TY  - JOUR
A1  - Beyer, Katharina
A1  - Baukloh, Ann-Kathrin
A1  - Stoyanova, Ani
A1  - Kamphues, Carsten
A1  - Sattler, Arne
A1  - Kotsch, Katja
T1  - Interactions of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) with the immune system: implications for inflammation and cancer
T2  - Cancers
N2  - Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily. TRAIL has historically been distinct from the Fas ligand and TNFα in terms of selective apoptosis induction in tumor cells and has a nearly non-existent systemic toxicity. Consequently, in the search for an ideal drug for tumor therapy, TRAIL rapidly drew interest, promising effective tumor control with minimal side effects. However, euphoria gave way to disillusionment as it turned out that carcinoma cells possess or can acquire resistance to TRAIL-induced apoptosis. Additionally, studies on models of inflammation and autoimmunity revealed that TRAIL can influence immune cells in many different ways. While TRAIL was initially found to be an important player in tumor defense by natural killer cells or cytotoxic T cells, additional effects of TRAIL on regulatory T cells and effector T cells, as well as on neutrophilic granulocytes and antigen-presenting cells, became focuses of interest. The tumor-promoting effects of these interactions become particularly important for consideration in cases where tumors are resistant to TRAIL-induced apoptosis. Consequently, murine models have shown that TRAIL can impair the tumor microenvironment toward a more immunosuppressive type, thereby promoting tumor growth. This review summarizes the current state of knowledge on TRAIL’s interactions with the immune system in the context of cancer.
Y1  - 2019
UR  - https://opus.bibliothek.uni-augsburg.de/opus4/frontdoor/index/index/docId/123950
UR  - https://nbn-resolving.org/urn:nbn:de:bvb:384-opus4-1239508
SN  - 2072-6694
VL  - 11
IS  - 8
SP  - 1161
PB  - MDPI AG
CY  - Basel
ER  -