6. CD23 mediated immune response
The consequence of CD23 mediated IgE- immune complex processing or
trafficking is still not understood in detail. However, it is thought
that IgE modulates immune responses to an antigen via CD23, as was shown
in mice for antibody and T cell responses (73,80). The mechanism of
antigen presentation mediated by CD23 has been referred to as
IgE-facilitated antigen presentation (FAP) (Fig. 3). As B cells are
antigen presenting cells expressing MHC class II, B cells could
potentially also degrade antigen and display peptides on MHC class II
for antigen presentation. This was indeed shown using EBV-transformed
human B cells which directly present IgE-immune complexes to T cells
(45,81–84). However, as previously mentioned, experiments with primary
B cells have shown that IgE-immune complexes are protected from
degradation. This difference in processing between normal B cells and
EBV-transformed cells requires more detailed investigations, in order to
better understand the mechanism of immunomodulation. Despite the fact
that primary human B cells failed to directly induce T cell
proliferation, they are able to transfer the IgE-immune complexes to
human dendritic cells to induce T cell proliferation (70). Fittingly, it
was shown in mice that IgE-mediated antigen presentation was, though
initiated by B cells, ultimately dependent on dendritic cells (73, 85).
The mechanism by which antigen could be transferred from B cells to
other cell types is not entirely clear. A potential role in CD23-induced
IgE or antigen shipping between immune cells could be attributed to
exosomes. It was shown that B cell-derived exosomes can play a role in
presenting allergen peptides to activate T cells (86,87) (Fig. 3).
Independently, it has been described that the CD23 sheddase ADAM10 can
mediate sorting of CD23 into B cell-derived exosomes (88,89). The
concept of exosome transfer between B cells and dendritic cells has also
been put forth in mice (90). The consequence of CD23-mediated T cell
proliferation and whether it is pro- or anti-inflammatory in the
allergic context has not been resolved yet, and evidence is generally
conflicting. In mouse models of allergic asthma it was both postulated
that CD23 could positively (91) as well as negatively regulate allergic
airway inflammation (92, 93).