Impaired Th2 subset development in the absence of CD4

Immunity. 1997 May;6(5):559-69. doi: 10.1016/s1074-7613(00)80344-1.


Prior studies in CD4-deficient mice established the capacity of T helper (Th) lineage cells to mature into Th1 cells. Unexpectedly, challenge of these mice with Nippostrongylus brasiliensis, a Th2-inducing stimulus, failed to result in the development of Th2 cells. Additional studies were performed using CD4+ or CD4-CD8- (double-negative) T cell receptor (TCR) transgenic T cells reactive to LACK antigen of Leishmania major. Double-negative T cells were unable to develop into Th2 cells in vivo, and, unlike CD4+ T cells, could not be primed for interleukin-4 production in vitro. Similarly, CD4+ TCR transgenic T cells primed on antigen-presenting cells expressing mutant MHC class II molecules unable to bind CD4 did not differentiate into Th2 cells. These data suggest that interactions between the TCR, MHC II-peptide complex and CD4 may be involved in Th2 development.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigen-Presenting Cells / metabolism
  • CD4 Antigens / genetics*
  • CD4 Antigens / metabolism
  • Cell Differentiation / genetics
  • Cell Differentiation / immunology
  • Cells, Cultured
  • Female
  • Histocompatibility Antigens Class II / genetics
  • Interleukin-4 / biosynthesis
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mutation
  • Protein Binding / genetics
  • Protein Binding / immunology
  • Receptors, Antigen, T-Cell / genetics
  • Th2 Cells / immunology*
  • Th2 Cells / metabolism*
  • Th2 Cells / pathology
  • Transgenes / immunology


  • CD4 Antigens
  • Histocompatibility Antigens Class II
  • Receptors, Antigen, T-Cell
  • Interleukin-4