Abstract
Immunoglobulin E (IgE), though constitutively present at low levels, is most commonly studied in atopic disease where it plays a vital role in mast cell degranulation and in initiating a T helper 2 (Th2) response. With the advent of better detection assays, however, researchers are discovering the importance of IgE in actively contributing to many disease states and pathologies. This review will discuss the latest findings in IgE beyond its role in allergies and recently discovered roles for IgE in its cell-bound form on FcεRI-expressing effector cells like monocytes and dendritic cells. In terms of parasites, we will discuss helminth-induced IgE that appears to protect the worms from immune recognition and a tick-borne illness that elicits an IgE response against red meat. Next, we describe recent findings of how auto-reactive IgE can contribute to the progression of lupus and induce organ damage. Finally, we summarize the emerging roles of IgE in tumor surveillance and antibody-dependent cytotoxicity. We additionally discuss recent or ongoing clinical trials that either target harmful IgE or use the unique characteristics of the isotype.
Highlights
There are many hypotheses regarding the origin of the immunoglobulin E (IgE) response and its conservation throughout evolution
A 2015 report described a novel mechanism by which dendritic cell (DC) can capture low levels of free antigen on FcεRI-bound IgE56
Conclusions and Future directions IgE is normally the least abundant antibody found in circulation because of its short half-life, there are certain conditions that exhibit high levels of IgE
Summary
There are many hypotheses regarding the origin of the immunoglobulin E (IgE) response and its conservation throughout evolution. The authors showed that auto-reactive IgE ICs activate basophils to produce interleukin-4 (IL-4) and contribute to an overall Th2 skewing[31] This inflammatory environment resulted in increased auto-antibody production by plasma cells and the development of severe lupus nephritis[31]. These exogenous antigens can be routed through a specialized pathway for presentation on MHC class I This process, known as crosspresentation, permits antigen-specific activation of CD8+ CTLs. A 2015 report described a novel mechanism by which DCs can capture low levels of free antigen on FcεRI-bound IgE56. Using mice that lacked either IgE (IgH-7−/−) or FcεRI (FcεRIα−/−), they showed that IgE signaling was playing a protective role, as the genetic-deficient mice developed more aggressive tumors[57] This gives important insight into a previously unexplored immune mechanism that prevents the progression to epithelial malignancy. These experiments suggest that tumor antigen–specific IgE can play a powerful role in eliciting and maintaining an immune response at the tumor site
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