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

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 immunohistoch...

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Veröffentlicht in:Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 1998-03, Vol.114 (3), p.482-492
Hauptverfasser: Bamford, Kathleen B., Fan, Xuejun, Crowe, Sheila E., Leary, James F., Gourley, William K., Luthra, Gurinder K., Brooks, Edward G., Graham, David Y., Reyes, Victor E., Ernst, Peter B.
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container_end_page 492
container_issue 3
container_start_page 482
container_title Gastroenterology (New York, N.Y. 1943)
container_volume 114
creator Bamford, Kathleen B.
Fan, Xuejun
Crowe, Sheila E.
Leary, James F.
Gourley, William K.
Luthra, Gurinder K.
Brooks, Edward G.
Graham, David Y.
Reyes, Victor E.
Ernst, Peter B.
description 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-γ) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8 + and CD4 + T cells expressed IFN-γ. 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 β. 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. GASTROENTEROLOGY 1998;114:482-492
doi_str_mv 10.1016/S0016-5085(98)70531-1
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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-γ) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8 + and CD4 + T cells expressed IFN-γ. 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 β. 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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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-γ) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8 + and CD4 + T cells expressed IFN-γ. 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 β. 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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subjects Adult
AIDS/HIV
Bacterial diseases
Bacterial diseases of the digestive system and abdomen
Biological and medical sciences
Cells, Cultured
Gastric Mucosa - immunology
Helicobacter Infections - immunology
Helicobacter pylori
Human bacterial diseases
Humans
Infectious diseases
Interferon-gamma - biosynthesis
Ki-1 Antigen - analysis
Medical sciences
Middle Aged
Th1 Cells - physiology
title Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype
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