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However, macrophage involvement is clearly different than their participation in overt inflammatory disorders characterized by widespread cellular infiltration. In early AMD, macrophages have been detected along the choriocapillaris-side of Bruch’s membrane underlying areas of thick deposits. Processes from choroidal monocytes have been noted to insert into Bruch’s membrane deposits, presumably for the purpose of scavenging debris. The identity of these cells is uncertain, but they seem to lack typical phagocytic vacuoles and express human leukocyte antigen DR, suggesting that the cells may represent DC or nonactivated macrophages (22).

Recruitment of blood-derived reparative macrophages develops early in the course of glomerulosclerosis in proportion to the severity of the injury (151,152). Various innate injury stimuli, including renal hypertension, hyperlipidemia, and glomerular capillary endothelial injury by oxidized LDL, can upregulate macrophage chemotactic factors and adhesion molecules in the capillaries to induce macrophage recruitment (156–158). Experimental data suggest that reparative macrophages release mediators that induce mesangial cell proliferation, amplify the accumulation of extracellular matrix and might induce killing of endothelial cells.

Abbreviation: MAC, membrane attack complex. , antigen trapped in the extracellular matrix). These “in situ” or locally formed complexes sometimes activate the complement pathway to produce complement fragments called anaphylatoxins. This mechanism should be differentiated from deposition of circulating ICs which are preformed in the blood. Typically, the histology is dominated by neutrophils and monocytes, but at low level of activation minimal cellular infiltration may be observed. Many types of glomerulonephritis and vasculitis are thought to represent this mechanism.

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