T cell subsets in (responder x nonresponder)F1 mice regulating antibody responses to L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT)

Academic Article


  • Immune responses to GAT are controlled by H-2-linked Ir genes; soluble GAT stimulates antibody responses in responder mice (H-2(b)) but not in non-responder mice (H-2(q)). In nonresponder mice, soluble GAT stimulates suppressor T cells that preempt function of helper T cells. After immunization with soluble GAT, spleen cells from (responder x nonresponder: H-2(b) x H-2(q))F1 mice develop antibody responses to responder H-2(b) GAT-M∅ but not to nonresponder H-2(q) GAT-M∅. This failure of immune F1 spleen cells to respd is due to an active suppressor T cell mechanism that is activated by H-2(q), but not H-2(b), GAT-M∅ and involves two regulatory T cell subsets. Suppressor-inducer T cells are immune radiosensitive Lyt-1+2-, I-A-, I-J+, Qa-1+ cells. Suppressor-effector T cells can be derived from virgin or immune spleens and are radiosensitive Lyt-1-2+, I-A-, I-J+, Qa-1+ cells. This suppressor mechanism can suppress responses of virgin or immune F1 helper T cells and B cells. Helper T cells specific for H-2(b) GAT-M∅ are easily detected in F1 mice after immunization with soluble GAT; helper T cells specific for H-2(q) GAT-M∅ are demonstrated after elimination of the suppressor-inducer and -effector cells. These helper T cells are radioresistant Lyt-1+2-, I-A+, I-J-, Qa-1- cells. These data indicate that the Ir gene defect in responses to GAT is not due to a failure of nonresponder M∅ to present GAT and most likely is not due to a defective T cell repertoire, because the relevant helper T cells are primed in F1 mice by soluble GAT and can be demonstrated when suppressor cells are removed. These data are discussed in the context of mechanisms for expression of Ir gene function in responses to GAT, especially the balance between stimulation of helper vs suppressor T cells.
  • Authors

    Published In

    Author List

  • Pierce CW; Kapp JA; Sorensen CM; Trial JA
  • Start Page

  • 2874
  • End Page

  • 2881
  • Volume

  • 133
  • Issue

  • 6