INKT cells prevent obesity-induced hepatic steatosis in mice in a C-C chemokine receptor 7-dependent manner

H. M. Kim, B. R. Lee, E. S. Lee, M. H. Kwon, J. H. Huh, B. E. Kwon, E. K. Park, S. Y. Chang, M. N. Kweon, P. H. Kim, H. J. Ko, C. H. Chung

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis are characterized by an increase in hepatic triglyceride content with infiltration of immune cells, which can cause steatohepatitis and hepatic insulin resistance. C-C chemokine receptor 7 (CCR7) is primarily expressed in immune cells, and CCR7 deficiency leads to the development of multi-organ autoimmunity, chronic renal disease and autoimmune diabetes. Here, we investigated the effect of CCR7 on hepatic steatosis in a mouse model and its underlying mechanism. Our results demonstrated that body and liver weights were higher in the CCR7 '/' mice than in the wild-type (WT) mice when they were fed a high-fat diet. Further, glucose tolerance and insulin sensitivity were markedly diminished in CCR7 '/' mice. The number of invariant natural killer T (iNKT) cells was reduced in the livers of the CCR7 '/' mice. Moreover, liver inflammation was detected in obese CCR7 '/' mice, which was ameliorated by the adoptive transfer of hepatic mononuclear cells from WT mice, but not through the transfer of hepatic mononuclear cells from CD1d '/' or interleukin-10-deficient (IL-10 '/') mice. Overall, these results suggest that CCR7 + mononuclear cells in the liver could regulate obesity-induced hepatic steatosis via induction of IL-10-expressing iNKT cells.

Original languageEnglish
Pages (from-to)270-279
Number of pages10
JournalInternational Journal of Obesity
Volume42
Issue number2
DOIs
Publication statusPublished - 2018 Feb 1

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C Chemokines
CC Chemokines
Chemokine Receptors
Obesity
Liver
Natural Killer T-Cells
Fatty Liver
Interleukin-10
Insulin Resistance
Hepatocytes
Adoptive Transfer
High Fat Diet
Autoimmunity
Type 1 Diabetes Mellitus
Chronic Renal Insufficiency
Triglycerides
Body Weight
Inflammation
Glucose

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Cite this

Kim, H. M. ; Lee, B. R. ; Lee, E. S. ; Kwon, M. H. ; Huh, J. H. ; Kwon, B. E. ; Park, E. K. ; Chang, S. Y. ; Kweon, M. N. ; Kim, P. H. ; Ko, H. J. ; Chung, C. H. / INKT cells prevent obesity-induced hepatic steatosis in mice in a C-C chemokine receptor 7-dependent manner. In: International Journal of Obesity. 2018 ; Vol. 42, No. 2. pp. 270-279.
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title = "INKT cells prevent obesity-induced hepatic steatosis in mice in a C-C chemokine receptor 7-dependent manner",
abstract = "Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis are characterized by an increase in hepatic triglyceride content with infiltration of immune cells, which can cause steatohepatitis and hepatic insulin resistance. C-C chemokine receptor 7 (CCR7) is primarily expressed in immune cells, and CCR7 deficiency leads to the development of multi-organ autoimmunity, chronic renal disease and autoimmune diabetes. Here, we investigated the effect of CCR7 on hepatic steatosis in a mouse model and its underlying mechanism. Our results demonstrated that body and liver weights were higher in the CCR7 '/' mice than in the wild-type (WT) mice when they were fed a high-fat diet. Further, glucose tolerance and insulin sensitivity were markedly diminished in CCR7 '/' mice. The number of invariant natural killer T (iNKT) cells was reduced in the livers of the CCR7 '/' mice. Moreover, liver inflammation was detected in obese CCR7 '/' mice, which was ameliorated by the adoptive transfer of hepatic mononuclear cells from WT mice, but not through the transfer of hepatic mononuclear cells from CD1d '/' or interleukin-10-deficient (IL-10 '/') mice. Overall, these results suggest that CCR7 + mononuclear cells in the liver could regulate obesity-induced hepatic steatosis via induction of IL-10-expressing iNKT cells.",
author = "Kim, {H. M.} and Lee, {B. R.} and Lee, {E. S.} and Kwon, {M. H.} and Huh, {J. H.} and Kwon, {B. E.} and Park, {E. K.} and Chang, {S. Y.} and Kweon, {M. N.} and Kim, {P. H.} and Ko, {H. J.} and Chung, {C. H.}",
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Kim, HM, Lee, BR, Lee, ES, Kwon, MH, Huh, JH, Kwon, BE, Park, EK, Chang, SY, Kweon, MN, Kim, PH, Ko, HJ & Chung, CH 2018, 'INKT cells prevent obesity-induced hepatic steatosis in mice in a C-C chemokine receptor 7-dependent manner', International Journal of Obesity, vol. 42, no. 2, pp. 270-279. https://doi.org/10.1038/ijo.2017.200

