Monocytes are effector immune cells but a precise anal-ysis of their role in immune response has been preclud-ed by their heterogeneity. Indeed, human monocytesare composed of at least three different subsets withdiff...Monocytes are effector immune cells but a precise anal-ysis of their role in immune response has been preclud-ed by their heterogeneity. Indeed, human monocytesare composed of at least three different subsets withdifferent phenotypic characteristics and functional prop-erties, the so-called classical, intermediate and non-classical monocytes. A review of the literature showsthat these monocyte subsets are differently affectedduring viral, bacterial, parasitic and fungal infections.The expansion of the CD16＋ compartment （intermedi-ate and non-classical monocytes） is typically observedin the majority of infectious diseases and the increasedproportion of CD16＋ monocytes is likely related totheir activation through their direct interaction with thepathogen or the infammatory context. In contrast, thenumber of non-classical and intermediate monocytesis decreased in Q fever endocarditis, suggesting thatcomplex mechanisms govern the equilibrium among monocyte subsets. The measurement of monocyte sub-sets would be useful in better understanding of the role of monocyte activation in the pathophysiology of infec-tious diseases.展开更多
文摘Monocytes are effector immune cells but a precise anal-ysis of their role in immune response has been preclud-ed by their heterogeneity. Indeed, human monocytesare composed of at least three different subsets withdifferent phenotypic characteristics and functional prop-erties, the so-called classical, intermediate and non-classical monocytes. A review of the literature showsthat these monocyte subsets are differently affectedduring viral, bacterial, parasitic and fungal infections.The expansion of the CD16＋ compartment （intermedi-ate and non-classical monocytes） is typically observedin the majority of infectious diseases and the increasedproportion of CD16＋ monocytes is likely related totheir activation through their direct interaction with thepathogen or the infammatory context. In contrast, thenumber of non-classical and intermediate monocytesis decreased in Q fever endocarditis, suggesting thatcomplex mechanisms govern the equilibrium among monocyte subsets. The measurement of monocyte sub-sets would be useful in better understanding of the role of monocyte activation in the pathophysiology of infec-tious diseases.
