Production of lymphotoxin by isolated human tonsillar B lymphocytes and B lymphocyte cell lines.

Sung, S.-S. J.; Jung, Lawrence; Walters, Jay A.; Jeffes, Edward W. B.; Granger, Gale A.; Fu, Shu Man

doi:10.1172/jci114146

Cited by 31 publications

(8 citation statements)

References 28 publications

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“…The proliferative e ect of TNFa on B-cells is well known (Cordingley et al, 1988;Jelinek and Lipsky, 1987;Kehrl et al, 1987). In vitro, EBV infection is associated with TNFa secretion (Jochems et al, 1991;Klein et al, 1996;Sung et al, 1988). Our results suggest that TNFa could be a target gene of NF-kB in EBV-infected cells.…”

Section: Roles Of Nf-kb Activation In Ebv-infected B-lymphocytes M Assupporting

confidence: 59%

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

et al. 1998

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In order to understand the role of NF-kB in EBV transformation we have established stably transfected IkBa into lymphoblastoid cells. Two clones were obtained in which the loss of NF-kB binding activity correlated with the constitutive expression of the transgenic IkBa. Protein latency expression was determined by immunocytochemistry. Expression of surface markers, intracytoplasmic content of cytokines cell cycle analysis after BrdU incorporation and DNA staining with propidium iodide were studied by¯ow cytometry. Percentage of apoptotic cells was determined by in-situ labelling of DNA strand breaks. No signi®cative changes in EBV latency nor in cell surface marker expression was found. In contrast, intracytoplasmic TNFa levels were strongly reduced in transfected clones. Furthermore, 30% of IkBa transfected cells were apoptotic after 8 h of TNFa treatment. This correlated with a strong reduction of BrdU incorporation after 24 h of TNFa treatment. No e ect was seen with non transfected cells or with cells transfected with a control plasmid. Our results suggest that the TNFa gene could be one of the targets of NF-kB in EBV infected cells and that NF-kB protects EBV-infected cells from apoptosis induced by TNFa, which may favour the proliferative e ect of this cytokine.

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Section: Roles Of Nf-kb Activation In Ebv-infected B-lymphocytes M Assupporting

confidence: 59%

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

et al. 1998

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“…It is produced primarily from activated T and B lymphocytes, which are found both in atherosclerotic lesions and rheumatoid synovial tissue and peripheral blood 6 49 50. The secreted form is composed of a homotrimeric protein (LTα3) with actions resembling TNF: LT-A induces adhesion molecule expression by endothelial cells, vascular smooth muscle cells and leucocytes contributing to the inflammatory process in atheromatous plaques,19 rendering them unstable and thus prone to cause an acute coronary syndrome.…”

Section: Discussionmentioning

confidence: 99%

Lymphotoxin 252A>G polymorphism is common and associates with myocardial infarction in patients with rheumatoid arthritis

Panoulas

Nikas

Smith

et al. 2008

Annals of the Rheumatic Diseases

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“…Being a pleiotropic molecule with broad regulatory functions in inflammation and immune response, TNF is produced by a great variety of cells including T and B lymphocytes (Sung et al, 1988a,b). In contrast, lymphotoxin-a expression is restricted to lymphocytes [T cells, B cells and LAK cells Miyake et al, 1992;Sung et al, 1989)l. Depending on the target cell and the cell-surface expression of TNF receptor proteins, TNF has been reported to induce proliferation, differentiation, apoptosis or necrosis.…”

mentioning

confidence: 99%

Lymphotoxin‐α/β heterodimer is expressed on leukemic hairy cells and activated human B lymphocytes

Mapara

Bargou

Beck

et al. 1994

Intl Journal of Cancer

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The expression of human lymphotoxin (LT) alpha/beta cell-surface complex was studied in human B-cell lines as well as in normal and neoplastic human B lymphocytes. In the absence of TNF receptors, only the human hairy-cell leukemia (HCL)-derived cell line JOK-I revealed constitutive cell-surface expression of LT but not TNF-alpha. Immunoprecipitation experiments with anti-LT monoclonal antibody (MAb) 9B9 from cell-surface radioiodinated JOK-I cells revealed that a cell-surface lymphotoxin molecule (25 kDa) is expressed in association with a 33-kDa molecule. Enzymatic digestion with F/N-glycosidase and O-glycosidase showed that both proteins contained N-linked carbohydrate residues, whereas only the 25-kDa molecule contained O-linked sugar residues. Analysis of mRNA expression revealed specific transcripts of LT-alpha and LT-beta in JOK-I cells. Resting tonsillar B cells did not express cell-surface LT. However, LT-beta mRNA was observable in unstimulated tonsillar B cells, whereas LT-alpha mRNA, cell-surface LT and LT secretion could only be detected upon in vitro activation. Thus LT-beta and alpha appear to be sequentially expressed in human B cells. Neoplastic B cells from chronic lymphocytic leukemia (BCLL), being devoid of constitutive cell-surface LT expression, could be induced to express surface LT by in vitro stimulation with Staphylococcus aureus Cowan I (SAC). Constitutive LT-beta transcripts, however, could also be detected in 4 out of 5 cases of BCLL. In contrast, human HCL cells displayed constitutive cell expression of lymphotoxin-alpha and beta. These findings demonstrate that cell-surface LT-alpha is expressed in association with LT-beta on activated normal B cells and neoplastic B cells representing an activated state.

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Production of lymphotoxin by isolated human tonsillar B lymphocytes and B lymphocyte cell lines.

Abstract: The expression of lymphotoxin (LT)

Cited by 31 publications

References 28 publications

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

Lymphotoxin 252A>G polymorphism is common and associates with myocardial infarction in patients with rheumatoid arthritis

Lymphotoxin‐α/β heterodimer is expressed on leukemic hairy cells and activated human B lymphocytes

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