

1

Damoiseaux, Jan G. M. C., ed. Macrophage heterogeneity established by immunocytochemistry. Stuttgart: Gustav Fischer, 1993.

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Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.

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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ‎ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.

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Book chapters on the topic "Macrophage heterogeneity"

1

Dehne, Nathalie, Michaela Jung, Christina Mertens, Javier Mora, and Andreas Weigert. "Macrophage Heterogeneity During Inflammation." In Encyclopedia of Inflammatory Diseases, 1–10. Basel: Springer Basel, 2015. http://dx.doi.org/10.1007/978-3-0348-0620-6_131-1.

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Dehne, Nathalie, Michaela Jung, Christina Mertens, Javier Mora, and Andreas Weigert. "Macrophage Heterogeneity During Inflammation." In Compendium of Inflammatory Diseases, 865–74. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_131.

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Dukhinova, Marina, Ekaterina Kopeikina, and Eugene D. Ponomarev. "Usage of Multiparameter Flow Cytometry to Study Microglia and Macrophage Heterogeneity in the Central Nervous System During Neuroinflammation and Neurodegeneration." In Cellular Heterogeneity, 167–77. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7680-5_10.

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Chao, D., and G. G. MacPherson. "Lymph Node Macrophage Heterogeneity: A Subpopulation Fails to Express Activation Phenotype." In Advances in Experimental Medicine and Biology, 771–76. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5535-9_115.

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Dijkstra, C. D., E. A. Döpp, P. Joling, and G. Kraal. "The Heterogeneity of Mononuclear Phagocytes in Lymphoid Organs: Distinct Macrophage Subpopulations in Rat Recognized by Monoclonal Antibodies ED1, ED2 and ED3." In Microenvironments in the Lymphoid System, 409–19. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2463-8_50.

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Zhang, Xia, and David M. Mosser. "The Functional Heterogeneity of Activated Macrophages." In Phagocyte-Pathogen Interactions, 325–40. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch20.

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Unkeles, Jay C. "Heterogeneity of Human and Murine Fcγ, Receptors." In Ciba Foundation Symposium 118 - Biochemistry of Macrophages, 89–101. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720998.ch7.

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Fidler, Isaiah J., J. Milburn Jessup, Eugenie S. Kleinerman, William E. Fogler, and Amitabha Mazumder. "Circumvention of Neoplastic Heterogeneity by Systemically Activated Macrophages." In Biology and Treatment of Colorectal Cancer Metastasis, 311–22. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2301-3_25.

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Morahan, Page S., Meryle Melnicoff, and Walla L. Dempsey. "Macrophage Heterogeneity." In Macrophages and Cancer, edited by Alvin Volkman, 1–26. CRC Press, 2019. http://dx.doi.org/10.1201/9780429276149-1.

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Aderem, Alan, and David M. Underhill. "Heterogeneity in macrophage phagocytosis." In Phagocytosis: The Host, 195–213. Elsevier, 1999. http://dx.doi.org/10.1016/s1874-5172(99)80032-7.

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Conference papers on the topic "Macrophage heterogeneity"

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Coleman, Fadie T., Mathew T. Blahna, Joseph D. Ferrari, Zachary A. Pepper-Cunningham, Kazuko Yamamoto, Andrew A. Wilson, Lee J. Quinton, et al. "Heterogeneity In Activation Of Macrophage NF-κB By Patient Isolates Of Pneumococci." 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.a4253.

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Hostetter, Galen, Arkadeep Sinha, and Brian Haab. "Abstract A34: Characterizing macrophage adaptive function in tumor stroma." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a34.

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Heaster, Tiffany, Karla Esbona, Paul M. Sondel, and Melissa C. Skala. "Abstract 375:In vivometabolic autofluorescence imaging of macrophage heterogeneity across normal and cancerous tissue." 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.am2020-375.

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Mazzone, Massimiliano. "Abstract IA02: Macrophage entry in hypoxia: Implications for cancer and angiogenesis." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-ia02.

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Shiao, Stephen L., David G. DeNardo, Bruce A. Faddegon, David M. Underhill, Catherine C. Park, and Lisa M. Coussens. "Abstract A28: Impact of macrophage function on the efficacy of radiation therapy." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a28.

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Dakhlallah, Duaa, Ivory Patterson, Amy C. Gross, Randall Evans, and Tim D. Eubank. "Abstract PR03: Macrophage phenotype drives tumor program via epigenetic machinery carried in secreted microvesicles." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-pr03.

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Hardaway, Aimalie Lynnette, Mackenzie K. Herroon, Erandi N. Rajagurubandara, and Izabela Podgorski. "Abstract A18: Investigating the role of bone marrow adiposity on macrophage function and osteoclast differentiation." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a18.

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Neisen, Jessica L., Nuala McCabe, Richard D. Kennedy, and David JJ Waugh. "Abstract A49: Cabozantinib attenuates CXCL8-driven macrophage-dependent migration and invasion of PTEN-deficient prostate cancer." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a49.

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Kunz, Lisette I., Thérèse S. Lapperre, Wim Timens, Simone van Wijngaarden, Dirkje S. Postma, Peter J. Sterk, and Pieter S. Hiemstra. "Macrophage Heterogeneity and Soluble Mediators in Sputum And Bronchoalveolar Lavage from Current Smokers And Ex-smokers With COPD." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3867.

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Moughon, Diana, Huanhuan He, Shiruyeh Schokrpur, Ziyue Jiang, Madeeha Yaqoob, John David, Luisa Iruela-Arispe, Oliver Dorigo, and Lily Wu. "Abstract A48: M2 macrophage inhibition reverses vascular leaks that cause malignant ascites in late-stage epithelial ovarian cancer." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a48.

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