Increased expression of the inflammatory chemokine CXC chemokine ligand 9/monokine induced by interferon-γ in lymphoid tissues of rhesus macaques during simian immunodeficiency virus infection and acquired immunodeficiency syndrome

Reinhart, Todd A.; Fallert, Beth A.; Pfeifer, Melanie E.; Sanghavi, Sonali; Capuano, Saverio; Rajakumar, Premeela A.; Murphey‐Corb, Michael; Day, Richard; Fuller, Craig L.; Schaefer, Todd M.

doi:10.1182/blood.v99.9.3119

Cited by 73 publications

(109 citation statements)

References 57 publications

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“…Earlier work on the SIV/rhesus macaque model addressing this issue demonstrated that during acute infection, despite widespread virus replication in the lymphoid tissues, virus replication in the lungs proceeded only minimally and was not evident in CD68-positive macrophages. 29 Furthermore, these studies also demonstrated that during chronic SIV infection, the lung tissues of macaques harbored many virus-positive CD68-positive cells that localized in large foci in diaphragmatic lobes. Similar to the findings reported by these authors, 30 we found large numbers of CD68-postive, virus-positive cells in the lungs of SHIV-infected macaques with lung disease, even though the patholog- Goat anti-MCP-1 polyclonal antibody (A) or mouse anti-CXCL10 monoclonal antibody (B) was used as primary antibody to stain the lung sections, followed by treatment with Alexa Fluor 594-conjugated secondary antibody.…”

Section: Discussionmentioning

confidence: 83%

Simian Human Immunodeficiency Virus-Associated Pneumonia Correlates with Increased Expression of MCP-1, CXCL10, and Viral RNA in the Lungs of Rhesus Macaques

Sui

Pinson

et al. 2005

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 83%

Simian Human Immunodeficiency Virus-Associated Pneumonia Correlates with Increased Expression of MCP-1, CXCL10, and Viral RNA in the Lungs of Rhesus Macaques

Sui

Pinson

et al. 2005

The American Journal of Pathology

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“…6, 8, and 14; this study) may allow pDCs to roll on resting or on minimally activated ECs and, thus, to constantly screen peripheral sites and lymph nodes for chemokine signatures of viral infection. In this respect, the CXCR3Ls may be of particular significance as they are among the gene products that are extremely rapidly and robustly up-regulated after viral encounter (42,43). In aggregate, these observations allow for speculation that pDC traffic into virally infected sites is maximal at early time points and may decrease with the onset of overt EC activation and EC activationdependent recruitment of effector cells of the innate and adaptive immune system.…”

Section: Discussionmentioning

confidence: 96%

Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

Kohrgruber

Gröger

Meraner

et al. 2004

The Journal of Immunology

109

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Plasmacytoid dendritic cells (pDCs) recognize microbes, viruses in particular, and provide unique means of innate defense against them. The mechanism of pDC tissue recruitment remained enigmatic because the ligands of CXCR3, the cardinal chemokine receptor on pDCs, have failed to induce in vitro chemotaxis of pDCs in the absence of additional chemokines. In this study, we demonstrate that CXCR3 is sufficient to induce pDC migration, however, by a migratory mechanism that amalgamates the features of haptotaxis and chemorepulsion. To mediate “haptorepulsion” of pDCs, CXCR3 requires the encounter of its cognate ligands immobilized, optimally by heparan sulfate, in a form of a negative gradient. This is the first report of the absolute requirement of chemokine immobilization and presentation for its in vitro promigratory activity. The paradigmatic example of pDC haptorepulsion described here may represent a new pathophysiologically relevant migratory mechanism potentially used by other cells in response to other chemokines.

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“…In previous studies we and others have found that SIV infection alters the levels of IFN-␥-inducible CXCR3 ligands 33 and lymphoid homing chemokines 34 in lymph nodes. In this study we focused on lung mucosal tissues in cynomolgus macaques and found that inflammatory modulators (eg, IFN-␥, CXCR3 ligands, and CCR5 ligands), were also up-regulated during SIV infection, particularly in animals with clear P. carinii coinfection.…”

Section: Discussionmentioning

confidence: 99%

Simian Immunodeficiency Virus Infection Alters Chemokine Networks in Lung Tissues of Cynomolgus Macaques

Qin

Junecko

Trichel

et al. 2010

The American Journal of Pathology

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Infection by HIV-1 frequently leads to pulmonary complications, including alterations to local immune environments. To better understand these alterations, we have examined in detail the patterns and levels of expression of chemokine, cytokine, and chemokine receptor mRNAs in lung tissues from 16 uninfected or simian immunodeficiency virus ( Pulmonary diseases are frequent complications of HIV-1 infection, affecting 75% to 85% of patients with AIDS.1 In addition, Pneumocystis carinii (now called Pneumocystis jirovecii in humans) pneumonia (PCP) is one of most frequent pulmonary opportunistic infections in HIV-1 infected individuals. However, little is known about the mechanisms leading to changes in pulmonary immune function and how these changes ultimately contribute to pathogenesis. Identifying alterations of overall immune function and the local mediators of these changes in the lungs during HIV-1 infection and AIDS will be useful for understanding and treating HIV-1-associated pulmonary complications.Chemokines are soluble immune factors that recruit cells bearing appropriate receptors into local environments as part of homeostatic immune cell trafficking and inflammatory reactions. There are approximately 50 known chemokines and 18 chemokine receptors.2 Chemokines play an important role in the control of infectious agents by recruiting effector cells to local inflammatory sites of infection and by serving directly as antimicrobial peptides.

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Increased expression of the inflammatory chemokine CXC chemokine ligand 9/monokine induced by interferon-γ in lymphoid tissues of rhesus macaques during simian immunodeficiency virus infection and acquired immunodeficiency syndrome

Cited by 73 publications

References 57 publications

Simian Human Immunodeficiency Virus-Associated Pneumonia Correlates with Increased Expression of MCP-1, CXCL10, and Viral RNA in the Lungs of Rhesus Macaques

Simian Human Immunodeficiency Virus-Associated Pneumonia Correlates with Increased Expression of MCP-1, CXCL10, and Viral RNA in the Lungs of Rhesus Macaques

Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

Simian Immunodeficiency Virus Infection Alters Chemokine Networks in Lung Tissues of Cynomolgus Macaques

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