Chitin is highly abundant in organisms with allergenic potential such as house dust mites, fungi, nematodes, and arthropods. Several observations suggest a role for chitin in allergic disease, although the mechanism of action is poorly understood. Humans and mice express highly conserved chitin-degrading chitinases: acidic mammalian chitinase (AMCase; encoded by CHIA in humans and Chia in mice) and chitotriosidase (Chit1; encoded by CHIT1 in humans and Chit1 in mice), which have been suggested to modulate allergic responses through enzymatic degradation of chitins. Humans with nasal polyposis and mice with type 2 immune responses had increased chitinolytic activity in their airways, emanating from two different enzymes. Due to redundancy between both enzymes and lack of a mouse model completely devoid of all chitinolytic activity, their precise role in regulating type 2 immunity to chitin remains controversial. Using transgenic mice with single or combined deficiency of Chia and Chit1, we investigated the impact of chitin and chitinases on type 2 immunity. Our data demonstrate that chitin is a potent adjuvant for type 2 inflammation by triggering increased activation and migration of type 2 dendritic cells, with consequent increased polarization of T helper 2 cells. This adjuvant potential of chitin is however unaffected by the absence of endogenous chitinolytic activity in different models of allergic airway disease. Taken together, we here highlight the role of chitin as an allergenic adjuvant and question if the strength of this response is influenced by endogenous chitinases.
Declercq et al. (Fri,) studied this question.