Abstract
Allergic diseases represent a global health and economic burden of increasing significance. The lack of disease-modifying therapies besides specific allergen immunotherapy (AIT) which is not available for all types of allergies, necessitates the study of novel therapeutic approaches. Exosomes are small endosome-derived vesicles delivering cargo between cells and thus allowing inter-cellular communication. Since immune cells make use of exosomes to boost, deviate, or suppress immune responses, exosomes are intriguing candidates for immunotherapy. Here, we review the role of exosomes in allergic sensitization and inflammation, and we discuss the mechanisms by which exosomes could potentially be used in immunotherapeutic approaches for the treatment of allergic diseases. We propose the following approaches: (a) Mast cell-derived exosomes expressing IgE receptor FcεRI could absorb IgE and down-regulate systemic IgE levels. (b) Tolerogenic exosomes could suppress allergic immune responses via induction of regulatory T cells. (c) Exosomes could promote TH1-like responses towards an allergen. (d) Exosomes could modulate IgE-facilitated antigen presentation.
Highlights
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We argue that exosomes hold this therapeutic potential in allergic diseases, which are becoming a major global health threat and represent a significant economic burden
It has to be noted that allergic diseases, as well as allergy immunotherapy, are peculiar in that they are still not completely understood from an immunological standpoint
Summary
Allergic diseases are a global issue as more and more people are affected by allergies [1]. Symptomatic treatment options for allergies involve down-regulation of the mediators released by mast cells or basophils (e.g., anti-histamine) or aim to down-regulate IgE levels, such as the monoclonal anti-IgE antibody Omalizumab [6]. The only disease modifying treatment available for some but not all allergies is allergen-specific immunotherapy (short AIT or SIT). AIT induces regulatory T cells and B cells that are able to produce anti-inflammatory cytokines, such as IL-10 and TGF-β. This leads to suppression in TH2 responses but increased IgG4 production [9–11]. It is accepted that IgG antibodies can suppress IgE-mediated effector functions by competing for the allergen epitope neutralizing IgE, or by ligation of inhibitory FcγRIIb receptors on mast cells/basophils [13–15]. There is a need for novel treatment strategies that reduce side effects while maintaining efficacy
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