The MAP kinases are differently utilized by CD28 and CD2 adhesion pathways in superantigen-activated Jurkat T cells

Edward Visse, J Inostroza, G Cabello, E Parra

Research output: Contribution to journalArticlepeer-review

6 Citations (SciVal)

Abstract

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/137-1-CHO transfected cells (signal 2). LFA-3 costimulation was able to induce T cell proliferation as well as IFN-gamma 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-gamma 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 costiniulation 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.
Original languageEnglish
Pages (from-to)263-278
JournalBiological Research
Volume36
Issue number2
Publication statusPublished - 2003

Subject classification (UKÄ)

  • Neurology
  • Surgery

Keywords

  • c-Jun N-terminal kinase
  • signal regulated kinase
  • extracellular
  • CD28 response element
  • staphylococcal enterotoxin A-E
  • interleukin-2

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