To explore the role of immune regulating cytokines in pathogenesis of the idiopathic thrombocytopenic purpura (ITP) and its clinical significance, the levels of IL-18, TNF-alpha and Sc5b-9 in plasma of 32 ITP patients and 18 normal individuals were detected using ELISA methods. The results showed that IL-18, TNF-alpha and sC5b-9 levels in plasma of ITP patients were higher than that in normal individuals. The level of IL-18 was positively correlated with the levels of TNF-alpha and sC5b-9. In conclusion, The rising levels of the IL-18, TNF-alpha and sC5b-9 were correlated with disorder of Th1/Th2 subsets, and may contribute to the immune dysfunction in ITP patients. The dynamic observation of these cytokines may be useful in directing the clinical treatment for ITP patients.
Adolescent ; Adult ; Child ; Child, Preschool ; Complement Membrane Attack Complex ; analysis ; Female ; Humans ; Interleukin-18 ; blood ; Male ; Middle Aged ; Purpura, Thrombocytopenic, Idiopathic ; immunology ; Tumor Necrosis Factor-alpha ; analysis

Asthma ; blood ; Child ; Child, Preschool ; Complement Membrane Attack Complex ; analysis ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Intercellular Adhesion Molecule-1 ; blood ; Male ; Vascular Cell Adhesion Molecule-1 ; blood

PURPOSE: Local activation of the complement system plays a role in target organ damage. The aim of our study was to investigate the influence of cyclosporine (CsA)- induced renal injury on the complement system in the kidney. MATERIALS AND METHODS: Mice fed a low salt (0.01%) diet were treated with vehicle (VH, olive oil, 1mL/kg/day) or CsA (30mg/kg/day) for one or four weeks. Induction of chronic CsA nephrotoxicity was evaluated with renal function and histomorphology. Activation of the complement system was assessed through analysis of the expression of C3, C4d, and membrane attack complex (MAC), and the regulatory proteins, CD46 and CD55. CsA treatment induced renal dysfunction and typical morphology (tubulointerstitial inflammation and fibrosis) at four weeks. RESULTS: CsA-induced renal injury was associated with increased the expression of C3, C4d, and MAC (C9 and upregulation of complement regulatory proteins (CD 46 and CD55). Immunohistochemistry revealed that the activated complement components were mainly confined to the injured tubulointerstitium. CONCLUSION: CsA-induced renal injury is associated with activation of the intrarenal complement system.
Animals ; Antigens, CD45/analysis ; Antigens, CD46/analysis ; Antigens, CD55/analysis ; Complement C3/analysis ; Complement C4b/analysis ; Complement Membrane Attack Complex/analysis ; Complement System Proteins/*analysis ; Cyclosporine/*toxicity ; Disease Models, Animal ; Immunity, Innate/drug effects ; Immunoblotting ; Immunohistochemistry ; Immunosuppressive Agents/toxicity ; Kidney/*drug effects/immunology/pathology ; Kidney Diseases/*chemically induced/immunology ; Mice ; Microscopy, Confocal ; Peptide Fragments/analysis