| Idiopathic chronic glomerulonephritis (CG) is characterized by proteinuria, hematuria, hypertension and edema. Many different pathogenic factors man induce this disease. Although CG contains multiple pathological types ,the prognosis of all of them would have no difference. Finally they will become chronic renal failure.The beginning of CG is immune-induced inflammation. The initiation of the immune response depends on T cell activation .T cell activation requires two signals. The first signal is specific, requiring T cell receptor recognition and binding to MHC/Antigen presented by an antigen-presenting cell. The second signal is nonspecific costimulatory molecules. T cells cannot activate, proliferate and differeriate without costimulatory molecules .Autoimmune diseases will occur when costimulatory molecules express abnormally. Inflammatory response is one of the important factors which may cause glomerular damage. The cells including infiltrating lymphocytes, macrophages may secrete many cytokines such as IL-1, IL-6, IL-8, TNF a , TGF ?and these cytokines cooperatively induce the renaldamage. The kidney cells (mesangial cells, endothelial cells, epithelial cells) may also produce these cytokines when giomerular damage initiates and facilitate the renal damage. Therefore it's very important to study the abnormal expression and significance of costimulatory melecules and the level of cytokines in the pathogenesis of CG.1. Significance of dynamic changes of T lymphocyte and its sebsets, as well as the expression of costimulatory molecules in 50 patients with chronic nephritis before and after treatment.We reported here the investigation of 50 patients with chronicnephritis for T cell subsets(CD3, CD4, CDS, CD21 and CD25), costmulatory molecu!es(CD28, 4-lBB, CD40, CD401, OX40 and CD80) before and after treatment by immunopheotying and flow cytometry analysis. The results demonstrated that the T cell subsets from patients with minor giomerular abnormalities , focal and segmental proliferative nephritis has no significant changes compared to that of normal controls. But the T cell subsets from patients with mesangial proliferative nephritis, crescentic nephritis and sclerosing nephritis were showed an obvious imbalance with reversing CD4/CD8 ratio, decreasing CD4*T cells and increasing CDS^ cells, meanwhile the CD3 expression of sclerosing nephritis decreased significantly. The expression of costimulatory molecule CD28 on T cells from patients with chronic nephritis was significantly lower compared to that of normal controls(P<0.001), meanwhile the percentage . of both CD4+CD28+T cells and CD8+CD28+T cells was decreased markedly. There are no difference among different pathologicaltypes' nephritis about the percentage of both CD4+CD28+T cells and CD8+CD28+T cells. After treatment the patients were in remission of their disease ,the imbalance of T cell subsets improved greatly , CD28+T cells, especially . CD4+CD28~T cells, increased significantly . In addition, a prefect negative collection was found between CD4+CD28+T cell numbers and the total amount of 24h urinary protein(r=-0.47,P<0.01). The 4-1BB expression on T cells in active patients was much higher in comparison with that of normal controls (P<0.01). After treatment the 4-1BB expression in remission patients was decreased significantly. Moreover, negative correlations were found between the 4-1BB expression and the CD4+ T cell counts(r=-0.84, P<0.01). The abnormal expression of the costimulatory molecules CD28 and 4-1BB needed for autoreative T cells and the imbalance of T cell subsets may play an important role in the pathogenesis of chronic nephritis. In particular, analysis the ratio of CD4/CD8, the expression levels of CD4+CD28+T cells and 4-lBB+ T cells has important value to evaluate the patients' remedial effect and prognosis.2. The levels and significance of IL-2, IL-6 and their soluble receptors in chronic nephritis.We also studied the serum levels of cytokines(IL-2 and its soluble receptor , IL-6 and its solu... |
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