AI Article Synopsis
- C-type lectin receptors (CLRs) play a role in immune responses by recognizing sugars on pathogens and body components, with Dectin-1 being a key CLR that targets β-glucan.
- Human Dectin-1 interacts with CLEC-2, another CLR on platelets, and is identified as a mucin-like protein with a specific glycan that allows this interaction, unlike its mouse counterpart.
- The study shows that introducing human Dectin-1 in mice can correct issues caused by a lack of another ligand, demonstrating that an innate immune receptor can also act as a physiological regulator through glycosylation.
Article Abstract
C-type lectin receptors (CLRs) elicit immune responses upon recognition of glycoconjugates present on pathogens and self-components. While Dectin-1 is the best-characterized CLR recognizing β-glucan on pathogens, the endogenous targets of Dectin-1 are not fully understood. Herein, we report that human Dectin-1 is a ligand for CLEC-2, another CLR expressed on platelets. Biochemical analyses revealed that Dectin-1 is a mucin-like protein as its stalk region is highly -glycosylated. A sialylated core 1 glycan attached to the EDxxT motif of human Dectin-1, which is absent in mouse Dectin-1, provides a ligand moiety for CLEC-2. Strikingly, the expression of human Dectin-1 in mice rescued the lethality and lymphatic defect resulting from a deficiency of Podoplanin, a known CLEC-2 ligand. This finding is the first example of an innate immune receptor also functioning as a physiological ligand to regulate ontogeny upon glycosylation.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9788829 | PMC |
| http://dx.doi.org/10.7554/eLife.83037 | DOI Listing |
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