Intercellular adhesion molecule-1 mediated interactions and leucocyte infiltration in IgA nephropathy

Background: Mononuclear leucocytes have a role in IgAnephropathy (IgAN). Renal leucocyte recruitment is mediated by adhesiveinteractions between leucocytes and their ligands on renal cells.Methods: We have assessed interstitial and glomerularleucocytes by avidin-biotin-peroxidase with monoclonal antibodies (MA)against leucocytes (CD45), {beta}2-integrin (CD18), monocyte-macrophages(CD14), T (CD3) and T-cell subsets (CD4, CD8), and intercellular adhesionmolecule 1 (ICAM-1) (CD54), and analysed their relation with the abnormalexpression of ICAM-1 on proximal tubule epithelium in sequential renalsections from 48 patients with IgAN stratified according to the severity ofthe interstitial cellular infiltration observed by light microscopy.Results: In IgAN without (n=15) and with (n=7)interstitial cellular infiltration of 1+, ICAM-1 expression on vascularendothelium was unchanged with respect to that observed in the normalkidney; the proximal tubule epithelium was negative for this stain. In IgANwith interstitial cellular infiltration of 2+ (n=10), 3+ (n=11), and 4+(n=5), ICAM-1⁺ stain was observed on the proximaltubule epithelium, the median value of its quantitative expression being0.3, 0.1, and 0.2 (P=0.0008), respectively. The tubularICAM-1⁺ stain was significantly associated with theinterstitial leucocytes identified by MA, and correlated withCD45⁺ (r=0.59, P=0.02), CD14⁺(r=0.54, P<0.02), and CD3⁺ (r=0.51, P=0.02)interstitial leucocytes in IgAN with interstitial cellular infiltration.Interstitial ICAM-1⁺ andCD18⁺ leucocytes were correlated (r=0.56,P<0.001). Correlation was found between the quantitative tubularexpression of ICAM-1⁺ and the number ofCD45⁺ (r=0.98, P<0.0001),CD3⁺ (r=0.48, P=0.02), andCD8⁺ (r=0.76, P<0.02) glomerular leucocytes.Conclusion: Our results suggest that tubular andinterstitial ICAM-1⁺ cells may participate inadhesive interactions with interstitial leucocytes. Interstitial T-cellsand macrophages as well as glomerular T-cells bearing predominantlyCD8⁺ phenotype could play a role in the induction ofthe tubular expression of ICAM-1 in IgAN.