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Similarly, for TRAIL, off-target toxicity of uncontrolled oligomeric forms of TRAIL has been reported.
Like CD95L, TRAIL has been reported to be a potent inhibitor of autoimmune arthritis [ 24].
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No TRAIL variants other than the full length TRAIL have been reported in murine cells.
To overcome the resistance of tumour cells to TRAIL, enhanced effects using combinations of anticancer drugs and TRAIL have been reported (Lacour et al, 2001).
Since trailing has been reported, we measured both MIC50 and MIC100 for fluconazole.
In addition, an agonistic monoclonal antibody that binds to the TRAIL death receptor, TRAIL R2, has been reported to induce apoptosis in RA synovial fibroblasts [ 18, 19].
In our experiment, we found that the over-expression of IPS-1 promoted the induction of the pro-apoptotic gene TRAIL, which has been reported to have an important role in the induction of apoptosis in various types of cancers.
TRAIL gene therapy has been reported to inhibit development of arthritis in a collagen-induced mouse model [ 17, 22].
As TRAIL receptor-2 regulation has been reported to be a central determinant of TRAIL sensitivity, overexpression of TRAIL receptor-2 was performed, but did not have an impact on the TRAIL response, arguing against a dominant role of TRAIL receptor-2 expression levels in the regulation of TRAIL sensitivity in our experimental setting (Supplementary Figure S1D).
The importance of CASP8 in TRAIL resistance in gliomas has been reported as well [ 23], while the data of other studies have strongly suggested TRAIL sensitivity to be CASP8-independent and DR4-specific [ 21].
So far, no correlation between TRAIL resistance and TRAIL decoy receptor gene expression has been reported.
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