Abstract: 【Abstract】Objective Glomerulonephritis (GN) is a major cause of end-stage renal failure in China. Tubulointerstitial cell infiltration is involved in the tissue destruction and therefore in renal dysfunction. The infiltration cells in renal tissue are mostly T lym¬phocytes and monocytes/macrophages. Activation of T-cells requires costimulatory signals through binding of CD28 receptor with cognate ligands (CD80 and CD86) located on antigen-presenting cells (APC). The aim of this study was to define the mechanisms by which CD80 and CD86 regulate the development of primary glomerulonephritis. Methods Eighty-nine patients with primary glomerulonephritis were studied. Tubulointerstitial lesions were divided into grade 1 to grade 4 (negative to severe tissue damage) by using Katafuchi scale. The expression of CD80 and CD86 in renal tissues was detected by immunohistochemical methods. Results The expression and distribution patterns of CD80 and CD86 were different in patients with primary glomerulonephritis. CD86 was expressed extensively in glomerulus, periglomerular area, tubular epithelial cells, and peritubular interstitium, while CD80 was ex¬pressed only in some tubular epithelial cells and peritubular interstitium. Moreover, the percent¬age of CD80+ and CD86+ cells in peritubular interstitium showed a tendency to increase with tubulointerstitial damage (r=0.741, P<0.001; r=0.736, P<0.001, respectively). The expression of CD80 and CD86 significantly correlated with the amount of 24-hour proteinuria and creatinine clearance. Conclusion This study clearly shows that the increase of CD80 and CD86 expression with the progression of tubulointerstitial lesion may play an important role in primary glomerulonephritis. The expression of CD80 and CD86 correlates with renal function at the time of biopsy. The costimulatory molecules CD80 and CD86 may involve in the pathogenesis of primary glomerulonephritis.

Key words: CD80, CD86, Renal tubulointerstitial lesions