Meta-Biol

• Pathways

Collectin kidney 1 (CL-K1, CL-11, COLEC11) (Keshi et al. 2006) forms disulfide-bridged stable heteromers with collectin liver 1 (CL-L1, COLEC10) (Otahani et al. 1999), with a ratio of one COLEC10 to two COLEC11 polypeptide chains. The majority of plasma COLEC11 was found in complex with COLEC10 (Henriksen et al. 2013). The resulting COLEC10:2xCOLEC11 heterocomplex, termred CL-LK, contains multiple Ca2+ -dependent carbohydrate-recognition domains (CRDs) and collagen-like regions, which allow high-avidity binding (KD ~10-9 M) to target cell surface carbohydrate patterns (Bajic et al. 2015); COLEC11 recognizes L-fucose and D-mannose and the disaccharide D-mannose(alpha1-2)-D-mannose (Keshi et al. 2006, Hansen et al. 2010, Selman & Hansen 2012, ). CL-LK can bind mannose-rich patterns on M. tuberculosis (Troegeler et al. 2015). The CL-LK complex was able to bind mannan-binding lectin-associated serine proteases (MASPs) in vitro with affinities in the nM range, and was associated with MASP1/3 and MASP2 in plasma. Upon binding to mannan or DNA in the presence of MASP2, the COLEC10:COLEC11 complex mediated deposition of C4b (Henriksen et al. 2013). Polymorphisms in the COLEC11 gene cause 3MC syndrome (Rooryck et al. 2011).