6533b7dbfe1ef96bd126ffb6
RESEARCH PRODUCT
Immune escape mechanism: defective resting and stimulated leukocyte-endothelium interaction in hepatocellular carcinoma of the rat.
Jan SchmidtMartha Maria GebhardSasa-marcel MaksanPatrick Morad AraibEduard Ryschichsubject
MalePathologymedicine.medical_specialtyCell signalingCarcinoma HepatocellularEndotheliumPhysiologyCell CommunicationBiologyMetastasisMicrocirculationNeovascularizationmedicineLeukocytesAnimalsChemotactic FactorsNeovascularization PathologicCell adhesion moleculeMicrocirculationLiver NeoplasmsGastroenterologyHemodynamicsChemotaxismedicine.diseaseRatsRats Inbred ACImedicine.anatomical_structureLiverModels AnimalEndothelium Vascularmedicine.symptomLiver cancerCell Adhesion MoleculesBlood Flow Velocitydescription
Hepatocellular carcinoma represents an increasing therapeutic challenge due to its high incidence and early metastasis. Numerous studies have demonstrated the influence of the vascular system on tumor growth and development. In addition, the role of leukocyte-endothelium interaction in tumor vessels is of particular significance with regard to immunological tumor therapy. In this study we used an experimental in vivo animal model that allows a quantitative analysis on vessel morphology, microcirculation, and leukocyte-endothelium interaction. The vessel architecture in tumor tissue was found to be extremely heterogeneous, with a consecutively variable blood flow velocity. Following superfusion with chemotactic factors (fMLP, LB4), the leukocyte-endothelium interaction in tumor tissue with respect to leukocyte sticking was significantly reduced in comparison to healthy liver tissue. In conclusion, one of the main mechanisms for the reduced leukocyte-endothelium interaction in tumor tissue seems to be a decreased expression of adhesion molecules such as ICAM-1, indicating an effective immune escape mechanism for this tumor.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2004-07-21 | Digestive diseases and sciences |