Journal
IMMUNOLOGICAL INVESTIGATIONS
Volume 36, Issue 1, Pages 25-46Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/08820130600991893
Keywords
FasL; TRAIL; inflammation; cancer; tumor escape
Categories
Funding
- NATIONAL CANCER INSTITUTE [R01CA111786] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [P01DE012321, R01DE013918] Funding Source: NIH RePORTER
- NCI NIH HHS [R0-1 CA111786] Funding Source: Medline
- NHLBI NIH HHS [N0-1 HB37165] Funding Source: Medline
- NIDCR NIH HHS [P0-1 DE12321, R0-1 DE13918] Funding Source: Medline
Ask authors/readers for more resources
Death receptor ligands (FasL, TRAIL) activate apoptosis in cells expressing the cognate receptors. Evidence suggests that these ligands also deliver pro-inflammatory signals. In the tumor microenvironment, Fas counterattack mounted by tumors against immune cells is mediated by tumor-associated FasL. But death ligands crosslinking their receptors also induce inhibition of apoptosis and activation of the transcription factor, NF kappa B, with a subsequent burst of pro-inflammatory cytokine production and tumor growth promotion. NF kappa B, a key link between inflammation and cancer, regulates dual activities of death ligands, depending on molecular signals in the tumor microenvironment. This paper focuses on death ligands as an example of the extensive repertoire of strategies devised by tumors for escape from immune control.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available