Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype

被引:488
作者
Bamford, KB
Fan, XJ
Crowe, SE
Leary, JF
Gourley, WK
Luthra, GK
Brooks, EG
Graham, DY
Reyes, VE
Ernst, PB
机构
[1] Univ Texas, Med Branch, Dept Med, Galveston, TX 77550 USA
[2] Univ Texas, Med Branch, Dept Pathol, Galveston, TX 77550 USA
[3] Univ Texas, Med Branch, Dept Pediat, Galveston, TX 77550 USA
[4] Univ Texas, Med Branch, Sealy Ctr Mol Sci, Galveston, TX 77550 USA
[5] Queens Univ Belfast, Dept Microbiol & Immunol, Belfast, Antrim, North Ireland
[6] Baylor Coll Med, Houston, TX 77030 USA
[7] Vet Adm, Dept Med, Houston, TX USA
关键词
D O I
10.1016/S0016-5085(98)70531-1
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: Studies have shown that gastric T cells are increased during Helicobacter pylori infection. The purpose of this study was to characterize the human gastric T-cell responses in the presence or absence of H. pylori. Methods: T-cell surface antigens were examined by immunohistochemistry or after isolation for evaluation of surface antigens and cytoplasmic cytokines using flow cytometry. Results: CD4(+) and CD8(+) T cells were increased in situ during infection with H. pylori. Freshly isolated gastric T cells expressed cytoplasmic interferon gamma (IFN-gamma) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8(+) and CD4(+) T cells expressed IFN-gamma. Because stimulation through CD30 favors the induction of IL-5 and Th2 cells, gastric and colonic T cells were examined for CD30 expression. Consistent with the notion that Th2 cells are found in the intestine, CD30 was evident throughout the lamina propria of the colon but was virtually absent in the stomach. Furthermore, freshly isolated gastric T cells produced little IL-4 and virtually no IL-5 or tumor necrosis factor beta. Conclusions: These observations show that gastric T cells resemble the Th1 type, which may explain their failure to induce immunity to H. pylori and their ability to contribute to the pathogenesis of gastric disease.
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收藏
页码:482 / 492
页数:11
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