The Role of Extracellular Vesicles in Type I Hypersensitivity: A Systematic Review
Abstract
Type I hypersensitivity is an allergic reaction that has numerous clinical manifestations.
Extracellular vesicles (EVs), which play a significant role in cell to cell communication, are
secreted from many cells in the body and microorganisms. EVs are involved in upregulating or
downregulating the pathogenesis of type I hypersensitivity disorders. This systematic review
aims to focus on all research available currently on the role of EVs in type I hypersensitivity,
focusing on atopic dermatitis (AD), allergic rhinitis (AR), food allergy and anaphylaxis. Using
the PRISMA statement method, an electronic search was conducted using PubMed and Web
of Science databases which returned a total of 140 papers. After screening for eligibility, 15
papers were included in this review. EVs derived from microorganisms such as staphylococcus
aureus release EVs that have a deleterious effect on the immune system, which enhances
inflammation in AD. Also, Adipose tissue-derived mesenchymal stem cell-derived exosomes
are shown to alleviate inflammation in AD. In AR, epithelial cells derived exosomes can
downregulate Th2 polarisation and upregulate the expression of IL-10 which can alleviate
inflammation. Also, EVs showed a suppressor effect on food allergy through induction of mast
cells (MCs) apoptosis by EVs derived from Bifidobacterium longum (B. longum). Poly- (lactideco-glycolide) microparticles combined with specific immunotherapy (SIT) was able to suppress
anaphylaxis which decreased IgE induction during SIT. Also, EVs derived from dendritic cells
(DCs) carried antigens and microbial products that enhanced anaphylaxis by activating mast
cells. In conclusion, EVs derived from cells in the body or microorganisms have a significant
role in driving or regulating inflammation in type I hypersensitivity. EVs seem to have multiple
functions in which they impact the immune system both positively or negatively. Therefore,
further research is needed.