Induction of G protein-coupled peptide receptor EBI 1 by human herpesvirus 6 and 7 infection in CD4+ T cells

Hasegawa, Hitoshi; Utsunomiya, Y; Yasukawa, Masaki; Yanagisawa, Kohsuke; Fujita, Shigeru

doi:10.1128/jvi.68.8.5326-5329.1994

Cited by 54 publications

(15 citation statements)

References 34 publications

(21 reference statements)

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“…The ELC receptor was identified originally as a molecule upregulated in EBV-transformed B cells (34). Other studies indicated that CCR7 is also upregulated by treatment of PBLs with phorbol ester, PHA, or anti-CD3 (35, 36). In preliminary experiments with cells cultured overnight in phorbol ester, we observed an increase in the magnitude of the B cell response to ELC (data not shown).…”

Section: Resultsmentioning

confidence: 99%

“…The only receptor characterized to date for ELC, EBV-induced molecule 1 (EBI-1) or CC chemokine receptor (CCR)7 (32), was first identified as a molecule upregulated in EBV-transformed Burkitt's lymphoma cells (34). The gene was later isolated from CD4 T cells that had been infected with herpesvirus (35) and by PCR as a molecule homologous to BLR1 (36). Northern blot analysis demonstrated that CCR7 is expressed in several B and T cell lines but not on monocytic or myeloid cell lines or cells of nonlymphoid origin.…”

mentioning

confidence: 99%

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Epstein-Barr Virus–induced Molecule 1 Ligand Chemokine Is Expressed by Dendritic Cells in Lymphoid Tissues and Strongly Attracts Naive T Cells and Activated B Cells

Ngo

Tang

Cyster

1998

The Journal of Experimental Medicine

430

299

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Movement of T and B lymphocytes through secondary lymphoid tissues is likely to involve multiple cues that help the cells navigate to appropriate compartments. Epstein-Barr virus– induced molecule 1 (EBI-1) ligand chemokine (ELC/MIP3β) is expressed constitutively within lymphoid tissues and may act as such a guidance cue. Here, we have isolated mouse ELC and characterized its expression pattern and chemotactic properties. ELC is expressed constitutively in dendritic cells within the T cell zone of secondary lymphoid tissues. Recombinant ELC was strongly chemotactic for naive (L-selectinhi) CD4 T cells and for CD8 T cells and weakly attractive for resting B cells and memory (L-selectinlo) CD4 T cells. After activation through the B cell receptor, the chemotactic response of B cells was enhanced. Like its human counterpart, murine ELC stimulated cells transfected with EBI-1/CC chemokine receptor 7 (CCR7). Our findings suggest a central role for ELC in promoting encounters between recirculating T cells and dendritic cells and in the migration of activated B cells into the T zone of secondary lymphoid tissues.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Epstein-Barr Virus–induced Molecule 1 Ligand Chemokine Is Expressed by Dendritic Cells in Lymphoid Tissues and Strongly Attracts Naive T Cells and Activated B Cells

Ngo

Tang

Cyster

1998

The Journal of Experimental Medicine

430

299

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“…In addition to this, EBV as well as HHV6 and HHV7 have been shown to upregulate certain endogenous chemokine receptors in their target cells. Thus, EBV actively upregulates the expression of endogenous CCR7, previously called EBVinduced molecule (EBI) 1, as well as an orphant receptor, EBI 2, in infected B cell lines (19), whereas HHV6 and HHV7 actively upregulate CCR7 in infected CD4 ϩ T cells (20). As CCR7 is believed to be a receptor that mediates migration of cells to lymph nodes, this could be a way that the virus obtains tissue targeting to secondary lymphoid tissues, i.e., by "telling the infected cell" where it would like to go by upregulating or expressing a suitable chemokine receptor.…”

Section: Introductionmentioning

confidence: 99%

A Highly Selective Cc Chemokine Receptor (Ccr)8 Antagonist Encoded by the Poxvirus Molluscum Contagiosum

