Background Recognition of antigen bound to the major histocompatibility complex by the T cell receptor is insufficient to lead to T cell proliferation and effector function, which require co-stimulatory signals, such as those resulting from the interaction of CD28 expressed on T lymphocytes and CD80/CD86 expressed on APCs. Lack of interaction between these accessory molecules during antigen stimulation leads to a state of antigen-specific lymphocyte unresponsiveness. Previous studies have shown that rush venom immunotherapy decreases venom-specific T cell proliferation very early after the initiation of the rush.
Objective In order to see whether this hyporeactivity was associated with a down regulation of accessory molecules, we studied CD28 surface expression on T lymphocytes from 10 non-atopic controls and from 10 non-atopic patients undergoing rush venom immunotherapy.
Methods Peripheral blood samples were collected before the rush (day 0), at the end of the rush (day 1), at day 15 and at day 45. CD28 expression was analysed using flow cytometry with double labelling of the CD4+ and CD8+ lymphocyte subpopulations.
Results At baseline CD28 was expressed at a higher level on T lymphocytes from allergic patients than from control subjects (P < 0.04), and in particular on the CD8 subset (P < 0.01), reflecting a decrease in the suppressive CD8+CD28– subpopulation. No changes were found in the percentages of total CD28+ T cells, CD4+ CD28+ or CD8+CD28+ cells at the different time points after the initiation of immunotherapy.
Conclusion These results suggest that the CD28 pathway is probably involved in the development of allergic reactions, but at least at the phenotypic level, CD28 expression remained unchanged after rush venom immunotherapy.