Despite the lack of endogenous chitin synthesis, mammalian genomes encode two enzymatically active true chitinases (chitotriosidase and acidic mammalian chitinase) and a variable number of chitinase-like proteins (CLPs) that have no enzyme activity but bind chitin. Chitinases and CLPs are prominent components of type-2 immune response-mediated respiratory diseases. However, despite extensive research into their role in allergic airway disease, there is still no agreement on whether they are mere biomarkers of disease or actual disease drivers. Functions ascribed to chitinases and CLPs include, but are not limited to host defense against chitin-containing pathogens, directly promoting inflammation, and modulating tissue remodeling and fibrosis. Here, we discuss in detail the chitin-dependent and -independent roles of chitinases and CLPs in the context of allergic airway disease, and recent advances and emerging concepts in the field that might identify opportunities for new therapies.
|Journal||Seminars in Immunology|
|Publication status||Published - May 2023|
Bibliographical noteFunding Information: This work was funded by an Excellence of Science UHEAD (Contract Nr G0G2318N ) and BENEFICIARIES (Contract Nr GoH1222N ) consortium grant, an ERC Advanced grant (Contract Nr 789384 ) and Concerted Research Action grant of the University of Ghent (Contract Nr 01GA2817 , BOF17/GOOA/028 . to B.N.L.) and an FWO Project grant (Contract Nr 3G068319 ) J.D. was supported by an FWO PhD Fellowship (Contract Nr 3F015119 ). U.S. was supported by a RESPIRE4 Marie Sklodowska-Curie Research Fellowship (Contract Nr R4202007-00839 ) and an FWO MSCA Seal of Excellence fellowship (Contract Nr 312ZZR22 ).
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