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

Review article
Authors Karin Enarsson
Erik Johnsson
Catharina Lindholm
Anna Lundgren
Q. Pan-Hammarström
Erika Strömberg
Philip Bergin
E. L. Baunge
Ann-Mari Svennerholm
Marianne Quiding-Järbrink
Published in Clin Immunol
Volume 118
Issue 1
Pages 24-34
Publication year 2006
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Clinical Sciences, Department of Gastrosurgical Research and Education
Pages 24-34
Language en
Keywords Adenocarcinoma/*immunology, Aged, Aged, 80 and over, Antigens, Surface/metabolism, CD4-Positive T-Lymphocytes/immunology, CD8-Positive T-Lymphocytes/immunology, Cell Movement/*immunology, Female, Gastric Mucosa/*immunology, Humans, Immunoglobulins/metabolism, Male, Membrane Proteins/metabolism, Middle Aged, Mucoproteins/metabolism, Receptors, Cell Surface/metabolism, Receptors, Chemokine/metabolism, Receptors, Lymphocyte Homing/*immunology, Stomach Neoplasms/*immunology, T-Lymphocyte Subsets/immunology, T-Lymphocytes/*immunology
Subject categories Medical and Health Sciences


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 alpha4beta7+ 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.

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