Background. An important aspect in glomerular nephritic processes is the enhanced influx of leukocytes into the glomerulus. Methods. To investigate the mechanisms of intraglomerular leukocyte infiltration in IgA nephropathy (IgA-N) and membranoproliferative glomerulonephritis type I (MPGN-I), we immunohistochemically examined the intraglomerular expression of leukocyte function-associated antigen-1 (LFA-1, CD11a/CD18), macrophage-1 (Mac-1, CD11b/CD18) and intercellular adhesion molecule-1 (ICAM-1, CD54) together with glomerular deposition of C3c and fibrinogen. Results. In IgA-N (n = 42), LFA-1+ cells were distributed mainly in glomeruli with intense expression of ICAM-1, and there was a positive correlation (P < 0.001) between the number of LFA-1+ cells and the degree of ICAM-1 expression. Mac-1+ cells had no correlation with glomerular C3c deposition, but had a significant correlation with fibrinogen deposition (P < 0.05). The number of LFA-1+ cells was significantly greater than of Mac-1+ cells (P < 0.05). The number of LFA-1+ cells was strongly correlated with that of CD68+ cells (P < 0.00001). In MPGN-I n = 43), on the contrary, Mac-1+ cells correlated only with C3c deposition (P < 0.001), and they were observed mainly in peripheral loops of glomerular capillaries where C3c was deposited with a similar distribution. However, there was no relationship between LFA-1+ cells and ICAM-I expression. The number of Mac-1+ cells was greater than that of LFA-1+ cells (P < 0.0001), and most Mac-1+ cells were identical to CD15+ cells. Conclusion. These results indicate the possibility that different mechanisms may cause glomerular leukocyte infiltration in various forms of human glomerulonephritis. The LFA-1/ICAM-1 pathway may play an important role in glomerular leukocyte infiltration in IgA-N, while the Mac-1/complement pathway may be important in MPGN-I. The former may promote mainly the infiltration of CD68+ cells, and the latter may promote that of CD15+ cells. In addition, Mac-1+ cells may act as fibrinogen and complement receptors in IgA-N and MPGN-I, respectively.
- Adhesion molecules
- Glomerular leukocytes infiltration
- IgA nephropathy
- Membranoproliferative glomerulonephritis
ASJC Scopus subject areas