Ahlbrand YI

In order to reflect this difference in mechanism of heterogeneity, recently suggested nomenclature systems present the argument that macrophage diversity is more appropriately classified on the basis of similarity of the expression profile of the macrophage with expression profiles observed during in vitro stimulation with IL-4, immune complexes, IL-10, TGFβ, glucocorticoids, lipopolysaccharide (LPS), LPS and IFNγ, and IFNγ alone. S. Mattila

Ellis

In the context of human mycobacterial infection, circulating monocytes are skewed significantly toward the non-classical or CD16+ phenotype as compared to uninfected individuals, where greater than 90% of circulating monocytes are of the ‘classical’ or CD16− phenotype (Balboa et al.2011). Divangahi Ahlbrand Strong autocrine induction of IL-10 during early infection has been shown to reduce protective responses to Mtb such as IL-12p40 and TNF production in animal models (Turner et al.2002; Beamer et al.2008) and to be involved in blocking phagosome maturation in human alveolar macrophages (O'Leary, O'Sullivan and Keane 2011). Schneider

K M A S

J et al. This allows for a more nuanced identification of macrophage activation state in vivo on the basis of marker repertoire expression or absence and placement along a spectrum. AK Belhadj Z, He B, Deng H, Song S, Zhang H, Wang X, Dai W, Zhang Q. J Extracell Vesicles. Cambier Gordon Remold Datta Blecher-Gonen However, even this graded categorization, while useful, may not be fully adequate to reflect macrophage heterogeneity.

RD S CC. O'Sullivan Ehlers S

Hirsch Haseley These findings indicate that even at the earliest stages of infection there are different populations of macrophages circulating within an organism or particular tissue at baseline, and these different populations play different roles in progression or control of mycobacterial infection.

H Mattila et al. M

They are large cells, and their cell bodies abound in granules of various content, partly foreign material that may have reached the alveoli, or cell debris originating from cell damage or normal cell death. et al. Turnover and replenishment of epithelioid and other macrophages in the granuloma has important implications for granuloma dynamics, but has been relatively inaccessible to experimental analysis. Cadena M et al. 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Mycobacterium tuberculosis infection, Manipulation of the mononuclear phagocyte system by, Mycobacterium tuberculosis modulates macrophage lipid-sensing nuclear receptors PPARgamma and TR4 for survival, Inflammatory signaling in human tuberculosis granulomas is spatially organized, Macrophage polarization drives granuloma outcome during, Dendritic cell trafficking and antigen presentation in the human immune response to, The M1 and M2 paradigm of macrophage activation: time for reassessment, Microenvironments in tuberculous granulomas are delineated by distinct populations of macrophage subsets and expression of nitric oxide synthase and arginase isoforms, Adventures within the speckled band: heterogeneity, angiogenesis, and balanced inflammation in the tuberculous granuloma, Host-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalk, Cytokine and lipid mediator networks in tuberculosis, Clash of the cytokine titans: counter-regulation of interleukin-1 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Lawrence These macrophages are associated with wound healing and tissue repair.

In mouse models of atherosclerosis, cholesterol crystals can result in lysosomal destabilization and activate the NLRP3 inflammasome and IL-1 secretion (Duewell et al.2010; Sheedy et al.2013). Introduction 2. Rothfuchs

Macrophages express a broad range of plasma membrane receptors that mediate their interactions with natural and altered-self components of the host as well as a range of microorganisms. CG Yeap et al. Varol

H Ando Latent tuberculosis: what the host “sees”? et al. CM Coleman DL S E TJ In vitro models of granuloma development have identified a shift from the IFNγ-stimulated-type to IL-4-stimulated-type macrophages over time following mycobacterial infection and implicating temporal variation as an important component of macrophage diversity during mycobacterial infection (Huang et al.2015). The role of inflammasome activation in mycobacterial infections is complex and the subject of more in-depth treatment in a number of reviews (Briken, Ahlbrand and Shah 2013; Mayer-Barber and Yan 2016). et al. Chambers Hulette

Get the latest public health information from CDC: https://www.coronavirus.gov. A, Mayer-Barber During mycobacterial infection, either as a result of inflammatory stimulus or through direction of infecting bacilli, cholesterol accumulates within macrophages (Kondo and Kanai 1976).

M Macrophages within the most central region in non-necrotic granulomas or just adjacent to the central necrotic core are frequently foam cells as identified by Oil Red O-staining (Peyron et al.2008; Russell et al.2009) and show elevated HAM56 staining, a reported marker for foam cell formation (Ihling et al.1996; Cummings et al.2001; Mattila et al.2013). Croix et al.

Epstein Cronan N et al. A

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