The MAP Kinases are Differently Utilized by CD28 and CD2 Adhesion Pathways in Superantigen-Activated Jurkat T cells

• EDWARD VISSE ^[3] ; JUAN INOSTROZA ^[1] ; GERTRUDIS CABELLO ^[2] ; EDUARDO PARRA ^[1]
  1. [1] Universidad de Chile

     Universidad de Chile

     Santiago, Chile

     
  2. [2] Universidad de Tarapacá

     Universidad de Tarapacá

     Arica, Chile

     
  3. [3] University of Lund Biomedical Center (BMC) B11 Glioma Immuno Therapy group

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• Localización: Biological Research, ISSN-e 0717-6287, ISSN 0716-9760, Vol. 36, Nº. 2, 2003, págs. 263-278
• Idioma: inglés
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• Resumen

  • To mimic the two-signal requirements for T cell activation mediated by ligands, we exposed the superantigens SEA or SEE (signal 1) to T cells incubated with HLA-DR/LFA-3 or HLA-DR/B7-1-CHO transfected cells (signal 2). LFA-3 costimulation was able to induce T cell proliferation as well as IFN-g and IL-4 production at similar levels as in cells induced by B7-1. Analysis of the CD28RE of the IL-2 promoter showed specific transcription factor recruitment at the CD28RE element upon induction by B7-1/SEE. Further functional studies with an IL-2 enhancer-promoter carrying either wild type or mutated versions of the CD28RE site revealed that this element is necessary for full activation upon B7-1 costimulation. While both CD28/B7-1 and CD2/LFA-3 costimulation resulted in the up-regulation of IL-4 and IFN-g promoters, IL-2 promoter activity and production of IL-2 were only seen after B7-1 costimulation. However, contrary to what has been previously proposed, we show that costimulation with either B7-1 or LFA-3 further enhanced the ERK-2 activity and strongly activated the p38 MAPK pathway, but only B7-1 costimulation induced high levels of JNK-1 activity. These data suggest that the differential effect of CD28 vs. CD2 can be related to the difference in the ability of the two pathways to induce JNK-1 activity.