A Novel Migration Pathway for Rat Dendritic Cells from the Blood: Hepatic Sinusoids–Lymph Translocation

Kudo, Shunsuke; Matsuno, Kenjiro; Ezaki, Taichi; Ogawa, Michio

doi:10.1084/jem.185.4.777

Cited by 130 publications

(99 citation statements)

References 12 publications

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“…DC are antigenpresenting cells and interact directly with both B and T lymphocytes (60)(61)(62)(63), some of which may be susceptible to HCV infection. Also, DC have been shown to migrate from the blood to the liver by translocation across the endothelium of hepatic sinusoids and may thus transport HCV to hepatocytes (64).…”

Section: Discussionmentioning

confidence: 99%

L-SIGN (CD209L) and DC-SIGN (CD209) mediate transinfection of liver cells by hepatitis C virus

Cormier

Durso

Tsamis

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

189

163

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Target cell tropism of enveloped viruses is regulated by interactions between viral and cellular factors during transmission, dissemination, and replication within the host. Binding of viral envelope glycoproteins to specific cell-surface receptors determines susceptibility to viral entry. However, a number of cell-surface molecules bind viral envelope glycoproteins without mediating entry. Instead, they serve as capture receptors that disseminate viral particles to target organs or susceptible cells. We and others recently demonstrated that the C type lectins L-SIGN and DC-SIGN capture hepatitis C virus (HCV) by specific binding to envelope glycoprotein E2. In this study, we use an entry assay to demonstrate that HCV pseudoviruses captured by L-SIGN؉ or DC-SIGN؉ cells efficiently transinfect adjacent human liver cells. Virus capture and transinfection require internalization of the SIGN-HCV pseudovirus complex. In vivo, L-SIGN is largely expressed on endothelial cells in liver sinusoids, whereas DC-SIGN is expressed on dendritic cells. Capture of circulating HCV particles by these SIGN؉ cells may facilitate virus infection of proximal hepatocytes and lymphocyte subpopulations and may be essential for the establishment of persistent infection.H epatitis C virus (HCV) is the etiologic agent of non-A non-B hepatitis in humans (1, 2). Only Ϸ15% of infected individuals clear the virus, and Ϸ170 million people worldwide are persistently infected with HCV (3, 4). These individuals may remain asymptomatic or may develop chronic hepatitis or cirrhosis, the latter often leading to hepatocellular carcinoma (5). Hepatocytes are the primary target cells for HCV infection (6-8). Virus-like particles have been visualized in liver biopsies of HCVϩ individuals (9-11), and in vitro infection, albeit inefficient, of primary hepatocytes and hepatoma cells has been documented (12)(13)(14). The existence of extrahepatic reservoirs of HCV is suggested by the detection of viral RNA in serum and peripheral blood mononuclear cells of HCVϩ individuals (15)(16)(17). Both B and T lymphocytes appear to be infected in vivo, which is supported by in vitro infection of B and T cell lines (7,8,18). One study, however, shows that replicating forms of HCV RNA are restricted to hepatocytes, whereas only nonreplicating forms are present in B lymphocytes, and none are in T lymphocytes (6).HCV envelope glycoproteins E1 and E2 mediate entry into target cells. We and others recently demonstrated that unmodified E1E2 heterodimers reach the cell surface and are incorporated into retroviral pseudoparticles, which can infect primary hepatocytes and some hepatoma cell lines (19 -22). Use of the soluble E2 ectodomain as a surrogate model for studying HCV interactions with cell-surface molecules has identified several potential HCV entry receptors, including CD81, scavenger receptor class B type 1, low-density lipoprotein receptor, and glycosaminoglycans (22-24). Several groups, including ours, have shown that CD81 is necessary but not sufficient for HCV pseu...

