Expression of Fas ligand by microglia: possible role in glioma immune evasion. J Neuroimmunol 2001 Nov 01;120(1-2):19-24
Date
11/06/2001Pubmed ID
11694315DOI
10.1016/s0165-5728(01)00361-7Scopus ID
2-s2.0-0034749035 (requires institutional sign-in at Scopus site) 99 CitationsAbstract
The immune-privileged status of the central nervous system is thought to limit the application of immunotherapy for treatment of malignant brain tumors. Because the Fas pathway has been proposed to play a role in immune evasion, we examined the effect of tumor environment on the expression of Fas ligand (FasL) in a mouse glioma model. Immunoblotting revealed the expression of membrane-bound FasL to nearly double when murine G26 gliomas were propagated intracranially (IC) as compared to subcutaneously (SC). Further analysis by flow cytometry revealed microglia, which were absent in the SC tumors, to account for half of the FasL expression in the IC tumors. Interestingly, when FasL activity was inhibited in IC tumors, the proportion of tumor-infiltrating leukocytes increased three-fold, reaching the same frequency as the SC tumors. These observations suggest that microglia are a major source of FasL expression in brain tumors and possibly contribute to the local immunosuppressive milieu of malignant gliomas.
Author List
Badie B, Schartner J, Prabakaran S, Paul J, Vorpahl JMESH terms used to index this publication - Major topics in bold
AnimalsAntibodies, Monoclonal
Antigens, Surface
Blood-Brain Barrier
Brain Neoplasms
Cell Movement
Drug Resistance, Neoplasm
Fas Ligand Protein
Flow Cytometry
Frontal Lobe
Glioma
Gliosis
Immune Tolerance
Immunologic Surveillance
Immunosuppressive Agents
Macrophages
Membrane Glycoproteins
Mice
Mice, Inbred C57BL
Microglia
Treatment Failure
Tumor Cells, Cultured