Cell-to-cell contact via measles virus haemagglutinin-CD46 interaction triggers CD46 downregulation

Krantic, Slavica; Gimenez, Cyrille; Rabourdin–Combe, Chantal

doi:10.1099/0022-1317-76-11-2793

Cited by 58 publications

(46 citation statements)

References 27 publications

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“…The murine fibroblast cell line L929, parental (L cells) or transfected with measles hemagglutinin (LH cells) (33), and HeLa cells were cultured in RPMI medium 1640 with 10% FCS.…”

Section: Methodsmentioning

confidence: 99%

Ligation of the cell surface receptor, CD46, alters T cell polarity and response to antigen presentation

Oliaro

Pasam

Waterhouse

et al. 2006

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

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Lymphocyte function in vivo is dictated by multiple external cues, but the integration of different signals is not well understood. Here, we show that competition for the axis of polarization dictates functional outcomes. We investigated the effect of ligation of the immunoregulatory cell surface receptor, CD46, on lymphocyte polarity during antigen presentation and cytotoxic effector function. Ligation of CD46 on human T cells prevented recruitment of the microtubule organizing center, CD3, and perforin to the interface with the antigen-presenting cell and caused a reduction in IFN-␥ production. In human NK cells, similar changes in polarity induced by CD46 ligation inhibited the recruitment of the microtubule organizing center and perforin to the interface with target cells and correlated with reduced killing. These data indicate that external signals can alter lymphocyte polarization toward antigen-presenting cells or target cells, inhibiting lymphocyte function.immunological synapse ͉ measles ͉ polar axis ͉ T cell signaling ͉ cytotoxicity L ymphocyte function is inf luenced by multiple extracellular cues, and the response to these signals is regulated by compartmentalization of proteins into distinct domains within the cell, for instance during migration or antigen presentation (1-3). Antigen presentation involves the formation of an immunological synapse (IS) proximal to the antigenpresenting cell (APC), remodeling of the actin and tubulin cytoskeletal networks, and clustering of signaling complexes at the distal pole of an axis perpendicular to the APC (4). Intracellular compartmentalization can control the sensitivity to signal, the duration of responsiveness to signal, and the direction of effector responses such as migration, cytotoxicity, and cytokine secretion (5). The signals that trigger polarization, such as ligation of chemokine receptors or the T cell receptor (TCR), are often modulated by the ensuing polarization state (2, 5), suggesting that cell polarity provides an inbuilt feedback mechanism.Recent reports suggest that extracellular signals compete to dictate both lymphocyte polarity and functional outcome. The intensity of signal from two target cells attached to the same T cell dictates the polarization of cytolytic granules (6). Competition between TCR and chemokine signaling determines whether a T cell adopts migratory polarization or forms an IS (7-9). To explore whether competition for polarization might provide a general means for controlling lymphocyte function, we investigated the effects of a competing polarizing signal on the response of lymphocytes to TCR or NK receptor signaling.CD46 is a cell surface receptor for complement C3b and a number of pathogens, including measles viruses (10 -12). CD46 ligation has been proposed to limit acquired immune function in response to complement and pathogens (12, 13) and facilitate the dramatic immunosuppression triggered by measles infection (14). Indeed, ligation of CD46 can mediate direct effects on T cell function, such as inducing regulat...

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“…The murine fibroblast cell line L929, parental (L cells) or transfected with measles hemagglutinin (LH cells) (33), and HeLa cells were cultured in RPMI medium 1640 with 10% FCS.…”

Section: Methodsmentioning

confidence: 99%

Ligation of the cell surface receptor, CD46, alters T cell polarity and response to antigen presentation

Oliaro

Pasam

Waterhouse

et al. 2006

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

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“…However, as described for CD46 (20,36), a rapid receptor modulation may also be induced by contact of MV glycoproteins with SLAM on uninfected cells. We measured contact-mediated downregulation by mixing persistently infected BJAB cells with uninfected SLAM-positive cells.…”

Section: Selection Of a Receptor Blocking Antibodymentioning

confidence: 99%

CD150 (SLAM) Is a Receptor for Measles Virus but Is Not Involved in Viral Contact-Mediated Proliferation Inhibition

