Differential mechanisms for T lymphocyte recruitment in normal and neoplastic human gastric mucosa

被引:20
|
作者
Enarsson, K
Johnsson, E
Lindholm, C
Lundgren, A
Pan-Hammarström, Q
Strömberg, E
Bergin, P
Baunge, EL
Svennerholm, AM
Quiding-Järbrink, M
机构
[1] Univ Gothenburg, Dept Med Microbiol & Immunol, S-40530 Gothenburg, Sweden
[2] Univ Gothenburg, Vaccine Res Inst, S-40530 Gothenburg, Sweden
[3] Sahlgrenska Univ Hosp, Dept Surg, Gothenburg, Sweden
[4] Univ Gothenburg, Dept Rheumatol & Inflammat Res, S-40530 Gothenburg, Sweden
[5] Karolinska Univ Hosp, Dept Lab Med, Huddinge, Sweden
关键词
Helicobacter pylori; gastric adenocarcinoma; human; cell recruitment; cell adhesion molecules; endothelial addressins;
D O I
10.1016/j.clim.2005.08.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Worldwide, gastric adenocarcinoma (GC) is the second most common cause of death from malignant disease. The reason why immune responses are unable to clear the tumour is not fully understood, although aberrant lymphocyte recruitment to the tumour site might be one factor. Therefore, we investigated the homing phenotype of mucosal T lymphocytes in GC, compared to tumour-free mucosa. We could detect significantly decreased frequencies of mucosal homing alpha 4 beta 7(+) T cells in the tumour tissues and increased frequencies of L-selectin(+) T cells. This was probably due to the correlated decrease in MAdCAM-1 positive and increase in PNAd positive blood vessels in the tumour mucosa. There were also fewer CXCR3(+) T lymphocytes in the tumour tissue. These findings provide evidence that endothelial cells within tumours arising at mucosal sites do not support extravasation of typical mucosa-infiltrating T cells. This may be of major relevance for future immunotherapeutic strategies for treatment of GC. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:24 / 34
页数:11
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