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-1 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.
