T Lymphocyte Reactivity to Glutamic Acid-Alanine-Tyrosine In Vitro Does Not Reflect Antibody Response In Vivo

Abstract Mechanisms responsible for the differences in humoral immune response to GAT (a random linear amino acid polymer) were investigated in a line of chickens consisting of four sublines homozygous for Ea-B (B1 or B19) and high or low antibody response to GAT (Ir-GATH or Ir-GATL). Previous research provided evidence of chromosomal recombination between the serologically determined regions of the MHC (encoded by B-F and B-G genes) and the gene or genes that control immune response to GAT, but immune response to GAT did not seem to be mediated through differences in B-L gene products. In the present study, proliferation of GAT-primed T lymphocytes indicated that reactivity in vitro was not associated with antibody levels produced in the animal. Cell surface markers were identified by flow cytometry. Lymphocytes from Ea-B19 chickens that were Ir-GATL had a higher percentage of suppressor T (CD8)-positive cells than did lymphocytes from Ir-GATH chickens. The Ea-B1 chickens that were Ir-GATL had a higher percentage of CD4-positive lymphocytes than did chickens that were Ir-GATH. This may indicate that low response to GAT in the Ea-B19 chickens, but not in Ea-B1 chickens, is mediated by CD8-positive cells. The ability of antigen-presenting cells (APC) to process and present GAT to antigen-primed T lymphocytes was tested in vitro. Measurements of lymphocyte proliferation indicated that, within the Ea-B1 blood type, APC from Ir-GATL chickens produced higher (P