Intrahepatic natural killer T cell populations are increased in human hepatic steatosis - PubMed (original) (raw)

Intrahepatic natural killer T cell populations are increased in human hepatic steatosis

Michael Adler et al. World J Gastroenterol. 2011.

Abstract

Aim: To determine if natural killer T cell (NKT) populations are affected in nonalcoholic fatty liver disease (NAFLD).

Methods: Patients undergoing bariatric surgery underwent liver biopsy and blood sampling during surgery. The biopsy was assessed for steatosis and immunocyte infiltration. Intrahepatic lymphocytes (IHLs) were isolated from the remainder of the liver biopsy, and peripheral blood mononuclear cells (PBMCs) were isolated from the blood. Expression of surface proteins on both IHLs and PBMCs were quantified using flow cytometry.

Results: Twenty-seven subjects participated in this study. Subjects with moderate or severe steatosis had a higher percentage of intrahepatic CD3+/CD56+ NKT cells (38.6%) than did patients with mild steatosis (24.1%, P = 0.05) or those without steatosis (21.5%, P = 0.03). Patients with moderate to severe steatosis also had a higher percentage of NKT cells in the blood (12.3%) as compared to patients with mild steatosis (2.5% P = 0.02) and those without steatosis (5.1%, P = 0.05).

Conclusion: NKT cells are significantly increased in the liver and blood of patients with moderate to severe steatosis and support the role of NKT cells in NAFLD.

Keywords: Hepatic steatosis; Lymphocytes; Natural killer T cells; Natural killer T-like cells; Nonalcoholic fatty liver disease.

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Figures

Figure 1

Figure 1

Flow cytometry of CD3+/CD56+/CD161+ intrahepatic lymphocytes in a patient with a normal liver versus a patient with moderate steatosis. Cells were initially selected via CD3+ gating prior to analysis for expression of CD56 and CD161. There are a greater percentage of natural killer T cells (CD56+/CD161+) in patients with moderate steatosis (20.1%) as compared to patients with normal livers (6.6%). A: Normal liver; B: Moderate steatosis.

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