Human Gene Set: CHEMNITZ_RESPONSE_TO_PROSTAGLANDIN_E2_DN


Standard name CHEMNITZ_RESPONSE_TO_PROSTAGLANDIN_E2_DN
Systematic name M2214
Brief description Genes down-regulated in CD4+ [GeneID=920] T lymphocytes after stimulation with prostaglandin E2 [PubChem=5280360].
Full description or abstract Many tumors, including Hodgkin's lymphoma, are associated with decreased cellular immunity and elevated levels of prostaglandin E(2) (PGE(2)), a known inhibitor of CD4+ T cell activation, suggested to be involved in immune deviation in cancer. To address the molecular mechanisms tumor-derived PGE(2) might have on primary human CD4+ T cells, we used a whole genome-based transcriptional approach and show that PGE(2) severely limited changes of gene expression induced by signaling through the T cell receptor and CD28. This data suggests an interference of PGE(2) at an early step of T cell receptor signaling: indeed, PGE(2) stimulation of T cells leads to inactivation of lck and reduced phosphorylation of ZAP70. Antiapoptotic genes escaped PGE(2)-induced inhibition resulting in partial protection from apoptosis in response to irradiation or Fas-mediated signaling. As a functional consequence, PGE(2)-treated CD4+ T cells are arrested in the cell cycle associated with up-regulation of the cyclin/cyclin-dependent kinase inhibitor p27(kip1). Most importantly, CD4+ T cells in Hodgkin's lymphoma show similar regulation of genes that were altered in vitro by PGE(2) in T cells from healthy individuals. These data strongly suggest that PGE(2) is an important factor leading to CD4+ T cell impairment observed in Hodgkin's lymphoma.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 16424048   Authors: Chemnitz JM,Driesen J,Classen S,Riley JL,Debey S,Beyer M,Popov A,Zander T,Schultze JL
Exact source Table 1S
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Source species Homo sapiens
Contributed by Arthur Liberzon (MSigDB Team)
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identifier namespace		 AFFY_HG_U133
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