摘要
C-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.
基金
D.A.M.is supported by the Howard Ostin Fund and the University Hospitals Coventry and Warwickshire Renal Medicine Department.J.N.A.is funded by a grant from Cancer Research UK(DCRPGF\100009)and is the recipient of a Cancer Research Institute/Wade F.B.Thompson CLIP grant(CRI3645).
