ϩ macrophages, with a few CD4 ϩ cells infiltrating the glomeruli. Necrotizing and crescentic glomerular lesions developed by day 7 with the increase of proteinuria. AT 1R was expressed on CD8 ϩ and CD4 ϩ cells and on ED1 ϩ macrophages. Low-dose ARB had no anti-inflammatory effects in anti-GBM GN. However, highdose ARB reduced glomerular infiltration of CD8 ϩ cells and ED1 ϩ macrophages and suppressed necrotizing and crescentic lesions by days 5 to 7 (P Ͻ 0.05). In addition, high-dose ARB reduced the numbers of ED3 ϩ -activated macrophages, suppressed glomerular TNF-␣ and IFN-␥ production, and downregulated M1-related chemokine and cytokines (monocyte chemoattractant protein type 1, IL-6, and IL-12). High-dose ARB also enhanced ED2 ϩ M2 macrophages by day 7 with upregulation of glomerular IL-4 and IL-13 and augmented CCL17, IL-1 receptor antagonist, and IL-10. We concluded that high-dose ARB inhibits glomerular inflammation by increasing the numbers of M2 macrophages and upregulation of anti-inflammatory cytokines and by suppressing M1 macrophage development with downregulation of M1-related proinflammatory cytokines.angiotensin II type 1 receptor blocker THE RENIN-ANGIOTENSIN-ALDOSTERONE system (RAAS) is a coordinated hormonal cascade that controls cardiovascular, renal, and adrenal function by regulating body fluid and electrolyte balances as well as arterial pressure (2, 41). ANG II is the principal RAAS effector peptide, and, through its binding to the ANG II type 1 receptor (AT 1 R), ANG II mediates a range of actions, including vasoconstriction, aldosterone and vasopressin release, sodium and water retention, and sympathetic activation. These activities may in turn induce hemodynamic alterations and hypertension. In addition to its systemic hemodynamic effects, ANG II was recently reported to be associated with several pathophysiological actions that facilitate specific tissue and organ injuries, including the production of proinflammatory mediators, cell proliferation, extracellular matrix synthesis, and release of reactive oxygen species (40,42).AT 1 R blockade (ARB) selectively inhibits the binding of ANG II to AT 1 R, and recent evidence indicated a role for ARB