Mononuclear inflammatory cells (MIC) in renal biopsies from 37 patients with renal disease were studied by avidin--biotin--immunoperoxidase complex (ABC) technique, utilizing monoclonal antibodies to cell surface antigens: T11 (total T), T4 (inducer/helper), T8 (suppressor/cytotoxic), B1 (B cells), M1 (monocytes), and Leu-7 (natural killer, NK cells). Renal MIC consisted mostly of T cells and monocytes. T cells were a predominating cell type in the renal interstitium of all patients studied (64-88% of MIC). The T4:T8 ratios ranged from 0.4 +/- 0.3 (mean +/- SEM) in interstitial nephritis to 2.5 +/- 0.9 in membranous glomerulonephritis. M1+ cells constituted from 10 to 62% of glomerular MIC and from 5 to 24% of interstitial MIC. Glomerular MIC were rare or absent in patients with IgA nephropathy (IgA N). These results support the concept that in situ interactions of T lymphocytes and monocytes may modulate the events leading to the development of human renal disease. The striking absence of glomerular MIC in IgA N could be related to persistence of immune deposits in the glomeruli of patients with this renal disorder.
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http://dx.doi.org/10.1016/0090-1229(84)90022-9 | DOI Listing |
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