Abstract
Our understanding of the pathologic processes leading to injury in human glomerulonephritis remains limited. Several mediation pathways have been suggested from observations of human biopsies and studies of experimental glomerulonephritis in animals, although the pathogenic mechanism of injury in many situations is obscure. However cells of the monocyte/macrophages series can be identified within glomeruli in glomerulonephritis, especially in more aggressive forms of the proliferative disease in humans. Experimental studies have confirmed the capacity of these cells to induce injury; thus, the role of monocytes as a mediator of glomerular injury is now established. Indirect evidence suggests that T cell-dependent mechanisms may also be involved in glomerulonephritis, but more data are needed to define the extent to which sensitised mononuclear leucocytes participate in the pathogenesis of human glomerulonephritis.
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