Abstract

IgE antigen complexes induce increased specific T cell proliferation and increased specific IgG production. Immediately after immunization, CD23+ B cells capture IgE antigen complexes, transport them to the spleen where, via unknown mechanisms, dendritic cells capture the antigen and present it to T cells. CD23, the low affinity IgE receptor, binds IgE antigen complexes and internalizes them. In this study, we show that these complexes are processed onto B-cell derived exosomes (bexosomes) in a CD23 dependent manner. The bexosomes carry CD23, IgE and MHC II and stimulate antigen specific T-cell proliferation in vitro. When IgE antigen complex stimulated bexosomes are incubated with dendritic cells, dendritic cells induce specific T-cell proliferation in vivo, similar to IgE antigen complexes. This suggests that bexosomes can provide the essential transfer mechanism for IgE antigen complexes from B cells to dendritic cells.

Highlights

  • Antibody, in complex with its antigen, provides the immune system with a feedback response against the complexed antigen

  • Combining antigen presentation properties of CD23 with the observed immunostimulation led to the hypothesis that antigen presentation by CD23+ B cells was responsible for these activities

  • Cells and were being transferred to dendritic cells (DCs). This led to the obvious question, what is the mechanism of this transfer? Henningson et al [4] suggested two possibilities; trogocytosis by DCs or exosomal mediated transfer from B cells to DCs

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Summary

Introduction

In complex with its antigen, provides the immune system with a feedback response against the complexed antigen. Culture of bexosomes with bone marrow derived DCs (BMDC), followed by isolation and injection of DCs did directly enhance in vivo antigen specific T cell proliferation.

Results
Conclusion
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