Collectin-11 detects stress-induced L-fucose pattern to trigger renal epithelial injury

Collectin-11 Is an Important Modulator of Retinal Pigment Epithelial Cell Phagocytosis and Cytokine Production

“…Although the SIPRα molecular structure to which collectin binds is unknown (based on our current knowledge), it has been suggested that SIRPα is a highly glycosylated membrane protein, so maybe CL-11 binds to carbohydrate moieties on SIPRα to exert its effect. CL-11 has been reported to be able to trigger complement activation upon binding to pathogens or stress-induced L -fucose patterns [15][16][17] . Given that RPE cells can synthesize a number of complement components [33] , the binding of CL-11 to RPE cells may cause complement activation, thus contributing to the effects of CL-11 on RPE cells that we observed in this study.…”

“…CL-11 has a wide tissue distribution; high-level expression has been found in the kidneys, liver, and adrenal glands [13,14] . It has been shown to bind to various molecules/molecular patterns through its CRD (e.g., monosaccharides, LPS, DNA, apoptotic cells, microorganisms, and the stress-induced L -fucose pattern on renal tubules) [6,13,15,16] . It has also been suggested that it plays an important role in host defense, waste removal, and embryonic development [6,17,18] , as well as participating in the pathogenesis of renal ischemia/reperfusion injury [15] .…”

“…It has been shown to bind to various molecules/molecular patterns through its CRD (e.g., monosaccharides, LPS, DNA, apoptotic cells, microorganisms, and the stress-induced L -fucose pattern on renal tubules) [6,13,15,16] . It has also been suggested that it plays an important role in host defense, waste removal, and embryonic development [6,17,18] , as well as participating in the pathogenesis of renal ischemia/reperfusion injury [15] . Given the important role of collectins in the opsonization and modulation of inflammatory responses, we hypothesized that CL-11 and, more specifically, locally produced CL-11, may play an important role in removing shedded POS by RPE cells and maintaining the homeostasis of the retinal microenvironment.…”

Complement activation, inflammation and relative ADAMTS13 deficiency in secondary thrombotic microangiopathies

“…Lectin pathway utilises 5 different recognition subcomponents such us mannose-binding lectin, ficolins 1, 2, and 3, and collectin-11. It will be an interesting task of future studies to tackle if additional lectin-recognition molecules including ficolins (Hein et al, 2015) and collectin-11 (Farrar et al, 2016) are also contributing to the development of secondary TMAs, and if specific inhibition of MBLassociated proteases has any clinical advantage in this disease. Finally, the strong, inverse correlation between Factor H level (an important regulator of alternative pathway), and between relative ADAMTS13 deficiency is surprising, and might have important implications regarding the observed alternative pathway activation and dysregulation (decreased alternative pathway activity, together with low Factor B levels and increased C3a concentrations).…”

Complement—here, there and everywhere, but what about the transplanted organ?

“…Identifying other triggers of the lectin pathway in IR may lead to novel specific therapeutic targets. A recent study demonstrates a role for collectin-11 (CL-11) in renal IR injury, whereby CL-11 produced by the renal tubuloepithelial cell appears to trigger complement activation along the basolateral tubuloepithelial surface [54].…”