Carbohydrate-binding lectin with a preference for chitin. Has no chitinase activity. May play a role in tissue remodeling and in the capacity of cells to respond to and cope with changes in their environment. Plays a role in T-helper cell type 2 (Th2) inflammatory response and IL-13-induced inflammation, regulating allergen sensitization, inflammatory cell apoptosis, dendritic cell accumulation and M2 macrophage differentiation. Facilitates invasion of pathogenic enteric bacteria into colonic mucosa and lymphoid organs. Mediates activation of AKT1 signaling pathway and subsequent IL8 production in colonic epithelial cells. Regulates antibacterial responses in lung by contributing to macrophage bacterial killing, controlling bacterial dissemination and augmenting host tolerance. Also regulates hyperoxia-induced injury, inflammation and epithelial apoptosis in lung. Monomer. Detected in bronchoalveolar lavage (BAL) fluids. Localizes mainly to endoplasmic reticulum when overexpressed in cells, with some protein also detected throughout the cytoplasm. Detected in lung in pulmonary macrophages and alveolar type 2 cells and in bronchoalveolar lavage (BAL) fluids. Expressed in mammary tumor cells (at protein level). Expressed in lung. Not detected in non-inflammatory colon. Up-regulated in colon under several inflammatory conditions. Up-regulated upon pulmonary inflammation elicited by sensitization and challenge with the chitin-free aeroallergen ovalbumin or with chitin-containing antigen house dust mite (HDM) extract. Up-regulated in lungs after S.pneumoniae infection. Up-regulated in splenic cells of mammary tumor-bearing animals. Down-regulated by hyperoxia in lung. Mice are viable, fertile and appear normal, but have defective antigen-induced Th2 inflammatory responses and defective IL-13-induced responses, displaying accelerated cell death responses and diminished M2 macrophage differentiation. Mutant mice are more sensitive to S.pneumoniae infection, displaying enhanced mortality, exacerbated lung injury and decreased bacterial clearance compared to wild-type mice. Mutant mice also have an exacerbated response to hyperoxia, displaying enhanced protein leak, tissue inflammation and chemokine production and premature death. Produced by alternative initiation at Met-9 of isoform 1. May be produced by alternative splicing of isoform 1. Belongs to the glycosyl hydrolase 18 family. Although it belongs to the glycosyl hydrolase 18 family, Leu-149 is present instead of the conserved Glu which is an active site residue. Therefore this protein lacks chitinase activity. Truncated N-terminus. Truncated N-terminus. Truncated N-terminus. Truncated N-terminus.