+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: not found

      Transforming growth factor beta is a growth-inhibitory cytokine of B cell lymphoma in SIV-infected macaques.

      AIDS Research and Human Retroviruses

      Tumor Cells, Cultured, Animals, pharmacology, metabolism, Transforming Growth Factor beta, Simian immunodeficiency virus, immunology, Simian Acquired Immunodeficiency Syndrome, Sequence Analysis, DNA, Reverse Transcriptase Polymerase Chain Reaction, genetics, Receptors, Transforming Growth Factor beta, Molecular Sequence Data, Macaca mulatta, pathology, Lymphoma, AIDS-Related, Immunohistochemistry, Growth Inhibitors, Enzyme-Linked Immunosorbent Assay, DNA, Complementary, Base Sequence

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Cytokine dysregulation is accepted as one of the pivotal factors in the pathogenesis of B cell lymphomas in HIV-positive patients. So far no data exist on inhibitory cytokines in the regulatory network of HIV-associated B-NHL. Simian immunodeficiency virus (SIV)-infected macaques are a well-established in vivo model of HIV infection in humans. We used this model for the identification of TGF-beta as a growth-inhibitory cytokine of SIV-associated B cell lymphomas. Fifty-seven rhesus macaques were infected with SIVmac. Nine animals developed B cell lymphomas: eight with high-grade lymphomas of the immunoblastic, centroblastic, and "Burkitt-like" type, and one with the centroblastic/centrocytic type according to the Kiel classification. Six of seven analyzed lymphomas were infected with the macaque EBV, herpes virus macaca mulatta (HVMM). The lymphomas and the SIV-associated B cell lymphoma cell line H50 were positive for transcription of the TGF-beta gene. Protein expression and secretion of the active cytokine were proved by immunohistochemistry and ELISA. H50 transcribed the TGF-beta type I and type II receptor (R I/II), betaglycan, and endoglin. Furthermore, all primary lymphoma samples tested were positive for receptor type I/II transcription and protein expression. TGF-beta induced reduction of cell viability by 67% (range, 50-84% and enhanced apoptosis by 69% (range, 33-111%) compared with the control. TGF-beta activity was blocked by a specific anti-TGF-beta antibody. Thus, TGF-beta fulfilled the criteria of a negative autocrine inhibitor in H50. These data identify TGF-beta as a promising candidate as an inhibitory factor in the regulatory network of HIV-associated lymphomagenesis.

          Related collections

          Author and article information



          Comment on this article