INKT cells prevent obesity-induced hepatic steatosis in mice in a C-C chemokine receptor 7-dependent manner. / Kim, H. M.; Lee, B. R.; Lee, E. S.; Kwon, M. H.; Huh, J. H.; Kwon, B. E.; Park, E. K.; Chang, S. Y.; Kweon, M. N.; Kim, P. H.; Ko, H. J.; Chung, C. H.

In: International Journal of Obesity, Vol. 42, No. 2, 01.02.2018, p. 270-279.

Research output: Contribution to journalArticle

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T1 - INKT cells prevent obesity-induced hepatic steatosis in mice in a C-C chemokine receptor 7-dependent manner

AU - Kim, H. M.

AU - Lee, B. R.

AU - Lee, E. S.

AU - Kwon, M. H.

AU - Huh, J. H.

AU - Kwon, B. E.

AU - Park, E. K.

AU - Chang, S. Y.

AU - Kweon, M. N.

AU - Kim, P. H.

AU - Ko, H. J.

AU - Chung, C. H.

PY - 2018/2/1

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N2 - Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis are characterized by an increase in hepatic triglyceride content with infiltration of immune cells, which can cause steatohepatitis and hepatic insulin resistance. C-C chemokine receptor 7 (CCR7) is primarily expressed in immune cells, and CCR7 deficiency leads to the development of multi-organ autoimmunity, chronic renal disease and autoimmune diabetes. Here, we investigated the effect of CCR7 on hepatic steatosis in a mouse model and its underlying mechanism. Our results demonstrated that body and liver weights were higher in the CCR7 '/' mice than in the wild-type (WT) mice when they were fed a high-fat diet. Further, glucose tolerance and insulin sensitivity were markedly diminished in CCR7 '/' mice. The number of invariant natural killer T (iNKT) cells was reduced in the livers of the CCR7 '/' mice. Moreover, liver inflammation was detected in obese CCR7 '/' mice, which was ameliorated by the adoptive transfer of hepatic mononuclear cells from WT mice, but not through the transfer of hepatic mononuclear cells from CD1d '/' or interleukin-10-deficient (IL-10 '/') mice. Overall, these results suggest that CCR7 + mononuclear cells in the liver could regulate obesity-induced hepatic steatosis via induction of IL-10-expressing iNKT cells.

AB - Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis are characterized by an increase in hepatic triglyceride content with infiltration of immune cells, which can cause steatohepatitis and hepatic insulin resistance. C-C chemokine receptor 7 (CCR7) is primarily expressed in immune cells, and CCR7 deficiency leads to the development of multi-organ autoimmunity, chronic renal disease and autoimmune diabetes. Here, we investigated the effect of CCR7 on hepatic steatosis in a mouse model and its underlying mechanism. Our results demonstrated that body and liver weights were higher in the CCR7 '/' mice than in the wild-type (WT) mice when they were fed a high-fat diet. Further, glucose tolerance and insulin sensitivity were markedly diminished in CCR7 '/' mice. The number of invariant natural killer T (iNKT) cells was reduced in the livers of the CCR7 '/' mice. Moreover, liver inflammation was detected in obese CCR7 '/' mice, which was ameliorated by the adoptive transfer of hepatic mononuclear cells from WT mice, but not through the transfer of hepatic mononuclear cells from CD1d '/' or interleukin-10-deficient (IL-10 '/') mice. Overall, these results suggest that CCR7 + mononuclear cells in the liver could regulate obesity-induced hepatic steatosis via induction of IL-10-expressing iNKT cells.

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