The low affinity IgE receptor, CD23, expressed on antigen presenting cells alters T-cell response to allergen

Abstract

Rationale The low affinity IgE-receptor (FCERII/CD23) found on antigen presenting cells (APC) induces T cell activation in the presence of specific allergen and IgE. Previous studies have shown that CD23 expression is increased on peripheral blood mononuclear cells, bronchial epithelium, and smooth muscle cells from atopic individuals. Therefore these APCs may utilize CD23 as accessory molecules for T cell activation. Methods An in vitro model was created using EBV-transformed B cells as APCs and isolated CD4 + T-lymphocytes from the same atopic patient cultured in the presence of allergen (Timothy grass, natural Feld1). T cell lines were created from different atopic subjects. T cell line proliferative responses were analyzed with and without the presence of an anti-CD23 monoclonal antibody to determine if blocking the CD23 receptor would affect T cell responses. Flow cytometry performed on peripheral blood monocytes. Results Results have shown that by blocking CD23, allergen specific T cell proliferation is reduced as measured by thymidine incorporation. Furthermore, preliminary data shows that by blocking CD23, expression of the co-stimulatory molecules, CD86 and B7-H2 are down-regulated as measured by flow cytometry on CD23 expressing peripheral blood monocytes. Conclusions These results suggest that the low affinity IgE receptor, CD23, may be involved in APC functions in T cell responses and may also be co-expressed and regulated with other co-stimulatory molecules.