Macrophages in Innate and Acquired Immunity

Twigg, Homer L.

doi:10.1055/s-2004-822302

Cited by 52 publications

(39 citation statements)

References 65 publications

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“…The first observation regarding classical activation is novel and consistent with the published literature on HIV infection in the lung (33) and in macrophages (34). In particular, classical activa- tion is consistent with published measurements of raised cytokine levels in bronchoalveolar lavage fluid (35) and also with upregulation of receptors critical in phagocytosis of Mycobacterium tuberculosis (36).…”

Section: Discussionsupporting

confidence: 85%

The Alveolar Microenvironment of Patients Infected with Human Immunodeficiency Virus Does Not Modify Alveolar Macrophage Interactions with Streptococcus pneumoniae

Gordon

Jagoe

Jarman

et al. 2013

Clin Vaccine Immunol

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gWe tested the hypothesis that HIV infection results in activation of alveolar macrophages and that this might be associated with impaired defense against pneumococcus. We compared alveolar macrophages and lymphocytes in 131 bronchoalveolar lavage samples from HIV-infected and healthy controls using inflammatory gene microarrays, flow cytometry, real-time PCR, and enzyme-linked immunosorbent assay (ELISA) to determine the pattern of macrophage activation associated with HIV infection and the effect of this activation on defense against pneumococcus. We used gamma interferon (IFN-␥) priming to mimic the cellular milieu in HIV-infected lungs. InnateDB and BioLayout 3D were used to analyze the interactions of the upregulated genes. Alveolar macrophages from HIV-infected adults showed increased gene expression and cytokine production in a classical pattern. Bronchoalveolar lavage from HIV-infected subjects showed excess CD8 ؉ lymphocytes with activated phenotype. Tolllike receptor 4 (TLR4) expression was increased in macrophages from HIV-infected subjects, but function was similar between the groups; lung lavage fluid did not inhibit TLR function in transfected HeLa cells. Alveolar macrophages from HIV-infected subjects showed normal binding and internalization of opsonized pneumococci, with or without IFN-␥ priming. Alveolar macrophages from HIV-infected subjects showed classical activation compared to that of healthy controls, but this does not alter macrophage interactions with pneumococci.

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Section: Discussionsupporting

confidence: 85%

The Alveolar Microenvironment of Patients Infected with Human Immunodeficiency Virus Does Not Modify Alveolar Macrophage Interactions with Streptococcus pneumoniae

Gordon

Jagoe

Jarman

et al. 2013

Clin Vaccine Immunol

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“…Virus infections generally upregulate MHC antigens and co-stimulatory molecules on antigen-presenting cells and induce proinflammatory cytokines and chemokine expression, which enhances dendritic cell and macrophage activation of T lymphocytes. Macrophages play important roles in innate immunity, such as phagocytosis, containment of pathogens and the secretion of cytokines and chemokines important in the inflammatory responses that contain infection and augment immune regulation (Taylor et al, 2005;Twigg, 2004). In influenza virus-infected hosts, mononuclear cells become infected after the primary target cells, respiratory ciliated epithelial cells (Fujisawa et al, 1987;Kaufmann et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Modulation of the immune responses in chickens by low-pathogenicity avian influenza virus H9N2

Xing

Cardona

et al. 2008

Journal of General Virology

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Most low-pathogenicity avian influenza (LPAI) viruses cause no or mild disease in avian species. Little is known about the mechanisms of host defence and the immune responses of avian influenza-infected birds. This study showed that chicken macrophages are susceptible to infection with LPAI H9N2 and H6N2 viruses and that infection led to apoptosis. In H9N2 virus-infected chicken macrophages, Toll-like receptor 7 responded to infection and mediated the cytokine responses. Whilst pro-inflammatory cytokines were largely upregulated, the interferon (IFN) response was fairly weak and IFN-inducible genes were differentially regulated. Among the regulated genes, major histocompatibility complex (MHC) antigens II were downregulated, which also occurred in the lungs of H9N2-infected chickens. Additionally, interleukin (IL)-4, IL-4 receptor and CD74 (MHC class II invariable chain) were also downregulated, all of which are pivotal in the activation of CD4 + helper T cells and humoral immunity. Remarkably, in H9N2virus-infected chickens, the antibody response was severely suppressed. This was in contrast to the robust antibody response in chickens infected with H6N2 virus, in which expression of MHC class II antigens was upregulated. These data suggest that neutralizing antibodies and humoral immunity may not be developed efficiently in H9N2-infected chickens. These findings raise questions about how some LPAI viruses differentially regulate avian immune responses and whether they have similar effects on mammalian immune function.

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“…Differentiation Ags present on macrophages, such as CD14, are important for the initiation of macrophage-mediated immune responses to bacteria and other invading pathogens. Thus, accumulation of macrophages at the relevant sites of infection is beneficial to the host for resolution of infections (1)(2)(3)(4)(5). However, characterization of the basal/ homeostatic circuitry that prepares macrophages for diverse immune responses, while sustaining their survival remains incomplete.…”

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confidence: 99%

Wnt5a–Rac1–NF-κB Homeostatic Circuitry Sustains Innate Immune Functions in Macrophages

Naskar

Maiti

Chakraborty

et al. 2014

The Journal of Immunology

121

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Macrophages play a critical role in innate immunity. Differentiation Ags present on macrophages such as CD14 orchestrate the first line of defense against infection. The basal/homeostatic signaling scheme that keeps macrophages thus groomed for innate immune functions remains unresolved. Wnt5a–Fz5 signaling being a primordial event during cell differentiation, we examined the involvement of Wnt5a–Fz5 signaling in the maintenance of innate immune functions. In this study, we demonstrate that innate immune functions of macrophages ensue at least partly through a homeostatic Wnt5a–Fz5–NF-κB (p65) circuit, which is Rac1 dependent. The autocrine/paracrine Wnt5a–Fz5–Rac1–p65 signaling cascade not only maintains basal levels of the immune defense modulating IFNs and CD14; it also supports macrophage survival. Wnt5a–Fz5–Rac1 signaling mediated p65 homeostasis in turn sustains Wnt5a expression in a feed-forward mode. The natural immune response of macrophages to Escherichia coli/LPS and virus is accordingly sustained. The depiction of sustenance of innate immune functions as an outcome of a homeostatic Wnt5a–p65 axis unfolds previously unidentified details of immune regulation and provides new insight into homeostatic cell signaling.

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Macrophages in Innate and Acquired Immunity

Cited by 52 publications

References 65 publications

The Alveolar Microenvironment of Patients Infected with Human Immunodeficiency Virus Does Not Modify Alveolar Macrophage Interactions with Streptococcus pneumoniae

The Alveolar Microenvironment of Patients Infected with Human Immunodeficiency Virus Does Not Modify Alveolar Macrophage Interactions with Streptococcus pneumoniae

Modulation of the immune responses in chickens by low-pathogenicity avian influenza virus H9N2

Wnt5a–Rac1–NF-κB Homeostatic Circuitry Sustains Innate Immune Functions in Macrophages

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