The innate immune system provides the first line of defence against infection and is crucial for inducing protection. Invading pathogens are recognized by pathogen-recognition receptors, including Toll-like receptors and C-type lectins (CLRs) expressed on the cell-surface of dendritic cells (DCs). Once a DC has captured pathogen-derived antigens, it undergoes considerable changes that are focussed on elimination of the pathogen. CLRs specifically capture carbohydrate antigens present on the surface or secreted products of pathogens, resulting in antigen processing and presentation. Current data, however, suggest that CLRs have a dual function: in addition to recognition of pathogen-derived antigens, they also function as recognition elements for glycosylated self-antigens to induce homeostatic control and tolerance. Interestingly, pathogens have evolved strategies to suppress or modulate the host immune response by exploiting these CLR functions. For example, Mycobacterium tuberculosis secretes glycosylated antigens that target host CLRs resulting in immune suppression, and several pathogenic nematodes secrete CLRs that may compete with host CLRs for binding to their ligands and may so modulate immune function. A better understanding of the molecular basis of CLR-carbohydrate interactions in infections, and their functional effects on innate immunity is pivotal to develop strategies to fight infectious disease.
|Number of pages||15|
|Journal||Trends in Glycoscience and Glycotechnology|
|Publication status||Published - Jul 2004|