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Journal ArticleDOI

The chemokine system in diverse forms of macrophage activation and polarization.

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TLDR
Recent evidence suggests that differential modulation of the chemokine system integrates polarized macrophages in pathways of resistance to, or promotion of, microbial pathogens and tumors, or immunoregulation, tissue repair and remodeling.
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This article is published in Trends in Immunology.The article was published on 2004-12-01. It has received 5568 citations till now. The article focuses on the topics: Macrophage polarization & M2 Macrophage.

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Endothelial cells provide an instructive niche for the differentiation and functional polarization of M2-like macrophages.

TL;DR: It is shown that adult endothelial cells provide critical signals for the selective growth and differentiation of macrophages from several hematopoietic progenitors, and some of the molecules underlying the M2-like differentiation are highlighted.
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Mechanisms driving macrophage diversity and specialization in distinct tumor microenvironments and parallelisms with other tissues.

TL;DR: A better understanding of TAM diversity could provide a rationale for novel strategies aimed at targeting the most potent tumor-supporting macrophages, and parallels are drawn between TAM and macrophage in other tissues.
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Macrophage phenotypic plasticity in atherosclerosis: The associated features and the peculiarities of the expression of inflammatory genes.

TL;DR: Understanding of mechanisms of macrophages plasticity and resolving functional characteristics of distinct macrophage phenotypes should help in the development of new strategies for treatment of chronic inflammation in atherosclerosis and other cardiovascular diseases.
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Alternatively activated macrophages elicited by helminth infection can be reprogrammed to enable microbial killing.

TL;DR: Despite the long-term exposure to Th2 cytokines and antiinflammatory signals in vivo, it is found that NeMφ were not terminally differentiated but could develop a more classically activated phenotype in response to LPS and IFN-γ, and could become antimicrobial.
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Paired immunoglobin-like receptor-B regulates the suppressive function and fate of myeloid-derived suppressor cells

TL;DR: The studies indicated that MDSCs genetically ablated for PIR-B (Lilrb3(-/-) MDSC underwent a specific transition to M1-like cells when entering the periphery from bone marrow, resulting in decreased suppressive function, regulatory T cell activation activity, primary tumor growth, and lung metastases.
References
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Journal ArticleDOI

International Union of Pharmacology: Approaches to the Nomenclature of Voltage-Gated Ion Channels

TL;DR: This issue of Pharmacological Reviews includes a new venture in the collaboration between the International Union of Pharmacology (IUPHAR) and the American Society for Pharmacology and Experimental Therapeutics (ASPET), in that a new classification of voltage-gated ion channels is outlined.
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Alternative activation of macrophages

TL;DR: The evidence in favour of alternative macrophage activation by the TH2-type cytokines interleukin-4 (IL-4) and IL-13 is assessed, and its limits and relevance to a range of immune and inflammatory conditions are defined.
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Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes

TL;DR: These functionally polarized cells, and similarly oriented or immature dendritic cells present in tumors, have a key role in subversion of adaptive immunity and in inflammatory circuits that promote tumor growth and progression.
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NF-kappaB regulation in the immune system.

TL;DR: The role of NF-κB proteins as potential therapeutic targets in clinical applications and their role in the immune system and inflammatory diseases are discussed.
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Blood Monocytes Consist of Two Principal Subsets with Distinct Migratory Properties

TL;DR: Using a murine adoptive transfer system to probe monocyte homing and differentiation in vivo, two functional subsets among murine blood monocytes are identified: a short-lived CX(3)CR1(lo)CCR2(+)Gr1(+) subset that is actively recruited to inflamed tissues and a CX (3) CR1(hi)CCS1-dependent recruitment to noninflamed tissues.
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