Mechanisms Driving Macrophage Diversity and Specialization in Distinct Tumor Microenvironments and Parallelisms with Other Tissues

Overmeire, Eva Van; Laoui, Damya; Keirsse, Jiri; Ginderachter, Jo A. Van; Sarukhan, Adélaïda

doi:10.3389/fimmu.2014.00127

Cited by 153 publications

(125 citation statements)

References 225 publications

(267 reference statements)

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“…It is well established that tumour progression involves altered intercellular communication that establishes a distinct microenvironment of cancer cells with various stromal cell types to support growth, angiogenesis and invasion [165,181]. In addition, altered communication of cancer cells to immune cells allows malignant cells to escape immune surveillance, a process termed immune-evasion, which has been proposed as another emerging hallmark for tumourigenesis [163,180].…”

Section: Intercellular Communicationmentioning

confidence: 99%

Hallmarks of the ageing lung

2015

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Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, "dysregulation of the extracellular matrix", which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases. @ERSpublications Hallmarks of ageing are selecting factors for the pathogenesis of COPD, lung cancer and IPF

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Section: Intercellular Communicationmentioning

confidence: 99%

Hallmarks of the ageing lung

2015

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“…They have tremendous tissue-specific phenotypic variability, and although there is no single set of macrophagespecific surface markers, useful markers include the general myeloid-lineage marker CD11b and F4/80 (in mice) and CD14 and CD68 (in humans). Functional classification of macrophages as classically activated (M1) vs alternatively activated (M2) is a useful and commonly used paradigm to describe the extremes of a spectrum of macrophage phenotype based on patterns of gene expression and cytokine production [8][9][10][11]28,29 (Fig. 1).…”

Section: Macrophagesmentioning

confidence: 99%

Myeloid-Derived Cells in Tumors: Effects of Radiation

Vatner

Formenti

2015

Seminars in Radiation Oncology

115

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The discrepancy between the in vitro and in vivo response to radiation is readily explained by the fact that tumors do not exist independently of the host organism; cancer cells grow in the context of a complex microenvironment composed of stromal cells, vasculature, and elements of the immune system. As the antitumor effect of radiotherapy depends in part on the immune system, and myeloid-derived cells in the tumor microenvironment modulate the immune response to tumors, it follows that understanding the effect of radiation on myeloid cells in the tumor is likely to be essential for comprehending the antitumor effects of radiotherapy. In this review, we describe the phenotype and function of these myeloid-derived cells, and stress the complexity of studying this important cell compartment owing to its intrinsic plasticity. With regard to the response to radiation of myeloid cells in the tumor, evidence has emerged demonstrating that it is both model and dose dependent. Deciphering the effects of myeloid-derived cells in tumors, particularly in irradiated tumors, is key for attempting to pharmacologically modulate their actions in the clinic as part of cancer therapy.

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“…The regulation of macrophage function and the balance between inflammation and resolution is arguably the key event in most disease processes. Dysregulated macrophage function contributes to almost all chronic inflammatory conditions including obesity [10,19,[26][27][28][29], atherosclerosis [30][31][32][33], cancer [18,[34][35][36][37][38][39][40][41], chronic obstructive pulmonary diseases [42][43][44], chronic infections [17,45,46], and even Alzheimer's [47][48][49][50].…”

Section: Introductionmentioning

confidence: 99%