Immune evasion by tumours: involvement of the CD95 (APO-1/Fas) system and its clinical implications.
T cells can cause the death of tumour cells by two mechanisms, one involving CD95 and the other involving perforin. T-cell activity or reduced tumour-cell responsiveness towards CD95 stimulation might result in an impaired anti-tumour immune response and tumour cell outgrowth. Recent data suggest that de novo expression of the CD95 ligand (CD95L) in tumours might result in elimination of CD95+ anti-tumour lymphocytes, and that tumours might therefore be privileged sites. However, conflicting data on the role of CD95L in transplantation experiments indicate that CD95L expression alone might not be sufficient to confer the status of immune privilege.
Strand
S
S
University Hospital, Dept of Internal Medicine, Heidelberg, Germany.
Galle
P R
PR
D017209:Apoptosis; D053222:Fas Ligand Protein; D006801:Humans; D008562:Membrane Glycoproteins / Q000276:immunology* / Q000378:metabolism; D015166:Monitoring, Immunologic; D009369:Neoplasms / Q000276:immunology*; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology; D019139:Tumor Escape; D019014:fas Receptor / Q000276:immunology* / Q000378:metabolism
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D019014:fas Receptor; D054353:Perforin