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Collectin liver 1 (CL-L1, alias CL-10) and collectin kidney 1 (CL-K1, alias CL-11), encoded by the  COLEC10  and  COLEC11  genes, respectively, are highly homologous soluble pattern recognition molecules in the lectin pathway of complement. These proteins may be involved in anti-microbial activity and in tissue development as mutations in  COLEC11  are one of the causes of the developmental defect syndrome 3MC. We studied variations in  COLEC10  and  COLEC11 , the impact on serum concentration and to what extent CL-L1 and CL-K1 serum concentrations are correlated. We sequenced the promoter regions, exons and exon-intron boundaries of  COLEC10  and  COLEC11  in samples from Danish Caucasians and measured the corresponding serum levels of CL-L1 and CL-K1. The median concentration of CL-L1 and CL-K1 was 1.87 μg/ml (1.00–4.14 μg/ml) and 0.32 μg/ml (0.11–0.69 μg/ml), respectively. The level of CL-L1 strongly correlated with CL-K1 (ρ = 0.7405, P <0.0001). Both genes were highly conserved with the majority of variations in the non-coding regions. Three non-synonymous variations were tested:  COLEC10  Glu78Asp (rs150828850, minor allele frequency (MAF): 0.003),  COLEC10  Arg125Trp (rs149331285, MAF: 0.007) and  COLEC11  His219Arg (rs7567833, MAF: 0.033). Carriers of  COLEC10  Arg125Trp had increased CL-L1 serum levels (P = 0.0478), whereas promoter polymorphism  COLEC11-9570C>T  (rs3820897) was associated with decreased levels of CL-K1 (P = 0.044). In conclusion,  COLEC10  and  COLEC11  are highly conserved, which may reflect biological importance of CL-L1 and CL-K1. Moreover, the strong inter individual correlation between the two proteins suggests that a major proportion are found as heterooligomers or subjected to the same regulatory mechanisms.

Genetic Variation of COLEC10 and COLEC11 and Association with Serum Levels of Collectin Liver 1 (CL-L1) and Collectin Kidney 1 (CL-K1)