Lymphocyte subsets and cytokines in women with gestational diabetes mellitus and their newborn

被引:37
作者
Lapolla, A
Dalfrá, MG
Sanzari, M
Fedele, D
Betterle, C
Masin, M
Zanchetta, R
Faggian, D
Massotti, M
Nucera, V
Plebani, M
机构
[1] Univ Padua, Metab Disorders Sect, Dept Med & Surg Sci, I-35128 Padua, Italy
[2] Univ Hosp, Inst Lab Med, Padua, Italy
[3] Univ Padua, Endocrinol Sect, Dept Med & Surg Sci, I-35128 Padua, Italy
关键词
pregnancy; diabetes; lymphocyte subsets; immunological impairment;
D O I
10.1016/j.cyto.2005.05.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study aimed to identify potential immunological markers for predicting type 1 diabetes in patients with gestational diabetes mellitus (GDM) and any immunological impairment in their newborn. In 62 GDM patients and 74 women with normal glucose tolerance (NGT), and their babies, we assessed total lymphocytes, T lymphocyte subsets CD3 and CD8 expressing T cell receptor (TCR) alpha/beta or gamma/delta, CD16 and CD19, pancreatic autoantibodies and cytokines (IL-5, IL-2, soluble receptor IL-2). At delivery, umbilical cord blood samples were taken for lymphocyte subpopulations and cytokine measurements. GDM mothers had higher levels of total lymphocytes, CD8 expressing TCR gamma/delta, and lower levels of CD3 expressing TCR alpha/beta than NGT controls. Insulin-treated GDM mothers had lower CD4 and CD4/CD8 ratios, and higher CD8 and IL-5 than diet-treated GDM or controls. Five women were positive for pancreatic autoantibodies, with lower CD4 (p < 0.01) and CD4/CD8 ratios (p < 0.05), and higher CD8 (p < 0.03) and CD19 than GDM and control mothers negative for autoantibodies. GDM newborn had higher CD8 gamma/delta and lower CD16 than NGT babies. There were no significant differences in TNF-alpha concentrations in the cord blood obtained from the GDM and NGT newborn. In conclusion, GDM women and their newborn have lymphocyte subset impairments, which are more important in patients positive for autoantibodies and/or treated with insulin. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:280 / 287
页数:8
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