Abstract
BACKGROUND
Although pancreatic cancer tissue frequently induces an immune reaction, immunocompetent cells are not able to eliminate the
tumor. One potential cause for this ineffective immune response is that a number of active, tumor-cytotoxic T cells are not
able to invade into the tumor.
METHODS
A potential barrier for invading leukocytes can be the tumor endothelium, which controls recruitment of leukocytes from circulating
blood into the tissue. Although attenuated expression of adhesion molecules on the tumor endothelium has been proposed as
a mechanism which suppresses intratumoral leukocyte infiltration, the relevance of adhesion molecules for leukocyte recruitment
in tumor tissue is poorly understood.
RESULTS
The leukocyte extravasation in normal pancreas during acute pancreatitis follows the "classic" leukocyte recruitment cascade
and is controlled by the overexpression of endothelial adhesion molecules, such as selectins, intracellular adhesion molecule-1,
and platelet endothelial cell adhesion molecule-1. In contrast to acute inflammation in normal pancreas, leukocyte recruitment
in pancreatic cancer is a slow process, which does not show a strong dependence on intracellular adhesion molecule-1. In addition,
pancreatic cancer has a high degree of heterogeneity of both immunogenic properties and the distribution of tumor-infiltrating
leukocytes, such as CD8(+), CD4(+), or regulatory T cells.
CONCLUSION
Additional studies may clarify whether T cell recruitment and their activity in pancreatic cancer can be enhanced by modulation
of endothelial adhesion molecules.
Links
Authors
Schmidt J, Mocevicius P, Werner J, Ryschich E
Institution
Department of Surgery, University of Heidelberg, Germany.
Source
Surgery 152:3 Suppl 1 2012 Sep pg S89-94MeSH
Adaptive ImmunityCell Adhesion Molecules
Disease Progression
Endothelium
Humans
Immunity, Innate
Leukocytes
Pancreatic Neoplasms
T-Lymphocytes, Cytotoxic
T-Lymphocytes, Regulatory
Pub Type(s)
Journal ArticleReview
Language
eng
PubMed ID
22770953
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