Chitinase, Chitinase-like Protein과 알레르기 염증
Chitinase, Chitinase-like Protein and Allergic Inflammation
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Chitin, the second most abundant polysaccharide in nature after cellulose, consist exoskeleton of lower organisms such as fungi, crustaceans and insects except mammals. Mammalian chitinase and chitinase-like proteins (CLPs) are a family of mediators increasingly associated with infection, T cell-mediated inflammation, wound healing, allergy and asthma. Although our current knowledge of the function of mammalian chitinases and CLPs is very limited, important information can be deduced from research carried out in lower organisms, and in different immunopathological conditions. It is most striking that both chitinases and CLPs are up- regulated in T-helper type 2 (Th2)-driven conditions, and the first evidence is now emerging that these proteins may accentuate Th2 reactivity, and possibly contribute to the repair process that follows inflammation. In addition, regulatory SNPs in CHI3L1 were associated with asthma, atopy, and immunemediated diseases. In this review, recent findings on the role of chitinase and CLPs in allergic inflammation will be highlighted and the genetic studies in the genes encoding CHI3L1 will be discussed.
Abstract
Chitin, the second most abundant polysaccharide in nature after cellulose, consist exoskeleton of lower organisms such as fungi, crustaceans and insects except mammals. Mammalian chitinase and chitinase-like proteins (CLPs) are a family of mediators increasingly associated with infection, T cell-mediated inflammation, wound healing, allergy and asthma. Although our current knowledge of the function of mammalian chitinases and CLPs is very limited, important information can be deduced from research carried out in lower organisms, and in different immunopathological conditions. It is most striking that both chitinases and CLPs are up- regulated in T-helper type 2 (Th2)-driven conditions, and the first evidence is now emerging that these proteins may accentuate Th2 reactivity, and possibly contribute to the repair process that follows inflammation. In addition, regulatory SNPs in CHI3L1 were associated with asthma, atopy, and immunemediated diseases. In this review, recent findings on the role of chitinase and CLPs in allergic inflammation will be highlighted and the genetic studies in the genes encoding CHI3L1 will be discussed.
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