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Section: Discussionmentioning

confidence: 99%

L-SIGN (CD209L) and DC-SIGN (CD209) mediate transinfection of liver cells by hepatitis C virus

Cormier

Durso

Tsamis

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

189

163

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“…This interpretation is in agreement with the observation that intraportally injected dendritic cells are recovered from the hilar lymphatic vessels of the liver. 34 Although it is reported in human acive hepatitis that lymphocyte attachment to vascular wall termed ''endothelialitis'' is rather frequent in the portal veins, 4 this phenomenon does not seem to be primary reactions but secondary to portal lymphocyte infiltration, whereas ''endothelialitis'' in the central veins is associated with active concomitant parenchymal inflammation such as sinusoidal lymphocyte infiltration and hepatocyte necrosis. 4 We used here Con A-induced hepatitis as the experimental model because it shows several pathological features common to human hepatitis, i.e., massive hepatic necrosis and T-cell infiltration.…”

Section: Discussionmentioning

confidence: 99%

Sublobular veins as the main site of lymphocyte adhesion/transmigration and adhesion molecule expression in the porto-sinusoidal-hepatic venous system during concanavalin A-induced hepatitis in mice

et al. 2000

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Lymphocyte infiltration is a manifest feature of hepatitis. To reveal the main site and mechanism of lymphocyte adhesion/extravasation in the hepatic vasculature during inflammation, we morphometrically and histologically analyzed these events in relation to adhesion molecule expression using a murine model of T-cell mediated hepatitis induced by concanavalin A (Con A). Although lymphocyte adhesion was restricted to the sinusoids in untreated mice, it increased in all the segments of porto-sinusoidal-hepatic venous system 8 hours after Con A injection; the number of adhering lymphocytes per unit vascular circumference was the largest in the sublobular veins, relatively large in the central veins and small hepatic veins, and relatively small in the sinusoids and negligible in the portal veins. At 20 hours, extravascular lymphocytes showed similar distribution to lymphocyte adhesion at 8 hours except in the portal veins, around which they were possibly accumulated by the translocation of extrasinusoidal lymphocytes. E-selectin and vascular cell adhesion molecule-1 (VCAM-1) were transiently expressed at 4 to 6 hours, whereas P-selectin and intercellular adhesion molecule-1 were not changed between 0 and 48 hours. In particular, E-selectin expression coincided with that of lymphocyte adhesion in distribution.

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“…13,14 The precise molecular mechanisms about DC migration and interactions between DC and T cells are not yet well defined. However, it is becoming increasingly more evident that chemokines play an important role in the migration and recruitment of immune cells including DC and T cells in vivo.…”

Section: Ance To Tumor Challenge Most Effectively It Was Found That mentioning

confidence: 99%

Lymphotactin cotransfection enhances the therapeutic efficacy of dendritic cells genetically modified with melanoma antigen gp100

et al. 2002

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Lymphotactin (Lptn) is a C chemokine that attracts T cells and NK cells. Dendritic cells (DC) are highly efficient, specialized antigen-presenting cells and antigen-pulsed DC has been regarded as promising vaccines in cancer immunotherapy. The aim of our present study is to improve the therapeutic efficacy of DC-based tumor vaccine by increasing the preferential chemotaxis of DC to T cells. In this study, Lptnand/or melanoma-associated antigen gp100 were transfected into mouse bone marrow-derived DC, which were used as vaccines in B16 melanoma model.

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A Novel Migration Pathway for Rat Dendritic Cells from the Blood: Hepatic Sinusoids–Lymph Translocation

Cited by 130 publications

References 12 publications

L-SIGN (CD209L) and DC-SIGN (CD209) mediate transinfection of liver cells by hepatitis C virus

L-SIGN (CD209L) and DC-SIGN (CD209) mediate transinfection of liver cells by hepatitis C virus

Sublobular veins as the main site of lymphocyte adhesion/transmigration and adhesion molecule expression in the porto-sinusoidal-hepatic venous system during concanavalin A-induced hepatitis in mice

Lymphotactin cotransfection enhances the therapeutic efficacy of dendritic cells genetically modified with melanoma antigen gp100

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