Hepatitis B virus surface antigen suppresses the activation of monocytes through interaction with a serum protein and a monocyte-specific receptor

Vanlandschoot, Peter; Houtte, Freya Van; Roobrouck, Annelies; Farhoudi, Ali; Leroux‐Roels, Geert

doi:10.1099/0022-1317-83-6-1281

Cited by 42 publications

(82 citation statements)

References 23 publications

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“…In chronic hepatitis B infections, levels of sCD14 are increased but, interestingly, an inverse correlation between HBsAg levels and sCD14 levels is found (S. Steyaert et al, unpublished). Recently rHBsAg was shown to behave as an apoptotic-like particle [8,9]. Additionally, rHBsAg binds to monocytes through interaction with the LPS-binding protein and CD14 [31].…”

Section: Hbsag Interacts With Molecules That Bind Apcesmentioning

confidence: 99%

“…An increased nuclear degradation of mRNA was demonstrated [7]. Recently, yeast-expressed HBsAg (rHBsAg) was shown to behave as an apoptotic-like particle: rHBsAg suppressed LPS-induced secretion of proinflammatory cytokines but increased secretion of IL-10 by monocytes [8,9]. Similarly, binding and engulfment of APCEs suppresses secretion of proinflammatory cytokines and certain chemokines by macrophages [10,11].…”

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confidence: 99%

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Viral apoptotic mimicry: an immune evasion strategy developed by the hepatitis B virus?

Vanlandschoot

Leroux‐Roels

2003

Trends in Immunology

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Section: Hbsag Interacts With Molecules That Bind Apcesmentioning

confidence: 99%

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confidence: 99%

Viral apoptotic mimicry: an immune evasion strategy developed by the hepatitis B virus?

Vanlandschoot

Leroux‐Roels

2003

Trends in Immunology

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“…37 Several factors likely are responsible for these defects of the adaptive immunity, including intrahepatic recruitment and subsequent deletion of activated virus-specific CD8 ϩ T cells, 55 antigendriven T-or B-cell exhaustion, 56 the ability of liver sinusoidal endothelial cells to suppress the expansion of T-helper 1-type cells, 57 and the production of viral proteins with immunomodulatory effects. [58][59][60] In addition, late appearance, reduced size, and functional T-cell defects detected in both primary HBV and HCV infections also might be a consequence of the inability of the innate immune response to provide an efficient containment of early virus replication and to promote timely and appropriate T-cell priming. Do available data allow support of this concept?…”

Section: Profiles Of Adaptive Immune Responses Early After Hbv and Hcmentioning

confidence: 99%

Kinetics of the immune response during HBV and HCV infection

2003

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The innate immune system has a role not only in protecting the host during the initial period of virus infection, but also in shaping the nature of the adaptive immune response. In this review, we follow the kinetics of the virologic and immunologic events occurring from the time of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection. We primarily discuss how the early events after infection might influence the development of the adaptive immune response in these 2 important viral infections and how new strategies for more efficient preventive and therapeutic vaccines can be derived from this knowledge. (HEPATOLOGY 2003; 38:4-13.)H epatitis B (HBV) and hepatitis C (HCV) viruses are the 2 major causes of chronic liver inflammation worldwide. 1,2 Despite distinct virologic features, both viruses are preferentially hepatotropic, not directly cytopathic, and elicit liver diseases that share several aspects of their natural history. HBV and HCV infections share also some important features of the adaptive immune response. Multispecific antiviral CD4 and CD8 responses with a T-helper type 1 profile of cytokine production are detectable in the blood of subjects with a self-limited infection. [3][4][5][6][7][8][9][10][11][12][13][14][15][16] These responses are stronger than those found in patients with chronic infection. [17][18][19][20][21] Based on these observations, it has been proposed that the ability to mount an efficient cellular immune response is the main mechanism responsible for HBV and HCV control, whereas a defect in this response leads to chronicity. 2,22 However, the lack of suitable animal models to study the pathogenesis of HBV and HCV infections has so far hampered a definitive demonstration that associations between different infection outcomes and different vigor and breadth of T-cell responses have a causative effect. A recent report in HCV-infected chimpanzees, in which a clear association between T-cell response and virus clearance was not found, 23 added a further note of caution. Even so, it is difficult to argue against the importance of the cellular immune response in HBV and HCV control. In chimpanzees infected with HCV, expansion of a multispecific and sustained HCV-specific CD8 ϩ T-cell-mediated response was observed in 2 of 2 animals that cleared the virus, but not in the 4 animals that developed a chronic infection. 24 These results have been confirmed by recent reports showing that expansion of interferon ␥ (IFN-␥) ϩ , CD8 ϩ , and CD4 ϩ T cells precedes viral clearance in patients studied during the incubation phase of acute HCV infection in man 10 and in HCV-infected chimpanzees. 25 Similar findings have been reported in animal models of HBV infection 26 and in patients studied during the incubation phase of HBV infection, 27 in whom reduced early expansion of virusspecific T cells was associated with virus persistence. Moreover, the importance of virus-specific CD8 ϩ T cells in HBV control has been confirmed further by CD8 ϩ T-cell deletion experiments performed in HBV-i...

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“…These lines of evidence directly support our contention that the interaction between NY-ESO-1 and CRT is specific and not an interaction between a chaperone and its client protein. Similar binding affinities are present among other critical molecular interactions known to exert regulatory functions to the innate immune system, such as those between IgGA1/A2 and Fc␣RI (17), between the hepatitis B surface Ag and the CD14/TLR4 complex (18), and between heat shock proteins and CD91 (3). Thus, CRT represents an innate immune receptor that directly binds to NY-ESO-1 without mediators.…”

Section: Discussionmentioning

confidence: 99%

Dendritic Cell Surface Calreticulin Is a Receptor for NY-ESO-1: Direct Interactions between Tumor-Associated Antigen and the Innate Immune System

Zeng

Aldridge²,

Tian³

et al. 2006

The Journal of Immunology

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How the immune system recognizes endogenously arising tumors and elicits adaptive immune responses against nonmutated tumor-associated Ags is poorly understood. In search of intrinsic factors contributing to the immunogenicity of the tumor-associated Ag NY-ESO-1, we found that the NY-ESO-1 protein binds to the surface of immature dendritic cells (DC), macrophages, and monocytes, but not to that of B cells or T cells. Using immunoprecipitation coupled with tandem mass spectrometry, we isolated DC surface calreticulin as the receptor for NY-ESO-1. Calreticulin Abs blocked NY-ESO-1 binding on immature DC and its cross-presentation to CD8+ T cells in vitro. Calreticulin/NY-ESO-1 interactions provide a direct link between NY-ESO-1, the innate immune system, and, potentially, the adaptive immune response against NY-ESO-1.

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Hepatitis B virus surface antigen suppresses the activation of monocytes through interaction with a serum protein and a monocyte-specific receptor

Cited by 42 publications

References 23 publications

Viral apoptotic mimicry: an immune evasion strategy developed by the hepatitis B virus?

Viral apoptotic mimicry: an immune evasion strategy developed by the hepatitis B virus?

Kinetics of the immune response during HBV and HCV infection

Dendritic Cell Surface Calreticulin Is a Receptor for NY-ESO-1: Direct Interactions between Tumor-Associated Antigen and the Innate Immune System

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