Murine CD4 T-cell response to Helicobacter infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load
Murine CD4 T-cell response to Helicobacter infection: TH1 cells enhance gastritis and TH2 cells reduce bacterial load
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DOI：
10.1016/s0016-5085(97)70004-0
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发表时间：
1997-12-01
期刊：
影响因子：
29.4
通讯作者：
Czinn, SJ
中科院分区：
文献类型：
--
作者：
Mohammadi, M;Nedrud, J;Czinn, SJ
背景与目的：以往的研究结果表明，TH 1细胞免疫反应有助于螺杆菌相关性胃炎。为了进一步研究这个问题，白细胞介素4基因靶向小鼠感染猫螺杆菌，并进行了一系列过继转移实验，以评估TH 1和TH 2细胞的作用。研究方法：在活细菌攻击之前，将来自免疫/攻击或非免疫/感染小鼠的抗原特异性脾细胞或CD 4（+）T细胞系过继转移到幼稚受体中。结果：从两组供体以及TH 1或TH 2细胞系转移的细胞加重了受体的胃炎症。在来自感染小鼠的大量脾细胞的受体或TH 1细胞系的受体中未观察到对细菌负荷的影响。相比之下，当过继转移来自免疫攻击小鼠的TH 2细胞系或大量细胞时，受体显示出细菌负荷的显著减少。在白细胞介素4缺陷小鼠中也观察到细菌数量增加。结论：这些数据表明，TH 1和TH 2细胞介导的免疫应答在螺杆菌感染中的不同贡献：一个与疾病的发病机制（TH 1表型）相关，另一个与保护或控制感染（TH 2表型）相关。
Background & Aims: Previous findings suggest that TH1 cellular immune responses contribute to Helicobacter-associated gastritis. To further investigate this issue, interleukin 4 gene targeted mice were infected with Helicobacter felis, and a series of adoptive transfer experiments was performed to evaluate the role of both TH1 and TH2 cells. Methods: Antigen-specific spleen cells from immunized/challenged or nonimmunized/infected mice or CD4(+) T-cell lines were transferred adoptively into naive recipients before live bacterial challenge. Results: Transfer of cells from both groups of donors as well as TH1 or TH2 cell lines exacerbated gastric inflammation in the recipients. No effect on bacterial load was observed in recipients of bulk spleen cells from infected mice or recipients of TH1 cell lines. In contrast, when either a TH2 cell line or bulk cells from immunized challenged mice were transferred adoptively, recipients showed a dramatic reduction in bacterial load. Increased numbers of bacteria were also noted in interleukin 4-deficient mice. Conclusions: These data suggest a differential contribution of TH1 and TH2 cell-mediated immune responses in Helicobacter infection: one associated with the pathogenesis of disease (TH1 phenotype) and the other associated with protection from or control of infection (TH2 phenotype).