Erlenhoefer¹,

Wurzer²,

Löffler³

et al. 2001

J Virol

172

157

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Section: Cd46 Modulationmentioning

confidence: 99%

“…We and others have demonstrated previously that vaccine and laboratory strains effectively modulate CD46 (Krantic et al, 1995;Naniche et al, 1993b;Schneider-Schaulies et al, 1995a, b, 1996 and that MV wild-type strains modulate SLAM on the surface of infected cells and after contact of the cells with viral glycoproteins (Erlenhoefer et al, 2001;Tanaka et al, 2002). We infected HUVECs and HBMECs with MV strains Edm and the wild-type strains (m.o.i.=0?1) for 3 days and determined the CD46 and MV H expression by double staining and flow cytometry.…”

Section: Cd46 Modulationmentioning

confidence: 99%

CD46- and CD150-independent endothelial cell infection with wild-type measles viruses

Andrés¹,

Obojes²,

Kim

et al. 2003

Journal of General Virology

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Measles virus (MV) infects endothelial cells of the skin, the brain and other organs during acute or persistent infections. Endothelial cells are supposed to play an important role in virus spread from the blood stream to surrounding tissues. CD46 and CD150 (signalling lymphocytic activation molecule, SLAM) have been described as cellular receptors for certain MV strains. We found that human umbilical vein and brain microvascular endothelial cells (HUVECs and HBMECs) were CD46-positive, but did not express SLAM. Wild-type MV strains, which do not use CD46 as a receptor at the surface of transfected Chinese hamster ovary cells, infected HUVECs and HBMECs to varying extents in a strain-dependent way. This infection was not inhibited by antibodies to CD46. These data suggest the presence of an additional unidentified receptor for MV uptake and spread in human endothelial cells. INTRODUCTIONAfter acute infection of the upper respiratory tract, measles virus (MV) is rapidly transported to draining lymph nodes forming giant cells in the reticulo-endothelial system. MV then establishes a systemic infection and spreads to different organs, including the skin. In these organs, virus replicates primarily in endothelial cells (ECs), epithelial cells and monocytes/macrophages (Griffin & Bellini, 1996). ECs of dermal capillaries (Kimura et al., 1975) and small vessels throughout the body show clear evidence of MV infection. This appears to play a central role in pathogenesis, leading to changes in the skin, conjunctivae, mucous membranes and the brain (Cosby & Brankin, 1995), accompanied by vascular dilatation, increased vascular permeability, mononuclear cell infiltration and infection of surrounding tissues. In rare cases, the EC infection may extend to a severe haemorrhagic infection with confluent haemorrhagic skin eruptions and intravascular coagulopathy, so-called haemorrhagic or black measles. Brain ECs and capillary endothelium of lymph nodes and the thymus have been found to be infected in fatal cases of acute measles (Esolen et al., 1995; Moench et al., 1988). In subacute sclerosing panencephalitis (SSPE) patients, brain ECs appear to be infected in addition to various neural cells (Allen et al., 1996;Isaacson et al., 1996;Kirk et al., 1991).Following the identification of CD46 as a receptor for MV vaccine and laboratory strains (Dörig et al., 1993;Naniche et al., 1993a), evidence has accumulated that many wildtype isolates do not use CD46 as a receptor. Recently, the signalling lymphocytic activation molecule (SLAM, CD150) has been identified as a common receptor interacting with MV vaccine as well as wild-type strains (Erlenhoefer et al., 2001(Erlenhoefer et al., , 2002Hsu et al., 2001; Ono et al., 2001a, b;Tatsuo et al., 2000). SLAM is expressed on human B cell lines, primary activated B and T cells, memory cells and activated monocytes and monocyte-derived dendritic cells (Cocks et al., 1995;Minagawa et al., 2001;Ohgimoto et al., 2001;Polacino et al., 1996;Punnonen et al., 1997), and its usage as a receptor c...

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Cell-to-cell contact via measles virus haemagglutinin-CD46 interaction triggers CD46 downregulation

Cited by 58 publications

References 27 publications

Ligation of the cell surface receptor, CD46, alters T cell polarity and response to antigen presentation

Ligation of the cell surface receptor, CD46, alters T cell polarity and response to antigen presentation

CD150 (SLAM) Is a Receptor for Measles Virus but Is Not Involved in Viral Contact-Mediated Proliferation Inhibition

CD46- and CD150-independent endothelial cell infection with wild-type measles viruses

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