Collectin-11

Background

Collectin-11 (CL-11), also known as alias collectin kidney 1 (CL-K1) is a recently identified member of collectins, encoded by COLEC11. It is produced by several types of non-immune cells, including epithelial cells of the renal tract and mucosal cells in the intestinal and bronchial tracts. CL-11 has a classical collectin structure containing an N-terminal segment, a collagen-like region, an alpha-helical coiled neck region, and a C-terminal carbohydrate recognition domain (CRD) which is responsible for the recognition of multiple sugars with a preference for fucose and mannose. Similar to other collectins, CL-11 plays an important role in innate immunity through binding to carbohydrate antigens on microorganisms and activating complement through the recruitment of mannose-binding lectin (MBL)-associated serine proteases (MASPs). Also, CL-11 has been shown to play a role in apoptosis through binding to the DNA present at the surface of apoptotic cells in a calcium-independent manner and activating the complement in response to this binding. Interestingly, CL-11 is also involved in the development via guiding the migration of neural crest cells and other cell types during embryogenesis.

CL-11 plays a crucial role in innate defense against invading microorganisms. It has been revealed to play a protective role in uropathogenic Escherichia coli (UPEC)-induced urinary tract infection (UTI) through inducing innate immunity defense. Besides, CL-11 is also involved in the pathogenic progress of several diseases. It has been also shown to be associated with acute kidney injury (AKI) through recognizing an abnormal pattern of L-fucose on postischemic renal tubule cells and activating a destructive inflammatory response. Deficiencies of CL-11 are associated with 3MC syndrome-2 and Chagas disease.

Fig. 1 Conceptual model of epithelial stress-induced local complement activation initiated by CL-11.^{1, 3}

Collectin-11 Functional Service

Creative Biolabs provides a varied array of CL-11-centered products, featuring anti-CL-11 antibodies, ELISA kits, and human complement CL-11 proteins. These precisely designed resources are vital for progressing research projects focused on creating therapeutic strategies for numerous diseases.

Fig.2 CL-11 employs its carbohydrate-recognition domain to bind and suppress T cell proliferation.^{2, 3}

Researchers have explored retinal pigment epithelium (RPE) cell allotransplantation as a potential remedy for retinal diseases, though the RPE-complement system, activated by collectin-11 (CL-11), may obstruct this process due to complement-mediated inflammation that enhances T cell recognition. To clarify the impact of CL-11 on T cell immune response, findings revealed that RPE cells increase the expression of MHC class I and demonstrate MHC class II presence during inflammatory states. RPE-T cell co-cultures resulted in suppressed T cell proliferation, partially attributed to CL-11 binding, which impeded T cell growth through CD28 downregulation, researchers determine CL--11 binding to PRE and T cells by using anti-CL-11 antibody. Blocking CL-11’s collagen-like domain with RGD peptide reversed this suppression, suggesting CL-11’s role in RPE cells’ immunosuppressive capabilities. These findings highlight CL-11’s dual function—activating the complement cascade and modulating T cell responses—elucidating mechanisms governing RPE cell immunogenicity.

Creative Biolabs provides a comprehensive array of CL-11-focused services, featuring binding evaluations and supplementary functional studies, meticulously customized to assist their prestigious clientele in both research and clinical objectives.

References

1. Nauser, Christopher L., et al. "Collectin-11 (CL-11) is a major sentinel at epithelial surfaces and key pattern recognition molecule in complement-mediated ischaemic injury." Frontiers in Immunology 9 (2018): 2023.
2. Fanelli, Giorgia, et al. "Soluble Collectin 11 (CL-11) Acts as an Immunosuppressive Molecule Potentially Used by Stem Cell-Derived Retinal Epithelial Cells to Modulate T Cell Response." Cells 12.13 (2023): 1805.
3. Distributed under Open Access license CC BY 4.0, without modification.