Th1 and Th2 cytokines cooperate to stimulate mannose-receptor-mediated phagocytosis

Raveh, David; Kruskal, Benjamin A.; Farland, J.; Ezekowitz, R. A. B.

doi:10.1002/jlb.64.1.108

Cited by 55 publications

(38 citation statements)

References 28 publications

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“…The effect of IL-4 on uptake of antigens by macrophages is dependent on both antigen and pathway. Treatment of macrophages with IL-4 leads to increased uptake of soluble antigen as well as increased mannose receptor-dependent uptake of antigen (Montaner et al, 1999;Raveh et al, 1998). However, alternative activation of macrophages with IL-4 has been shown to impair phagocytosis of bacteria and microbial particles (Varin et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Susceptibility of bone marrow-derived macrophages to influenza virus infection is dependent on macrophage phenotype

Campbell

Nicol

Dransfield

et al. 2015

Journal of General Virology

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The role of the macrophage in influenza virus infection is complex. Macrophages are critical for resolution of influenza virus infections but implicated in morbidity and mortality in severe infections. They can be infected with influenza virus and consequently macrophage infection is likely to have an impact on the host immune response. Macrophages display a range of functional phenotypes, from the prototypical pro-inflammatory classically activated cell to alternatively activated anti-inflammatory macrophages involved in immune regulation and wound healing. We were interested in how macrophages of different phenotype respond to influenza virus infection and therefore studied the infection of bone marrow-derived macrophages (BMDMs) of classical and alternative phenotype in vitro. Our results show that alternatively activated macrophages are more readily infected and killed by the virus than classically activated. Classically activated BMDMs express the pro-inflammatory markers inducible nitric oxide synthase (iNOS) and TNF-a, and TNF-a expression was further upregulated following infection. Alternatively activated macrophages express Arginase-1 and CD206; however, following infection, expression of these markers was downregulated whilst expression of iNOS and TNF-a was upregulated. Thus, infection can override the anti-inflammatory state of alternatively activated macrophages. Importantly, however, this results in lower levels of proinflammatory markers than those produced by classically activated cells. Our results showed that macrophage phenotype affects the inflammatory macrophage response following infection, and indicated that modulating the macrophage phenotype may provide a route to develop novel strategies to prevent and treat influenza virus infection.

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Section: Discussionmentioning

confidence: 99%

Susceptibility of bone marrow-derived macrophages to influenza virus infection is dependent on macrophage phenotype

Campbell

Nicol

Dransfield

et al. 2015

Journal of General Virology

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“…When, however, a Th2 immune memory is generated following an infection or vaccination, a more pronounced and even detrimental inflammatory response will arise upon renewed contact with RSV, due to the secretion of IL-4 and IL-5 by Th2 cells. In addition, the Th1 and Th2 responses are known to downregulate each other's activation, as will be described below (13). For these reasons, a dominant Th2 response will result in an inefficient viral clearance and increased disease severity (1,8,12).…”

Section: Th1 Cells Th2 Cells and Rsvmentioning

confidence: 99%

The role of Th17 and Treg responses in the pathogenesis of RSV infection

et al. 2015

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“…Binding or internalization of natural or synthetic ligands of MR may modulate macrophage functions, including respiratory burst (6) and synthesis of proinflammatory cytokines, such as IL-1␤, IL-6, and GM-CSF (7) to increase their microbicidal capacity. Previous studies have shown that MR expression can be positively modulated in vitro by many agents, in particular by 1,25-dihydroxyvitamin D3 (8), prostaglandin E 2 (9), IL-4, and IL-13 (10,11). Further support for a role of IL-13 in the control of the innate immune response came from the characterization of susceptibility to infection of animals that were deficient in IL-13.…”

Section: Il-13 Attenuates Gastrointestinal Candidiasis In Normal Andmentioning

confidence: 99%

“…To evaluate MR surface expression on mouse peritoneal macrophages harvested from mice untreated or treated in vivo by IL-13, 15d-PGJ 2 , rosiglitazone, and/or GW9662, 1 ϫ 10 6 peritoneal cells were incubated directly with a mannosylated BSA (mBSA), an MR-specific ligand, conjugated with FITC (840 nM) (7,11). Labeling of MR was done during 1 h on ice.…”

Section: Mr Surface Expressionmentioning

confidence: 99%

IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation

Coste

Lagane

Filipe

et al. 2008

The Journal of Immunology

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We recently demonstrated that in vitro peroxisome proliferator-activated receptor-γ (PPARγ) activation of mouse peritoneal macrophages by IL-13 or PPARγ ligands promotes uptake and killing of Candida albicans through mannose receptor overexpression. In this study, we demonstrate that i.p. treatment of immunocompetent and immunodeficient (RAG-2−/−) mice with natural and synthetic PPARγ-specific ligands or with IL-13 decreases C. albicans colonization of the gastrointestinal (GI) tract 8 days following oral infection with the yeast. We also showed that Candida GI infection triggers macrophage recruitment in cecum mucosa. These mucosal macrophages, as well as peritoneal macrophages, overexpress the mannose receptor after IL-13 and rosiglitazone treatments. The treatments promote macrophage activation against C. albicans as suggested by the increased ability of peritoneal macrophages to phagocyte C. albicans and to produce reactive oxygen intermediates after yeast challenge. These effects on C. albicans GI infection and on macrophage activation are suppressed by treatment of mice with GW9662, a selective PPARγ antagonist, and are reduced in PPARγ+/− mice. Overall, these data demonstrate that IL-13 or PPARγ ligands attenuate C. albicans infection of the GI tract through PPARγ activation and hence suggest that PPARγ ligands may be of therapeutic value in esophageal and GI candidiasis in immunocompromised patients.

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Th1 and Th2 cytokines cooperate to stimulate mannose-receptor-mediated phagocytosis

Cited by 55 publications

References 28 publications

Susceptibility of bone marrow-derived macrophages to influenza virus infection is dependent on macrophage phenotype

Susceptibility of bone marrow-derived macrophages to influenza virus infection is dependent on macrophage phenotype

The role of Th17 and Treg responses in the pathogenesis of RSV infection

IL-13 Attenuates Gastrointestinal Candidiasis in Normal and Immunodeficient RAG-2−/− Mice via Peroxisome Proliferator-Activated Receptor-γ Activation

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