title: The collectins CL-L1, CL-K1 and CL-P1, and their roles in complement and innate immunity.
abstract: Both the complement system and collectins play important roles in our innate immune system. The collectins, which are characterized by their inclusion of a collagen-like region and a calcium-dependent carbohydrate recognition domain, are pattern recognition molecules and include the well characterized proteins mannan-binding lectin (MBL) and the surfactant proteins SP-A/-D. Collectin liver 1 (CL-L1), collectin kidney 1 (CL-K1) and collectin placenta 1 (CL-P1) are the most recently discovered collectins. Although their function is still under investigation, accumulating information suggests that CL-L1, CL-K1 and CL-P1 play important roles in host defense by recognizing a variety of microorganisms and interacting with effector proteins, including complement components. The recent establishment of the existence of CL-K1 in the circulation in form of heteromeric complexes with CL-L1 (known as CL-LK) and its activation of the lectin pathway via MASPs, drew new attention in the complement biology, which was further strengthened by the observed interactions between CL-P1 and CRP-C1q-factor H or properdin. Deficiency of either CL-K1 or MASP-3 has been demonstrated in 3MC syndrome patients with developmental abnormalities, showing that lectin pathway components, regulation and/or activation are essential during the embryonic development; another feature that they most likely share CL-P1. Herein, we discuss the recent characteristics and roles of the collectins CL-L1, CL-K1 and CL-P1 in the complement system, in innate immunity and their possible association with disease development and pathogenesis.
authors.affiliation: Department of Cancer and Inflammation Research, Institute of Molecular Medicine, University of Southern Denmark, Odense C, Denmark. Electronic address: shansen@health.sdu.dk.
authors.forename: Soren W K
authors.initials: SW
authors.lastname: Hansen
authors.affiliation: Department of Microbiology and Immunochemistry, Asahikawa Medical University, Asahikawa, Japan.
authors.forename: Katsuki
authors.initials: K
authors.lastname: Ohtani
authors.affiliation: Department of Microbiology and Immunochemistry, Asahikawa Medical University, Asahikawa, Japan.
authors.forename: Nitai
authors.initials: N
authors.lastname: Roy
authors.affiliation: Department of Microbiology and Immunochemistry, Asahikawa Medical University, Asahikawa, Japan. Electronic address: wakamiya@asahikawa-med.ac.jp.
authors.forename: Nobutaka
authors.initials: N
authors.lastname: Wakamiya
mesh_terms: D000818:Animals; D037222:Collectins / Q000737:chemistry / Q000502:physiology*; D003167:Complement Activation; D003165:Complement System Proteins / Q000502:physiology*; D004198:Disease Susceptibility; D005786:Gene Expression Regulation; D006801:Humans; D007113:Immunity, Innate; D008024:Ligands; D005810:Multigene Family; D009928:Organ Specificity / Q000235:genetics / Q000276:immunology; D011110:Polymorphism, Genetic; D013329:Structure-Activity Relationship
chemical_list: D037222:Collectins; D008024:Ligands; D003165:Complement System Proteins
keywords: 3MC syndrome; Collagen; Collectin; Complement; Embryogenesis; Innate immunity; MASP; Microbes; Scavenger receptor