Lüttichau

Stine²,

Boesen³

et al. 2000

The Journal of Experimental Medicine

135

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The MC148 CC chemokine from the human poxvirus molluscum contagiosum (MCV) was probed in parallel with viral macrophage inflammatory protein (vMIP)-II encoded by human herpesvirus 8 (HHV8) in 16 classified human chemokine receptors. In competition binding using radiolabeled endogenous chemokines as well as radiolabeled MC148, MC148 bound with high affinity only to CCR8. In calcium mobilization assays, MC148 had no effect on its own on any of the chemokine receptors, but in a dose-dependent manner blocked the stimulatory effect of the endogenous I-309 chemokine on CCR8 without affecting chemokine-induced signaling of any other receptor. In contrast, vMIP-II acted as an antagonist on 10 of the 16 chemokine receptors, covering all four classes: XCR, CCR, CXCR, and CX3CR. In chemotaxis assays, MC148 specifically blocked the I-309–induced response but, for example, not stromal cell–derived factor 1α, monocyte chemoattractant protein 1, or interleukin 8–induced chemotaxis. We thus concluded that the two viruses choose two different ways to block the chemokine system: HHV8 encodes the broad-spectrum chemokine antagonist vMIP-II, whereas MCV encodes a highly selective CCR8 antagonist, MC148, conceivably to interfere with monocyte invasion and dendritic cell function. Because of its pharmacological selectivity, the MC148 protein could be a useful tool in the delineation of the role played by CCR8 and its endogenous ligand, I-309.

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“…HHV-6 and HHV-7 are ␤-herpesviruses closely related to HCMV [Lawrence et al, 1990]. The lymphotrophic nature of HHV-6 and HHV-7; the in vitro observations that these viruses affect expression of interferon (IFN), interleukin (IL)-8, IL-1␤, and tumor necrosis factor-␣ (TNF-␣) [Kikuta et al, 1990;Inagi et al, 1996;Flamand et al, 1991]; and their ability to modulate other immunologically important cell surface molecules (CD3, CD4, and EB1) [Furukawa et al, 1994;Hasegawa et al, 1994] suggest that these viruses may have immunomodulatory potential. They may possibly play a role as cofactors of other infections [Osman et al, 1996] or in the pathogenesis of GVHD [Appleton et al, 1995].…”

Section: Introductionmentioning

confidence: 99%

Human herpesvirus-6 and human herpesvirus-7 infections in bone marrow transplant recipients

et al. 1997

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Human cytomegalovirus (HCMV), human herpesvirus-6 (HHV-6), and human herpesvirus-7 (HHV-7) DNA in peripheral blood leukocytes (PBL) of 61 bone marrow transplant recipients was monitored weekly during the first 12 weeks post-transplantation by a nested polymerase chain reaction (PCR). Thirty-seven (61%), 17 (28%), and 32 (53%) of patients had one or more PBL specimens positive for HCMV, HHV-6 or HHV-7 DNA, respectively. HHV-7 DNA in PBL during the early post-transplant period was associated with a longer time to neutrophil engraftment (mean 28.8 days vs 19.8 days; P = 0.01). In two patients who failed to engraft, HHV-6 DNA and HHV-7 DNA was detected in plasma and PBL, respectively, early in their post-transplant period. Patients with HCMV disease were more likely to have concurrent HHV-7 DNA in PBL prior to onset of disease than were patients with asymptomatic HCMV infection, suggesting that HHV-7 may be a cofactor in the progression from HCMV infection to HCMV disease. In the 17 patients (179 specimens) in whom viral DNA in plasma was studied (in addition to PBL), a positive result was found only in 3. In each, viral DNA in plasma appeared to correlate with clinically significant disease. HHV-7 DNA in plasma was associated with encephalitis in an allograft recipient.

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Induction of G protein-coupled peptide receptor EBI 1 by human herpesvirus 6 and 7 infection in CD4+ T cells

Cited by 54 publications

References 34 publications

Epstein-Barr Virus–induced Molecule 1 Ligand Chemokine Is Expressed by Dendritic Cells in Lymphoid Tissues and Strongly Attracts Naive T Cells and Activated B Cells

Epstein-Barr Virus–induced Molecule 1 Ligand Chemokine Is Expressed by Dendritic Cells in Lymphoid Tissues and Strongly Attracts Naive T Cells and Activated B Cells

A Highly Selective Cc Chemokine Receptor (Ccr)8 Antagonist Encoded by the Poxvirus Molluscum Contagiosum

Human herpesvirus-6 and human herpesvirus-7 infections in bone marrow transplant recipients

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