Th2 predominance and CD8+ memory T cell depletion in patients with severe acute respiratory syndrome.

Th2 predominance and CD8+ memory T cell depletion in patients with severe acute respiratory syndrome.
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DOI:
10.1016/j.micinf.2004.11.017
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发表时间:
2005-03
影响因子:
5.8
通讯作者:
Huang W
Huang W
中科院分区:
医学3区
文献类型:
--
作者:
Huang JL;Huang J;Duan ZH;Wei J;Min J;Luo XH;Li JG;Tan WP;Wu LZ;Liu RY;Li Y;Shao J;Huang BJ;Zeng YX;Huang W

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严重急性呼吸系统综合症(SARS)的免疫谱尚不清楚。采用酶联免疫吸附试验(ELISA)检测了95例SARS患者血清中抗SARS相关冠状病毒(SARS- cov)的细胞因子、趋化因子、免疫球蛋白、补体和特异性抗体水平,并采用流式细胞术分析了外周血淋巴细胞表型。结果显示,在整个SARS期间,白细胞介素(IL)-10和转化生长因子β (TGF-β)持续上调。正常活化受调控的T细胞表达和分泌(RANTES)水平降低,而单核细胞趋化蛋白-1 (MCP-1)在急性患者中升高。免疫球蛋白和补体在SARS的第一个月升高。针对SARS冠状病毒的特异性IgM和IgG抗体的血清阳性率和滴度在SARS发病后第41-60天达到峰值。急性期CD4+、CD8+ T淋巴细胞明显降低。恢复期患者CD3+CD8+CD45RO+ T淋巴细胞减少36.78%。结论:SARS-CoV可能引起有效的体液免疫,但随着时间的推移抑制细胞免疫,特别是CD8+记忆T淋巴细胞。IL-10和TGF-β的长期过量产生可能在该疾病中起重要作用。
The immune spectrum of severe acute respiratory syndrome (SARS) is poorly understood. To define the dynamics of the immune spectrum in SARS, serum levels of cytokines, chemokines, immunoglobulins, complement and specific antibodies against SARS-associated coronavirus (SARS-CoV) were assayed by enzyme-linked immunosorbent assay (ELISA), and phenotypes of peripheral lymphocytes were analyzed by flow cytometry in 95 SARS-infected patients. Results showed that interleukin (IL)-10 and transforming growth factor β (TGF-β) were continuously up-regulated during the entirety of SARS. Regulated on activation normally T cell-expressed and secreted (RANTES) levels were decreased, while monocyte chemoattractant protein-1 (MCP-1) was elevated in acute patients. Immunoglobulins and complement were elevated during the first month of SARS. Both serum-positive rates and titers of specific IgM and IgG antibodies responding to SARS-CoV peaked at days 41–60 from the onset of SARS. CD4+ and CD8+ T lymphocytes decreased significantly in acute-phase. CD3+CD8+CD45RO+ T lymphocytes were decreased by 36.78% in the convalescent patients. Conclusion: SARS-CoV seemed to elicit effective humoral immunity but inhibited cellular immunity, especially CD8+ memory T lymphocytes over time. Prolonged overproduction of IL-10 and TGF-β may play an important role in the disease.
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