Antigen-independent Th2 cell differentiation by stimulation of CD28: regulation via IL-4 gene expression and mitogen-activated protein kinase activation

J Immunol. 2001 Apr 1;166(7):4283-92. doi: 10.4049/jimmunol.166.7.4283.

Abstract

To delineate the molecular mechanisms regulating Th2 cell differentiation, CD28-mediated generation of Th2 effectors was analyzed. In the absence of TCR ligation CD28 stimulation induced Th2 differentiation of memory but not of naive CD4(+) T cells, whereas costimulation via CD28 and the TCR enhanced Th2 differentiation from naive T cells but suppressed it from memory T cells. Stimulation of T cells via the CD28 pathway, therefore, provided critical signals facilitating Th2 cell differentiation. By comparing the responses to CD28 stimulation in memory and naive T cells and by using specific inhibitors, signaling pathways were defined that contributed to Th2 differentiation. CD28-induced Th2 differentiation required IL-4 stimulation and the activation of the mitogen-activated protein kinases p38 and extracellular signal-regulated kinases 1/2. CD28 engagement directly initiated IL-4 gene transcription in memory T cells and induced activation of phosphatidylinositol 3-kinase, p38, and c-Jun NH(2)-terminal kinase/stress-activated protein kinase pathways. Extracellular signal-regulated kinase phosphorylation that was necessary for Th2 differentiation, however, required stimulation by IL-2. These results indicate that optimal TCR-independent generation of Th2 effectors requires coordinate signaling via the CD28 and IL-2 pathways. TCR-independent generation of Th2 effectors might provide a mechanism to control Th1-dominated cellular inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antibodies, Monoclonal / pharmacology
  • Antigens, CD / metabolism
  • Antigens, CD / physiology
  • B7-1 Antigen / metabolism
  • B7-1 Antigen / physiology
  • B7-2 Antigen
  • CD28 Antigens / immunology
  • CD28 Antigens / metabolism
  • CD28 Antigens / physiology*
  • CD4-Positive T-Lymphocytes / cytology
  • CD4-Positive T-Lymphocytes / enzymology
  • CD4-Positive T-Lymphocytes / immunology
  • Cell Differentiation / immunology
  • Cells, Cultured
  • Drug Synergism
  • Enzyme Activation / immunology
  • Fetal Blood
  • Gene Expression Regulation / immunology*
  • Humans
  • Immunologic Memory / genetics
  • Interleukin-4 / biosynthesis*
  • Interleukin-4 / genetics*
  • Interleukin-4 / physiology
  • Interphase / genetics
  • Interphase / immunology
  • Jurkat Cells
  • Ligands
  • Membrane Glycoproteins / metabolism
  • Membrane Glycoproteins / physiology
  • Mitogen-Activated Protein Kinases / metabolism*
  • Mitogen-Activated Protein Kinases / physiology
  • Phosphorylation
  • Protein Serine-Threonine Kinases*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Signal Transduction / immunology
  • T-Lymphocyte Subsets / cytology
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism
  • Th2 Cells / cytology*
  • Th2 Cells / enzymology*
  • Th2 Cells / immunology
  • Transcription, Genetic / immunology
  • Tyrosine / metabolism
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Antibodies, Monoclonal
  • Antigens, CD
  • B7-1 Antigen
  • B7-2 Antigen
  • CD28 Antigens
  • CD86 protein, human
  • Ligands
  • Membrane Glycoproteins
  • Proto-Oncogene Proteins
  • Interleukin-4
  • Tyrosine
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases