CCR8 on Human Thymocytes Functions as a Human Immunodeficiency Virus Type 1 Coreceptor

Lee, Shirley; Tiffany, H. Lee; King, Lisa R.; Murphy, Philip M.; Golding, Hana; Zaitseva, Marina

doi:10.1128/jvi.74.15.6946-6952.2000

Cited by 45 publications

(37 citation statements)

References 47 publications

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“…CCR8 is a beta chemokine receptor with a known role in induction of chemotaxis in Th2 cells via its two ligands CCL1 and CCL18 [50], and functions as a co-receptor for enveloped viruses including HIV [51,52]. The CCR8 axis has been found to be activated in urothelial and renal carcinomas resulting in immune response impairment, and it is responsible for apoptosis inhibition in lymphoma [53,54].…”

Section: Resultsmentioning

confidence: 99%

“…CCL5 was also shown to strongly induce uptake of (cellular, non-viral) EVs from uninfected T lymphocytes [84]. Of note, it was reported that enveloped viruses, such as HIV, can use chemokine receptors as co-receptors, including CCR8 [51,85–87]. Moreover, natural ligands can compete with these viruses for the co-receptors, inhibiting viral uptake [88,89].…”

Section: Discussionmentioning

confidence: 99%

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Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8

Berenguer

Lagerweij

Zhao

et al. 2018

J of Extracellular Vesicle

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Cancer cells release extracellular vesicles (EVs) that contain functional biomolecules such as RNA and proteins. EVs are transferred to recipient cancer cells and can promote tumour progression and therapy resistance. Through RNAi screening, we identified a novel EV uptake mechanism involving a triple interaction between the chemokine receptor CCR8 on the cells, glycans exposed on EVs and the soluble ligand CCL18. This ligand acts as bridging molecule, connecting EVs to cancer cells. We show that glioblastoma EVs promote cell proliferation and resistance to the alkylating agent temozolomide (TMZ). Using in vitro and in vivo stem-like glioblastoma models, we demonstrate that EV-induced phenotypes are neutralised by a small molecule CCR8 inhibitor, R243. Interference with chemokine receptors may offer therapeutic opportunities against EV-mediated cross-talk in glioblastoma.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8

Berenguer

Lagerweij

Zhao

et al. 2018

J of Extracellular Vesicle

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“…However, loss of CD4 ϩ thymocytes is also observed after infection with R5 isolates, although at a later time postinfection (32,66). The chemokine receptors CCR3, CCR4, CCR8, CCR9, and CXCR6 are also expressed in the thymus and may be used as coreceptors for HIV, as recently reported for CCR8 (20,30,44,45,52,87).…”

mentioning

confidence: 81%

“…7). In addition, recent studies in our laboratory have shown that the presence of the CD27 ϩ population at the moment of infection is essential for virus replication in thymocytes in vitro (Gurney and Uittenbogaart, unpublished), further delineating the mature thymocyte subset in which we and others observe HIV expression (10, 28,44,56). More-recent studies with an X4 variant suggest that IL-7 favors the persistence of HIV in mature CD4 ϩ CD8 Ϫ CD3 ϩ thymocytes, which we characterized here as being CD27 ϩ (28).…”

Section: Vol 76 2002 Replication In the Thymus Of Hiv Isolates Frommentioning

confidence: 94%

Impact of Cytokines on Replication in the Thymus of Primary Human Immunodeficiency Virus Type 1 Isolates from Infants

Pedroza-Martins

Boscardin

Anisman-Posner

et al. 2002

J Virol

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Early infection of the thymus with the human immunodeficiency virus (HIV) may explain the more rapid disease progression among children infected in utero than in children infected intrapartum. Therefore, we analyzed infection of thymocytes in vitro by HIV type 1 primary isolates, obtained at or near birth, from 10 children with different disease outcomes. HIV isolates able to replicate in the thymus and impact thymopoiesis were present in all infants, regardless of the timing of viral transmission and the rate of disease progression. Isolates from newborns utilized CCR5, CXCR4, or both chemokine receptors to enter thymocytes. Viral expression was observed in discrete thymocyte subsets postinfection with HIV isolates using CXCR4 (X4) and isolates using CCR5 (R5), despite the wider distribution of CXCR4 in the thymus. In contrast to previous findings, the X4 primary isolates were not more cytopathic for thymocytes than were the R5 isolates. The cytokines interleukin-2 (IL-2), IL-4, and IL-7 increased HIV replication in the thymus by inducing differentiation and expansion of mature CD27 ؉ thymocytes expressing CXCR4 or CCR5. IL-2 and IL-4 together increased expression of CXCR4 and CCR5 in this population, whereas IL-4 and IL-7 increased CXCR4 but not CCR5 expression. IL-2 plus IL-4 increased the viral production of all pediatric isolates, but IL-4 and IL-7 had a significantly higher impact on the replication of X4 isolates compared to R5 isolates. Our studies suggest that coreceptor use by HIV primary isolates is important but is not the sole determinant of HIV pathogenesis in the thymus.

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“…HIV-1 infects cells by recognition of the CD4 receptor in combination with a coreceptor, which is either the chemokine receptor CCR5 or CXCR4 (reviewed in refs. 7,8). HIV-1 can use other coreceptors to some extent in vitro, but these receptors do not seem to play a major role in vivo.…”

Section: Introductionmentioning

confidence: 99%

Construction of a Minimal HIV-1 Variant that Selectively Replicates in Leukemic Derived T-Cell Lines: Towards a New Virotherapy Approach

Jeeninga¹,

Jan²,

Linden

et al. 2005

Cancer Research

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T-cell acute lymphoblastic leukemia is a high-risk type of blood-cell cancer. We analyzed the possibility of developing virotherapy for T-cell acute lymphoblastic leukemia. Virotherapy is based on the exclusive replication of a virus in leukemic cells, leading to the selective removal of these malignant cells. We constructed a minimized derivative of HIV-1, a complex lentivirus encoding multiple accessory functions that are essential for virus replication in untransformed cells, but dispensable in leukemic T cells. This mini-HIV virus has five deletions (vif, vpR , vpU, nef, and U3) and replicated in the SupT1 cell line, but did not replicate in normal peripheral blood mononuclear cells. The stripped down mini-HIV variant was also able to efficiently remove leukemic cells from a mixed culture with untransformed control cells. In contrast to wild-type HIV-1, we did not observe bystander killing in mixed culture experiments with the mini-HIV variant. Furthermore, viral escape was not detected in long-term cultures. The mini-HIV variant that uses CD4 and CXCR4 for cell entry could potentially be used against CXCR4-expressing malignancies such as Tlymphoblastic leukemia/lymphoma, natural killer leukemia, and some myeloid leukemias. (Cancer Res 2005; 65(8): 3347-55)

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CCR8 on Human Thymocytes Functions as a Human Immunodeficiency Virus Type 1 Coreceptor

Cited by 45 publications

References 47 publications

Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8

Glycosylated extracellular vesicles released by glioblastoma cells are decorated by CCL18 allowing for cellular uptake via chemokine receptor CCR8

Impact of Cytokines on Replication in the Thymus of Primary Human Immunodeficiency Virus Type 1 Isolates from Infants

Construction of a Minimal HIV-1 Variant that Selectively Replicates in Leukemic Derived T-Cell Lines: Towards a New Virotherapy Approach

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