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Tae Hyun Kim1, Sang Geon Kim1,2,*
1College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea
2Interdisciplinary Program of Clinical Pharmacology, Seoul National University, Seoul, Republic of Korea
*Reprint requests Address requests for reprints to: Sang Geon Kim, PhD, College of Pharmacy, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 08826, Korea.
Abstract
Chronic damage to hepatocytes causes persistent inflammation, leading to chronic hepatitis, liver cirrhosis, and eventually hepatocellular carcinoma (HCC).1 Along with the concept that the HCC microenvironment is composed of a heterogeneous mixture of tumor cells, stromal cells, and immune cells, increasing evidence from experimental and clinical studies suggests the critical role of inflammatory tumor microenvironments in the development and progression of HCC.2 Although it is challenging to accurately assess whether HCC development occurs in a proinflammatory or anti-inflammatory fashion, the role of immune cells in the context of cancer-related inflammation is currently being studied intensively based on observations that immune cells and immune-related mediators are expressed in the tumor environments of different types of cancer,2, 3 highlighting the effects of antitumor immune responses on the inflammatory milieu. Because early clinical trials of therapeutic approaches targeting immune cells such as immune checkpoint inhibitors showed promising results in patients with HCC,4, 5 recent investigations have characterized anti-HCC immune responses mainly in the context of developing novel immunotherapies targeting a clinical setting wherein HCCs have already developed and progressed.6, 7 However, the impact of antitumor immune responses in the inflammatory milieu during hepatocarcinogenesis remains largely elusive. In this issue of Gastroenterology, Mossanen et al8 present the important, unrecognized function of CXCR6 in tumor surveillance in HCC progression by demonstrating the role of natural killer (NK) T and cluster of differentiation (CD)4+ T cell-dependent recognition and clearance of senescent hepatocytes in multiple HCC models.
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