L Wang

Sichuan University, Chengdu, Sichuan Sheng, China

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Publications (2)2.91 Total impact

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    ABSTRACT: Type 2 diabetes mellitus (T2DM) has been gradually considered as a micro- inflammatory disease. To explore the significance of peripheral CD4+ regulatory T cells and CD4+ effector T cells in T2DM, we analyzed inflammation, humoral and cellular immune state in patients with T2DM.118 patients with T2DM without complications and 116 healthy volunteers were included. Serum C-reactive protein (CRP), Complement 3 (C3), Complement 4 (C4), IgG, IgA, IgM, plasma sIL-2 R and peripheral T lymphocyte subsets (including CD4+ CD25high regulatory T cells (Treg) and CD4+ CD25low+median effector T cells (Teff)) were analyzed by rate nephelometry immunoassay, chemiluminescence immunoassay and flow cytometry, respectively.(1) micro-inflammation state in T2DM: Serum CRP, C3, IgA and plasma sIL-2 R were all significantly higher in T2DM than those in healthy control (HC) (all P<0.05). (2) Disturbance of cellular immune in T2DM: Compared with HC, the percentage of peripheral CD3+CD4+T cells and ratio of CD3+CD4+T cells to CD3+CD8+T cells in T2DM were both significantly increased (P<0.05); and the percentage of peripheral CD4+CD25+T cells, Teff cells increased (P>0.05), Treg cells strikingly decreased in T2DM (P<0.05). A positive correlation between sIL-2R levels and peripheral CD4+CD25+T cells or Teff cell percentages, as well as a negative correlation between plasma sIL-2 R levels and serum HDL, LDL or CHOL levels in T2DM were shown (all P <0.05).Micro-inflammation state in T2DM was characterized by increased sIL-2 R, elevated CD3+CD4+T cells and the imbalance of Treg cells and Teff cells, which as one of the pathogeneses took part in inflammation reaction in T2DM.
    Experimental and Clinical Endocrinology & Diabetes 04/2013; 121(4):214-9. · 1.56 Impact Factor
  • Y Li, Y Shi, J Chen, B Cai, B Ying, L Wang
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    ABSTRACT: Interleukin-18 (IL-18) is a potent proinflammatory cytokine, which can promote hepatitis B virus clearance. The latest studies find that genetic polymorphisms near the IL-28B gene are strongly associated with sustained viral response and spontaneous viral clearance in patients with chronically infected hepatitis C and hepatitis B. We investigated the effect of rs187238 and rs1946518 in IL-18 gene and rs8099917 in IL-28B gene on HBV recurrence in liver transplant patients. A total of 200 liver transplant recipients and relevant donors were enrolled in this study. The patients' mean follow-up was 39 month (range 10-65 month). All liver transplant recipients were in a stable stage. The total recipients (n = 200) were divided into end-stage liver disease secondary to hepatitis B (n = 140) and end-stage liver disease secondary to other diseases (n = 60) before transplantation. Recipients (n = 140) with hepatitis B before transplantation were defined to nonHBV recurrence group (n = 119) or HBV recurrence group (n = 21), which was positive for HBsAg or elevatory in HBV DNA (>2.0 × 10(2) IU mL(-1)) after transplantation. For the recipients (n = 140) had hepatitis B before transplantation, we studied the single-nucleotide polymorphisms (SNPs) of IL-18 gene (rs187238 and rs1946518) and IL-28B gene (rs8099917) by high-resolution melting (HRM) curve analysis. The serum levels of IL-18 and IFN-γ were tested by ELISA. The serums levels of IFN-γ were lower in HBV recurrence group than that in nonHBV recurrence group (P < 0.01). The genotype of IL-28B gene rs8099917 was associated with alanine aminotransferase (ALT) levels and aspartate aminotransferase (AST) levels in HBV-related liver transplant recipients (n = 140). The recipients with allele G (GG+GT) had higher ALT and AST levels (P < 0.05). No association was found between IL-18 gene and IL-28B gene polymorphisms with HBV recurrence in the liver transplant recipients or the donors. We identified that the IFN-γ was a protective factor of HBV recurrence after liver transplantation. The allele G of rs8099917 was associated with hepatitis B-related hepatocytes injury. The rs8099917 G allele subgroup should reinforce antiviral therapy.
    International Journal of Immunogenetics 02/2012; 39(4):346-52. · 1.36 Impact Factor