Abstract
Macrophage (MQ) infiltration within the glomerular and interstitial compartments is a common feature in most forms of glomerulonephritis (GN). We have studied role of MQs in the pathogenesis of chronic GN in both human and experimental model of GN, and reported that ‘activation’ of MQ is one of the most important processes during the initiation and the progression of chronic GN.
During the last decade, it has become clear that macrophages respond to various stimuli to generate phenotypically distinct states of activation. These activation states have been termed ‘classical (pro-inflammatory)’ and ‘alternative’ and represent a range of cellular phenotypes. Pro-inflammatory M1-type MQs (M1) are often associated with tissue damage, whereas alternatively activated M2-type MQs (M2) are usually associated with tissue repair and often involved in fibrosis. Thus, M1 or M2 may explain the underlying differences in pathology of chronic GN. Here we review the main functions of polarized macrophages and discuss the perspectives of this field.
