J Clin Invest.
T cell response to Id, peptides, or autologous tumor was HLA associated. (A) LE T cells were cultured with irradiated autologous PBMCs (LE) or HLA-matched (VS) or HLA-mismatched (HR, BE, RB, SG, and NC) heterologous PBMCs in the absence (_) or presence (+) of 100 ∝g/ml LE-Id. The proliferation response (cpm) was measured by [3H]thymidine incorporation. (B) The proliferation response of LE T cells to LE-CDR2-1 peptide was measured using irradiated EBV cells as APCs. (C and D) The proliferation and cytokine responses of TL T cells to TL-Id and TL-CDR3-1 peptide, respectively, were measured using autologous PBMCs or matched (JR) or unmatched (LK) heterologous PBMCs as APCs. (E and F) In the inhibition experiments, the indicated T cells were cultured with irradiated autologous PBMCs and 10 ∝M LE-CDR2-1 peptide (E) or TL-CDR3-1 (F) in the absence or presence of anti-HLA mAb’s or control (ctrl) Ig. (G and H) BL T cells were cultured with irradiated autologous tumor cells in the absence or presence of the indicated mAb’s. The proliferation responses in the absence of Ab’s (None) were 106,658 (LE-1), 86,511 (LE-2), 5,930 (TL-1), 23,461 (TL-2), 107,223 (BL-1), and 13,244 (BL-3). Results from a representative experiment are shown. Ag, antigen.