Affiliation:
1. School of Cancer and Pharmaceutical Sciences, King’s College London , London SE1 1UL , UK
2. Warwick Medical School, University of Warwick , Coventry CV2 2DX , UK
Abstract
AbstractC-type lectins (CTLs) represent a large family of soluble and membrane-bound proteins which bind calcium dependently via carbohydrate recognition domains (CRDs) to glycan residues presented on the surface of a variety of pathogens. The deconvolution of a cell’s glycan code by CTLs underpins several important physiological processes in mammals such as pathogen neutralization and opsonization, leukocyte trafficking, and the inflammatory response. However, as our knowledge of CTLs has developed it has become apparent that the role of this innate immune family of proteins can be double-edged, where some pathogens have developed approaches to subvert and exploit CTL interactions to promote infection and sustain the pathological state. Equally, CTL interactions with host glycoproteins can contribute to inflammatory diseases such as arthritis and cancer whereby, in certain contexts, they exacerbate inflammation and drive malignant progression. This review discusses the ‘dual agent’ roles of some of the major mammalian CTLs in both resolving and promoting infection, inflammation and inflammatory disease and highlights opportunities and emerging approaches for their therapeutic modulation.
Funder
Howard Ostin Fund
University Hospitals Coventry
Warwickshire Renal Medicine Department
Cancer Research UK
Cancer Research Institute
Wade F.B. Thompson CLIP
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Drug Discovery,Biochemistry,Biotechnology
Cited by
3 articles.
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