title: Differences in glomerular leukocyte infiltration between IgA nephropathy and membranoproliferative glomerulonephritis.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: The Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Soma
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: T
authors.initials: T
authors.lastname: Ootaka
authors.forename: H
authors.initials: H
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Abe
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D015932:Complement C3c / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005922:Glomerulonephritis, IGA / Q000473:pathology*; D015432:Glomerulonephritis, Membranoproliferative / Q000473:pathology*; D006801:Humans; D007124:Immunoenzyme Techniques; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D007962:Leukocytes / Q000473:pathology*; D016256:Lewis X Antigen / Q000032:analysis; D016169:Lymphocyte Function-Associated Antigen-1 / Q000032:analysis; D016177:Macrophage-1 Antigen / Q000032:analysis; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015932:Complement C3c; D005340:Fibrinogen; D018799:Intercellular Adhesion Molecule-1; D016256:Lewis X Antigen; D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; C067980:CD68 antigen, human; D000097382:CD68 Molecule