Metadata about: C-type lectins, originally defined as proteins binding carbohydrates in a Ca(2+)-dependent manner, form a large family containing soluble and membrane-bound proteins. Among them, those expressed on phagocytes and working as pathogen pattern-recognition receptors were designated as C-type lectin receptors (CLRs), in accordance with Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I–like receptors (RLRs). Most of the genes for CLRs are clustered in human chromosome 12 close to the natural killer gene complex. Similar to the killer lectin-like receptors whose genes are clustered in this complex, most of the CLRs induce activating or regulatory signal cascades in response to distinct pathogen- or self-derived components, through the immunoreceptor tyrosine-based activating or inhibitory motif, respectively. In this chapter, some representative CLRs are picked up and their structural features leading to the functional consequences are discussed, especially on the signaling cascades and pathogen interactions, including some impacts on cutaneous pathophysiology. These CLRs should provide targets to develop effective vaccination and therapeutics for distinct infectious and autoimmune/inflammatory diseases.

About: C-type lectins, originally defined as proteins binding carbohydrates in a Ca(2+)-dependent manner, form a large family containing soluble and membrane-bound proteins. Among them, those expressed on phagocytes and working as pathogen pattern-recognition receptors were designated as C-type lectin receptors (CLRs), in accordance with Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I–like receptors (RLRs). Most of the genes for CLRs are clustered in human chromosome 12 close to the natural killer gene complex. Similar to the killer lectin-like receptors whose genes are clustered in this complex, most of the CLRs induce activating or regulatory signal cascades in response to distinct pathogen- or self-derived components, through the immunoreceptor tyrosine-based activating or inhibitory motif, respectively. In this chapter, some representative CLRs are picked up and their structural features leading to the functional consequences are discussed, especially on the signaling cascades and pathogen interactions, including some impacts on cutaneous pathophysiology. These CLRs should provide targets to develop effective vaccination and therapeutics for distinct infectious and autoimmune/inflammatory diseases.

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