Suppressor T cell clones from patients with acute Epstein-Barr virus-induced infectious mononucleosis.

Wang, F; Blaese, R. Michael; Zoon, Kathryn C.; Tosato, Giovanna

doi:10.1172/jci112810

Cited by 19 publications

(10 citation statements)

References 45 publications

(32 reference statements)

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“…In contrast, other human suppressor cells have been found to inhibit antibody production by allogeneic PBMC (14). This lack of inhibition was seen even in the presence of autologous antigen-presenting cells, which should have been sufficent to induce activation of an acute immune response and that such CD4' cells may mediate the delayed hypersensitivity response.…”

Section: Discussionmentioning

confidence: 95%

“…Many of these clones produced high levels of both IL-2 and y-interferon in response to antigen, suggesting that they are mediators ofdelayed hypersensitivity. There are also reports of cloning CD8+ suppressor cells from skin lesions of patients with lepromatous CD8+ suppressor cells from skin lesions ofpatients with lepromatous (anergic) leprosy (12,13,24) and peripheral blood of patients with acute Epstein-Barr virus infection (14). The lepromintriggered suppressor clones share with RLB9-7 the properties of being triggered specifically by antigen to induce nonspecific suppression.…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, most of these studies are handicapped by the lack of a known relevant antigen. Exceptions include the cloning of lepromin-triggered CD8+ suppressor cells from lesions oflepromatous leprosy (11,12) the cloning of hepatitis B virus-specific clones from livers exhibiting chronic active hepatitis B (13), and suppressor cells from peripheral blood of patients with acute EBV infectious mononucleosis (14).…”

Section: Introductionmentioning

confidence: 99%

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Urushiol (poison ivy)-triggered suppressor T cell clone generated from peripheral blood.

Kalish

Morimoto²

1988

J. Clin. Invest.

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Allergic contact dermatitis to Toxicodendron radicans (poison ivy) is mediated by the hapten urushiol. An urushiol-specific, interleukin 2 (IL-2)-dependent T cell clone (RLB9-7) was generated from the peripheral blood of a patient with a history of allergic contact dermatitis to T. radicans. This clone proliferated specifically to both leaf extract and pure urushiol. Although the clone had the phenotype CD3+CD4+CD8', proliferation to antigen was blocked by anti-CD8 and anti-HLA-A, B, C but not by anti-CD4, suggesting that CD4 was not functionally associated with the T cell receptor. Furthermore, studies with antigen-presenting cells from MHC-typed donors indicated that the clone was MHC class 1 restricted. RLB9-7 was WT31 positive, indicating it bears the afi T cell receptor. The clone lacked significant natural killer cell activity and produced only low levels of IL-2 or y-interferon upon antigen stimulation. Addition of RLB9-7 to autologous peripheral blood mononuclear cells in the presence of urushiol inhibited the pokeweed mitogen-driven IgG synthesis. This suppression was resistant to irradiation (2,000 rad) and was not seen when RLB9-7 was added to allogeneic cells, even in the presence of irradiated autologous antigen-presenting cells, suggesting that suppression was MHC restricted and not mediated by nonspecific soluble factors. However, RLB9-7 cells in the presence of urushiol inhibited the synthesis of tetanus toxoid-specific IgG by autologous lymphocytes, indicating that the suppression, although triggered specifically by urushiol, was nonspecific.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Urushiol (poison ivy)-triggered suppressor T cell clone generated from peripheral blood.

Kalish

Morimoto²

1988

J. Clin. Invest.

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“…After a 3-d culture, splenocytes were harvested and washed twice in tissue culture medium. Then viable cells were counted and tested for cytotoxicity, as described (33). Lymphoblastoid cells (VDS-0 and TB) and murine T cell leukemia YAC-l cells (ATCC T1B 160) were used as 51Cr-labeled target cells.…”

Section: Methodsmentioning

confidence: 99%

Impairment of natural killer functions by interleukin 6 increases lymphoblastoid cell tumorigenicity in athymic mice.

Tanner

Tosato²

1991

J. Clin. Invest.

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Expression of the human IL-6 gene in EBV-immortalized normal human B lymphocytes following retroviral-mediated transduction rendered these cells highly tumorigenic in athymic mice. The tumors were lymphomas composed of the originally inoculated human lymphoblastoid cells. Co-injection of IL-6 expressing EBV-immortalized cells with IL-6 nonexpressing control cells resulted in increased tumorigenicity of the IL-6 nonexpressing cells. The lymphoblastoid cells expressing IL-6 were indistinguishable from parental cell lines in morphology and in a variety of cell surface characteristics, and did not exhibit growth advantage over parental cell lines in vitro, such that increased tumorigenicity is unlikely to depend upon a direct oncogenic effect of IL-6 on the B cells. Rather, at high concentrations, IL-6 markedly inhibits human lymphoblastoid cell killing by IL-2-activated murine splenocytes in vitro, suggesting that IL-6-related tumorigenicity might depend upon IL-6 inhibiting cytotoxicity at the tumor site. Thus, production of IL-6 by tumor cells that results in natural killer cell dysfunctions illustrates a novel mechanism of tumor cell escape from immune surveillance. (J. Clin. Invest. 1991. 88:239-247.)

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“…All cell lines were grown at greater than 90% viability in RPMI 1640 medium supplemented with 10% calf serum or in HL-1 medium (Ventrex Laboratories) without supplementation. Normal B lymphocytes were purified from whole blood (27) (11). Cells were photographed at x960 magnification on a Zeiss microscope.…”

Section: Methodsmentioning

confidence: 99%

An Epstein-Barr virus transforming protein associates with vimentin in lymphocytes.

Liebowitz¹,

Kopan²,

Fuchs³

et al. 1987

Mol. Cell. Biol.

118

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The Epstein-Barr virus (EBV) latent infection membrane protein (LMP) is likely to be an important mediator of EBV-induced cell proliferation, since it is one of the few proteins encoded by the virus in latent infection and since production of this protein in Rat-l cells results in their conversion to a fully transformed phenotype. LMP was previously noted to localize to patches at the cell periphery. In this paper we examine the basis of LMP patching in EBV-infected, transformed lymphocytes. Our data indicate that LMP is associated with the cytoskeletal protein vimentin. Although LMP is fully soluble in isotonic Triton X-100 buffer, only 50% of it is extracted from cells in this solution. The rest remains bound to the cytoskeleton. LMP undergoes phosphorylation, and phosphorylated LMP is preferentially associated with the cytoskeleton. As judged by both immunofluorescence and immunoelectron microscopy, the vimentin network in EBV-transformed lymphocytes or EBV-infected Burkitt tumor lymphocytes is abnormal. Vimentin and LMP often colocalize in a single patch near the plasma membrane. In response to Colcemid treatment of EBV-infected cells, vimentin reorganizes into perinuclear rings, as it does in uninfected cells. LMP is associated with these perinuclear rings. Vimentin (or a vimentin-associated protein) may be a transducer of an LMP transmembrane effect in lymphoproliferation.

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Suppressor T cell clones from patients with acute Epstein-Barr virus-induced infectious mononucleosis.

Cited by 19 publications

References 45 publications

Urushiol (poison ivy)-triggered suppressor T cell clone generated from peripheral blood.

Urushiol (poison ivy)-triggered suppressor T cell clone generated from peripheral blood.

Impairment of natural killer functions by interleukin 6 increases lymphoblastoid cell tumorigenicity in athymic mice.

An Epstein-Barr virus transforming protein associates with vimentin in lymphocytes.

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