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.