Elevated circulating CD14lowCD16+ monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization

Anping Peng; Peifeng Ke; Rong Zhao; Xinyi Lu; Cheng Zhang; Xianzhang Huang; Guangjun Tian; Jun Huang; Jinli Wang; Pietro Invernizzi; Qubo Chen; Junhua Zhuang

doi:10.1007/s10238-015-0381-2

Elevated circulating CD14^lowCD16⁺ monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization

Anping Peng, Peifeng Ke, Rong Zhao, Xinyi Lu, Cheng Zhang, Xianzhang Huang, Guangjun Tian, Jun Huang, Jinli Wang, Pietro Invernizzi, Qubo Chen, Junhua Zhuang

Rheumatology, Allergy, and Clinical Immunology

Research output: Contribution to journal › Article

4 Citations (Scopus)

Abstract

Primary biliary cirrhosis (PBC) is a progressive autoimmune liver disease in which monocytes/macrophages infiltration and skewed T helper type (Th) 1 and Th17 cell responses participate in the development of the disease. Human peripheral blood monocytes are heterogeneous and can be divided into classical CD14^highCD16⁻, intermediate CD14^highCD16⁺, and nonclassical CD14^lowCD16⁺ monocyte subsets. Compared to classical monocytes, CD16⁺ monocytes are generally termed pro-inflammatory monocytes and play an important pathogenic role in autoimmune diseases. However, little is known about the immunophenotype and immunopathogenic role of peripheral blood CD16⁺ monocytes in PBC. Thus, we investigated the phenotype and function of these circulating monocyte subsets from PBC patients. The frequencies of circulating CD14^highCD16⁺ and CD14^lowCD16⁺ subpopulation were increased in disease compared with healthy controls. Among them, CD14^lowCD16⁺ monocyte subset positively correlated with disease progress, liver damage indicators and serum C-reactive protein, respectively. Furthermore, the frequencies of Th1 and Th17 cells were upregulated and CD14^lowCD16⁺ monocyte subset was also positively associated with Th1 cell frequency in PBC. Using a vitro coculture model, we further found that CD14^lowCD16⁺ monocytes promoted Th1 cell polarization compared to classical monocytes. Interleukin-12 (IL-12) and direct contact of patient CD4⁺T cell and CD14^lowCD16⁺ monocytes, were responsible for CD14^lowCD16⁺ monocytes promotion of Th1 cells polarization in PBC. Our study demonstrated that the enhanced CD14^lowCD16⁺ monocyte subset participated in fostering liver damage and inflammatory responses, and promoted Th1 cells skewing in PBC.

Original language	English (US)
Journal	Clinical and Experimental Medicine
DOIs	https://doi.org/10.1007/s10238-015-0381-2
State	Accepted/In press - Sep 24 2015

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Biliary Liver Cirrhosis

Liver

Monocytes

Polarization

Wounds and Injuries

Th1 Cells

Blood

T-cells

Macrophages

Interleukin-12

Set theory

Infiltration

C-Reactive Protein

Th17 Cells

Autoimmune Diseases

Liver Diseases

Foster Home Care

Coculture Techniques

Keywords

CD16
Monocyte subsets
Primary biliary cirrhosis
T helper type 1 cells

ASJC Scopus subject areas

Medicine(all)
Biochemistry, Genetics and Molecular Biology(all)

Cite this

Peng, A., Ke, P., Zhao, R., Lu, X., Zhang, C., Huang, X., ... Zhuang, J. (Accepted/In press). Elevated circulating CD14^lowCD16⁺ monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization. Clinical and Experimental Medicine. https://doi.org/10.1007/s10238-015-0381-2

Elevated circulating CD14^lowCD16⁺ monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization. / Peng, Anping; Ke, Peifeng; Zhao, Rong; Lu, Xinyi; Zhang, Cheng; Huang, Xianzhang; Tian, Guangjun; Huang, Jun; Wang, Jinli; Invernizzi, Pietro; Chen, Qubo; Zhuang, Junhua.

In: Clinical and Experimental Medicine, 24.09.2015.

Research output: Contribution to journal › Article

Peng, A, Ke, P, Zhao, R, Lu, X, Zhang, C, Huang, X, Tian, G, Huang, J, Wang, J, Invernizzi, P, Chen, Q & Zhuang, J 2015, 'Elevated circulating CD14^lowCD16⁺ monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization', Clinical and Experimental Medicine. https://doi.org/10.1007/s10238-015-0381-2

Peng A, Ke P, Zhao R, Lu X, Zhang C, Huang X et al. Elevated circulating CD14^lowCD16⁺ monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization. Clinical and Experimental Medicine. 2015 Sep 24. https://doi.org/10.1007/s10238-015-0381-2

Peng, Anping ; Ke, Peifeng ; Zhao, Rong ; Lu, Xinyi ; Zhang, Cheng ; Huang, Xianzhang ; Tian, Guangjun ; Huang, Jun ; Wang, Jinli ; Invernizzi, Pietro ; Chen, Qubo ; Zhuang, Junhua. / Elevated circulating CD14^lowCD16⁺ monocyte subset in primary biliary cirrhosis correlates with liver injury and promotes Th1 polarization. In: Clinical and Experimental Medicine. 2015.

