H-2-linked Ir gene control of T cell proliferative responses to the synthetic terpolymer L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT). I. Requirements for T cell activation in responder and nonresponder mice

Academic Article


  • The immune response to the synthetic terpolymer L-glutamic acid60-L-alanine30- L-tyrosine10 (GAT) is controlled by an H-2-linked Ir gene(s). C57BL/10 (responder) and DBA/1 (nonresponder) mice develop GAT-specific plaque-forming cell responses after stimulation with GAT complexed to methylated bovine serum albumin (GAT-MBSA), whereas only responder mice produce antibodies after stimulation with soluble GAT. We have investigated the development of antigen-specific proliferative responses by nylon wool-enriched lymph node T cells from GAT- and GAT-MBSA-primed responder, nonresponder, and (responder x nonresponder)F1 mice. After immunization with GAT in complete Freund's adjuvant, T cells from C57BL/10, DBA/1, and (C57BL/10xDBA/1)F1 mice responded to PPD, but only C57BL/10 and F1 T cells responded to GAT and GAT-MBSA. By contrast, after immunization with GAT-MBSA in CFA, proliferative responses to soluble GAT, GAT-MBSA, and MBSA were developed by T cells from both DBA/1 and C57BL/10 mice. Development of GAT-specific T cell proliferative responses was strictly macrophage (Mphi) dependent. In addition, GAT-pulsed Mphi from responder and nonresponder mice stimulated comparable proliferative responses in Mphi-depleted lymph node T cells from GAT-primed (responder x nonresponder)F1 mice. Treatment of both responder and nonresponder parental macrophages with alloantisera specific for the I-region of the H-2 gene complex and complement abrogated their ability to stimulate F1 T cells. These experiments eliminate the possibility that antigen transfer from nonresponder parental Mphi to residual F1 Mphi accounts for reconstitution of F1 T cell responses by nonresponder Mphi and demonstrate that the antigen-presenting cells are Ia+ adherent Mphi.
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    Author List

  • Araneo BA; Kapp JA
  • Start Page

  • 1492
  • End Page

  • 1498
  • Volume

  • 124
  • Issue

  • 3