IgE enhances B cell-derived exosomal induced T cell proliferation. (P5013)

Abstract

Abstract The immunostimulatory potential of IgE immune complexes is known to be dependent on CD23, the low affinity IgE receptor. This was originally thought to be due to CD23 mediated uptake and subsequent stimulation of T cells by B cell processed antigen. Recent findings have indicated that dendritic cells (DC) are required in this process and B cells are primarily needed for antigen transportation. This has called into question the role of B cells in this interaction and leaves a gap in the knowledge of how the antigen is transferred to the DC. Given the resurgent interest in exosomes as having the capacity to mediate antigen presentation, we tested whether B cell derived exosomes might provide an explanation for this transfer. B cell derived exosomes express CD23 as well as the costimulatory molecules CD80 and CD86. Exosomes isolated from B cells that had been cultured with anti-TNP-IgE and TNP-OVA were shown to induce proliferation of ova specific DO11 T cells in a dose dependent manner. In the absence of either CD23 or anti-TNP-IgE, specific T cell stimulation was severely reduced. Thus, B cell derived exosomes alone have the capacity to induce antigen specific T cell activation and could represent the mechanism for antigen transfer to DCs. Ongoing testing involves whether injection of exosomes with processed antigen, either iv or intrasplenic will give an enhanced T cell and anti-OVA response in a manner similar to the classical IgE immune complex injection.