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abstract = "Primary biliary cirrhosis (PBC) is a progressive autoimmune liver disease in which monocytes/macrophages infiltration and skewed T helper type (Th) 1 and Th17 cell responses participate in the development of the disease. Human peripheral blood monocytes are heterogeneous and can be divided into classical CD14highCD16−, intermediate CD14highCD16+, and nonclassical CD14lowCD16+ monocyte subsets. Compared to classical monocytes, CD16+ monocytes are generally termed pro-inflammatory monocytes and play an important pathogenic role in autoimmune diseases. However, little is known about the immunophenotype and immunopathogenic role of peripheral blood CD16+ monocytes in PBC. Thus, we investigated the phenotype and function of these circulating monocyte subsets from PBC patients. The frequencies of circulating CD14highCD16+ and CD14lowCD16+ subpopulation were increased in disease compared with healthy controls. Among them, CD14lowCD16+ monocyte subset positively correlated with disease progress, liver damage indicators and serum C-reactive protein, respectively. Furthermore, the frequencies of Th1 and Th17 cells were upregulated and CD14lowCD16+ monocyte subset was also positively associated with Th1 cell frequency in PBC. Using a vitro coculture model, we further found that CD14lowCD16+ monocytes promoted Th1 cell polarization compared to classical monocytes. Interleukin-12 (IL-12) and direct contact of patient CD4+T cell and CD14lowCD16+ monocytes, were responsible for CD14lowCD16+ monocytes promotion of Th1 cells polarization in PBC. Our study demonstrated that the enhanced CD14lowCD16+ monocyte subset participated in fostering liver damage and inflammatory responses, and promoted Th1 cells skewing in PBC.",

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AU - Peng, Anping

AU - Ke, Peifeng

AU - Zhao, Rong

AU - Lu, Xinyi

AU - Zhang, Cheng

AU - Huang, Xianzhang

AU - Tian, Guangjun

AU - Huang, Jun

AU - Wang, Jinli

AU - Invernizzi, Pietro

AU - Chen, Qubo

AU - Zhuang, Junhua

PY - 2015/9/24

Y1 - 2015/9/24

N2 - Primary biliary cirrhosis (PBC) is a progressive autoimmune liver disease in which monocytes/macrophages infiltration and skewed T helper type (Th) 1 and Th17 cell responses participate in the development of the disease. Human peripheral blood monocytes are heterogeneous and can be divided into classical CD14highCD16−, intermediate CD14highCD16+, and nonclassical CD14lowCD16+ monocyte subsets. Compared to classical monocytes, CD16+ monocytes are generally termed pro-inflammatory monocytes and play an important pathogenic role in autoimmune diseases. However, little is known about the immunophenotype and immunopathogenic role of peripheral blood CD16+ monocytes in PBC. Thus, we investigated the phenotype and function of these circulating monocyte subsets from PBC patients. The frequencies of circulating CD14highCD16+ and CD14lowCD16+ subpopulation were increased in disease compared with healthy controls. Among them, CD14lowCD16+ monocyte subset positively correlated with disease progress, liver damage indicators and serum C-reactive protein, respectively. Furthermore, the frequencies of Th1 and Th17 cells were upregulated and CD14lowCD16+ monocyte subset was also positively associated with Th1 cell frequency in PBC. Using a vitro coculture model, we further found that CD14lowCD16+ monocytes promoted Th1 cell polarization compared to classical monocytes. Interleukin-12 (IL-12) and direct contact of patient CD4+T cell and CD14lowCD16+ monocytes, were responsible for CD14lowCD16+ monocytes promotion of Th1 cells polarization in PBC. Our study demonstrated that the enhanced CD14lowCD16+ monocyte subset participated in fostering liver damage and inflammatory responses, and promoted Th1 cells skewing in PBC.

AB - Primary biliary cirrhosis (PBC) is a progressive autoimmune liver disease in which monocytes/macrophages infiltration and skewed T helper type (Th) 1 and Th17 cell responses participate in the development of the disease. Human peripheral blood monocytes are heterogeneous and can be divided into classical CD14highCD16−, intermediate CD14highCD16+, and nonclassical CD14lowCD16+ monocyte subsets. Compared to classical monocytes, CD16+ monocytes are generally termed pro-inflammatory monocytes and play an important pathogenic role in autoimmune diseases. However, little is known about the immunophenotype and immunopathogenic role of peripheral blood CD16+ monocytes in PBC. Thus, we investigated the phenotype and function of these circulating monocyte subsets from PBC patients. The frequencies of circulating CD14highCD16+ and CD14lowCD16+ subpopulation were increased in disease compared with healthy controls. Among them, CD14lowCD16+ monocyte subset positively correlated with disease progress, liver damage indicators and serum C-reactive protein, respectively. Furthermore, the frequencies of Th1 and Th17 cells were upregulated and CD14lowCD16+ monocyte subset was also positively associated with Th1 cell frequency in PBC. Using a vitro coculture model, we further found that CD14lowCD16+ monocytes promoted Th1 cell polarization compared to classical monocytes. Interleukin-12 (IL-12) and direct contact of patient CD4+T cell and CD14lowCD16+ monocytes, were responsible for CD14lowCD16+ monocytes promotion of Th1 cells polarization in PBC. Our study demonstrated that the enhanced CD14lowCD16+ monocyte subset participated in fostering liver damage and inflammatory responses, and promoted Th1 cells skewing in PBC.

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10.1007/s10238-015-0381-2