TY  - JOUR
AU  - Ramadori, Pierluigi
AU  - Kam, Shing
AU  - Heikenwälder, Mathias
TI  - T Cells: Friends and Foes in NASH Pathogenesis and Hepatocarcinogenesis.
JO  - Hepatology
VL  - 75
IS  - 4
SN  - 0270-9139
CY  - New York [u.a.]
PB  - Wiley Interscience
M1  - DKFZ-2022-00109
SP  - 1038-1049
PY  - 2022
N1  - #EA:F180#LA:F180# / 2022 Apr;75(4):1038-1049 / #DKFZ-MOST-Ca197#
AB  - In association with the pandemic spreading of obesity and metabolic syndrome, the prevalence of NAFLD-related HCC is increasing almost exponentially. In recent years, many of the underlining multi-factorial causes of NAFLD have been identified, and the cellular mechanisms sustaining disease development have been dissected up to single-cell level. However, there is still an urgent need to provide clinicians with more therapeutic targets, with particular attention on NAFLD-induced HCC, where immune check-point inhibitors do not work as efficiently. Whereas much effort has been invested in elucidating the role of the innate immune response in the hepatic NAFLD microenvironment, only in the last decade novel critical roles were unraveled for T cells in driving chronic inflammation toward HCC. The metabolic and immune-microenvironment interact to recreate a tumor-promoting and immune-suppressive terrain, responsible for the resistance to anti-cancer therapy. In this article, we will review the specific functions of several T-cell populations involved in NAFLD and NAFLD-driven HCC. We will illustrate the cellular cross talk with other immune cells, the regulatory networks or stimulatory effects of these interactions and the role of the metabolic microenvironment in influencing immune-cell functionality. Finally, we will present the pros and cons of the current therapeutic strategies against NAFLD-related HCC and delineate possible novel approaches for the future.
LB  - PUB:(DE-HGF)16
C6  - pmid:35023202
DO  - DOI:10.1002/hep.32336
UR  - https://inrepo02.dkfz.de/record/178512
ER  -