Inflammatory monocyte effector mechanisms

Lauvau, Grégoire; Chorro, Laurent; Spaulding, Emily; Soudja, Saïdi M.

doi:10.1016/j.cellimm.2014.07.007

Cited by 55 publications

(45 citation statements)

References 91 publications

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“…Our study examined both myeloid and lymphoid cell compartments to provide a global analysis of blood immune leukocytes during severe human malaria. Data reveal both expansion and activation of inflammatory monocytes (CD14 + ), which express an exquisite machinery to sense pathogen-derived molecules, produce inflammatory cytokines and contribute to systemic inflammation [63]. We also found diminished pDC blood frequencies in severe malaria patients as reported before [51], yet our data further reveal that pDCs were activated.…”

Section: Discussionsupporting

confidence: 81%

STING-Licensed Macrophages Prime Type I IFN Production by Plasmacytoid Dendritic Cells in the Bone Marrow during Severe Plasmodium yoelii Malaria

et al. 2016

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Malaria remains a global health burden causing significant morbidity, yet the mechanisms underlying disease outcomes and protection are poorly understood. Herein, we analyzed the peripheral blood of a unique cohort of Malawian children with severe malaria, and performed a comprehensive overview of blood leukocytes and inflammatory mediators present in these patients. We reveal robust immune cell activation, notably of CD14+ inflammatory monocytes, NK cells and plasmacytoid dendritic cells (pDCs) that is associated with very high inflammation. Using the Plasmodium yoelii 17X YM surrogate mouse model of lethal malaria, we report a comparable pattern of immune cell activation and inflammation and found that type I IFN represents a key checkpoint for disease outcomes. Compared to wild type mice, mice lacking the type I interferon (IFN) receptor exhibited a significant decrease in immune cell activation and inflammatory response, ultimately surviving the infection. We demonstrate that pDCs were the major producers of systemic type I IFN in the bone marrow and the blood of infected mice, via TLR7/MyD88-mediated recognition of Plasmodium parasites. This robust type I IFN production required priming of pDCs by CD169+ macrophages undergoing activation upon STING-mediated sensing of parasites in the bone marrow. pDCs and macrophages displayed prolonged interactions in this compartment in infected mice as visualized by intravital microscopy. Altogether our findings describe a novel mechanism of pDC activation in vivo and precise stepwise cell/cell interactions taking place during severe malaria that contribute to immune cell activation and inflammation, and subsequent disease outcomes.

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Section: Discussionsupporting

confidence: 81%

STING-Licensed Macrophages Prime Type I IFN Production by Plasmacytoid Dendritic Cells in the Bone Marrow during Severe Plasmodium yoelii Malaria

et al. 2016

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“…[8][9][10] Akin to lymphocytes, these subsets may be endowed with specific functions. [4][5][6]11,12 Here, we demonstrate that an increase in the fraction of classical CD14…”

Section: /Cd16mentioning

confidence: 99%

Characteristic repartition of monocyte subsets as a diagnostic signature of chronic myelomonocytic leukemia

Selimoglu-Buet

Wagner-Ballon

Saada

et al. 2015

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“…In contrast to helminth infection, which results in tissue-resident macrophage proliferation in response to the Type II cytokine IL-4 37 (Figure 3), microbial infections typically engage Type I responses by promoting inflammatory monocyte recruitment 41,100 (Figure 3). Upon entering tissues, monocytes can remain “immature” or can differentiate into mature cells, including macrophages, to perform various effector functions.…”

Section: Macrophage Functionmentioning

confidence: 99%

Ontogeny of Tumor-Associated Macrophages and Its Implication in Cancer Regulation

2016

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Macrophages are innate immune cells with evolutionarily conserved functions in tissue maintenance and host defense. As such, macrophages are among the first hematopoietic cells that seed developing tissues, and respond to inflammatory insults by in situ proliferation or de novo differentiation from monocytes. Recent studies have revealed that monocyte-derived tumor-induced macrophages represent a major tumor-associated macrophage population, which can further expand following their differentiation in tumors. Compared to tissue-resident tumor-associated macrophages, these newly differentiated cells are phenotypically distinct, and likely play a unique role in tissue dysregulation and immune modulation in cancer. These findings imply that tumor growth elicits a specific innate immune response. In this review, we explore the different routes of macrophage seeding and maintenance in tissues during steady state and inflammation and how these principles underlie the responses observed during tumor development. In addition, we highlight the relationship between the origin and function of macrophages in different settings and how this knowledge may be used to create new opportunities for cancer immunotherapy.

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Inflammatory monocyte effector mechanisms

Cited by 55 publications

References 91 publications

STING-Licensed Macrophages Prime Type I IFN Production by Plasmacytoid Dendritic Cells in the Bone Marrow during Severe Plasmodium yoelii Malaria

STING-Licensed Macrophages Prime Type I IFN Production by Plasmacytoid Dendritic Cells in the Bone Marrow during Severe Plasmodium yoelii Malaria

Characteristic repartition of monocyte subsets as a diagnostic signature of chronic myelomonocytic leukemia

Ontogeny of Tumor-Associated Macrophages and Its Implication in Cancer Regulation

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