sirolimus and buparvaquone

sirolimus has been researched along with buparvaquone* in 1 studies

Other Studies

1 other study(ies) available for sirolimus and buparvaquone

Article	Year
Jun NH2-terminal kinase is constitutively activated in T cells transformed by the intracellular parasite Theileria parva. Proceedings of the National Academy of Sciences of the United States of America, 1997, May-13, Volume: 94, Issue:10 When T cells become infected by the parasite Theileria parva, they acquire a transformed phenotype and no longer require antigen-specific stimulation or exogenous growth factors. This is accompanied by constitutive interleukin 2 (IL-2) and IL-2 receptor expression. Transformation can be reversed entirely by elimination of the parasites using the specific drug BW720c. Extracellular signal-regulated kinase and jun NH2-terminal kinase (JNK) are members of the mitogen-activated protein kinase family, which play a central role in the regulation of cellular differentiation and proliferation and also participate in the regulation of IL-2 and IL-2 receptor gene expression. T. parva was found to induce an unorthodox pattern of mitogen-activated protein kinase expression in infected T cells. JNK-1 and JNK-2 are constitutively active in a parasite-dependent manner, but have altered properties. In contrast, extracellular signal-regulated kinase-2 is not activated even though its activation pathway is functionally intact. Different components of the T cell receptor (TCR)-dependent signal transduction pathways also were examined. The TCRzeta or CD3epsilon chains were found not to be phosphorylated and T. parva-transformed T cells were resistant to inhibitors that block the early steps of T cell activation. Compounds that inhibit the progression of T cells to proliferation, however, were inhibitory. Our data provide the first example, to our knowledge, for parasite-mediated JNK activation, and our findings strongly suggest that T. parva not only lifts the requirement for antigenic stimulation but also entirely bypasses early TCR-dependent signal transduction pathways to induce continuous proliferation. Topics: 8-Bromo Cyclic Adenosine Monophosphate; Animals; Antiprotozoal Agents; Calcium-Calmodulin-Dependent Protein Kinases; Cell Line; Enzyme Activation; Enzyme Inhibitors; Humans; Immunosuppressive Agents; Indoles; JNK Mitogen-Activated Protein Kinases; Kinetics; Lymph Nodes; Lymphocyte Activation; Maleimides; Mitogen-Activated Protein Kinase 9; Mitogen-Activated Protein Kinases; Naphthoquinones; Polyenes; Protein Kinase C; Protein Kinases; Receptor-CD3 Complex, Antigen, T-Cell; Sirolimus; T-Lymphocytes; Tacrolimus; Theileria parva	1997

Article

Year

Jun NH2-terminal kinase is constitutively activated in T cells transformed by the intracellular parasite Theileria parva.

Proceedings of the National Academy of Sciences of the United States of America, 1997, May-13, Volume: 94, Issue:10

When T cells become infected by the parasite Theileria parva, they acquire a transformed phenotype and no longer require antigen-specific stimulation or exogenous growth factors. This is accompanied by constitutive interleukin 2 (IL-2) and IL-2 receptor expression. Transformation can be reversed entirely by elimination of the parasites using the specific drug BW720c. Extracellular signal-regulated kinase and jun NH2-terminal kinase (JNK) are members of the mitogen-activated protein kinase family, which play a central role in the regulation of cellular differentiation and proliferation and also participate in the regulation of IL-2 and IL-2 receptor gene expression. T. parva was found to induce an unorthodox pattern of mitogen-activated protein kinase expression in infected T cells. JNK-1 and JNK-2 are constitutively active in a parasite-dependent manner, but have altered properties. In contrast, extracellular signal-regulated kinase-2 is not activated even though its activation pathway is functionally intact. Different components of the T cell receptor (TCR)-dependent signal transduction pathways also were examined. The TCRzeta or CD3epsilon chains were found not to be phosphorylated and T. parva-transformed T cells were resistant to inhibitors that block the early steps of T cell activation. Compounds that inhibit the progression of T cells to proliferation, however, were inhibitory. Our data provide the first example, to our knowledge, for parasite-mediated JNK activation, and our findings strongly suggest that T. parva not only lifts the requirement for antigenic stimulation but also entirely bypasses early TCR-dependent signal transduction pathways to induce continuous proliferation.

Topics: 8-Bromo Cyclic Adenosine Monophosphate; Animals; Antiprotozoal Agents; Calcium-Calmodulin-Dependent Protein Kinases; Cell Line; Enzyme Activation; Enzyme Inhibitors; Humans; Immunosuppressive Agents; Indoles; JNK Mitogen-Activated Protein Kinases; Kinetics; Lymph Nodes; Lymphocyte Activation; Maleimides; Mitogen-Activated Protein Kinase 9; Mitogen-Activated Protein Kinases; Naphthoquinones; Polyenes; Protein Kinase C; Protein Kinases; Receptor-CD3 Complex, Antigen, T-Cell; Sirolimus; T-Lymphocytes; Tacrolimus; Theileria parva

1997