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A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus
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Zeitschriftentitel: | The Journal of Immunology |
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Personen und Körperschaften: | , , , , , , |
In: | The Journal of Immunology, 199, 2017, 4, S. 1261-1274 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
The American Association of Immunologists
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Schlagwörter: |
author_facet |
Han, Shuhong Zhuang, Haoyang Shumyak, Stepan Wu, Jingfan Li, Hui Yang, Li-Jun Reeves, Westley H. Han, Shuhong Zhuang, Haoyang Shumyak, Stepan Wu, Jingfan Li, Hui Yang, Li-Jun Reeves, Westley H. |
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author |
Han, Shuhong Zhuang, Haoyang Shumyak, Stepan Wu, Jingfan Li, Hui Yang, Li-Jun Reeves, Westley H. |
spellingShingle |
Han, Shuhong Zhuang, Haoyang Shumyak, Stepan Wu, Jingfan Li, Hui Yang, Li-Jun Reeves, Westley H. The Journal of Immunology A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus Immunology Immunology and Allergy |
author_sort |
han, shuhong |
spelling |
Han, Shuhong Zhuang, Haoyang Shumyak, Stepan Wu, Jingfan Li, Hui Yang, Li-Jun Reeves, Westley H. 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.1700099 <jats:title>Abstract</jats:title> <jats:p>Dead cells accumulating in the tissues may contribute to chronic inflammation. We examined the cause of impaired apoptotic cell clearance in human and murine lupus. Dead cells accumulated in bone marrow from lupus patients but not from nonautoimmune patients undergoing myeloablation, where they were efficiently removed by macrophages (MΦ). Impaired apoptotic cell uptake by MΦ also was seen in mice treated i.p. with pristane (develop lupus) but not mineral oil (MO) (do not develop lupus). The inflammatory response to both pristane and MO rapidly depleted resident (Tim4+) large peritoneal MΦ. The peritoneal exudate of pristane-treated mice contained mainly Ly6Chi inflammatory monocytes; whereas in MO-treated mice, it consisted predominantly of a novel subset of highly phagocytic MΦ resembling small peritoneal MΦ (SPM) that expressed CD138+ and the scavenger receptor Marco. Treatment with anti-Marco–neutralizing Abs and the class A scavenger receptor antagonist polyinosinic acid inhibited phagocytosis of apoptotic cells by CD138+ MΦ. CD138+ MΦ expressed IL-10R, CD206, and CCR2 but little TNF-α or CX3CR1. They also expressed high levels of activated CREB, a transcription factor implicated in generating alternatively activated MΦ. Similar cells were identified in the spleen and lung of MO-treated mice and also were induced by LPS. We conclude that highly phagocytic, CD138+ SPM-like cells with an anti-inflammatory phenotype may promote the resolution of inflammation in lupus and infectious diseases. These SPM-like cells are not restricted to the peritoneum and may help clear apoptotic cells from tissues such as the lung, helping to prevent chronic inflammation.</jats:p> A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus The Journal of Immunology |
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10.4049/jimmunol.1700099 |
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The American Association of Immunologists, 2017 |
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The American Association of Immunologists, 2017 |
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2017 |
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The American Association of Immunologists |
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The Journal of Immunology |
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title |
A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_unstemmed |
A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_full |
A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_fullStr |
A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_full_unstemmed |
A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_short |
A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_sort |
a novel subset of anti-inflammatory cd138+ macrophages is deficient in mice with experimental lupus |
topic |
Immunology Immunology and Allergy |
url |
http://dx.doi.org/10.4049/jimmunol.1700099 |
publishDate |
2017 |
physical |
1261-1274 |
description |
<jats:title>Abstract</jats:title>
<jats:p>Dead cells accumulating in the tissues may contribute to chronic inflammation. We examined the cause of impaired apoptotic cell clearance in human and murine lupus. Dead cells accumulated in bone marrow from lupus patients but not from nonautoimmune patients undergoing myeloablation, where they were efficiently removed by macrophages (MΦ). Impaired apoptotic cell uptake by MΦ also was seen in mice treated i.p. with pristane (develop lupus) but not mineral oil (MO) (do not develop lupus). The inflammatory response to both pristane and MO rapidly depleted resident (Tim4+) large peritoneal MΦ. The peritoneal exudate of pristane-treated mice contained mainly Ly6Chi inflammatory monocytes; whereas in MO-treated mice, it consisted predominantly of a novel subset of highly phagocytic MΦ resembling small peritoneal MΦ (SPM) that expressed CD138+ and the scavenger receptor Marco. Treatment with anti-Marco–neutralizing Abs and the class A scavenger receptor antagonist polyinosinic acid inhibited phagocytosis of apoptotic cells by CD138+ MΦ. CD138+ MΦ expressed IL-10R, CD206, and CCR2 but little TNF-α or CX3CR1. They also expressed high levels of activated CREB, a transcription factor implicated in generating alternatively activated MΦ. Similar cells were identified in the spleen and lung of MO-treated mice and also were induced by LPS. We conclude that highly phagocytic, CD138+ SPM-like cells with an anti-inflammatory phenotype may promote the resolution of inflammation in lupus and infectious diseases. These SPM-like cells are not restricted to the peritoneum and may help clear apoptotic cells from tissues such as the lung, helping to prevent chronic inflammation.</jats:p> |
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author | Han, Shuhong, Zhuang, Haoyang, Shumyak, Stepan, Wu, Jingfan, Li, Hui, Yang, Li-Jun, Reeves, Westley H. |
author_facet | Han, Shuhong, Zhuang, Haoyang, Shumyak, Stepan, Wu, Jingfan, Li, Hui, Yang, Li-Jun, Reeves, Westley H., Han, Shuhong, Zhuang, Haoyang, Shumyak, Stepan, Wu, Jingfan, Li, Hui, Yang, Li-Jun, Reeves, Westley H. |
author_sort | han, shuhong |
container_issue | 4 |
container_start_page | 1261 |
container_title | The Journal of Immunology |
container_volume | 199 |
description | <jats:title>Abstract</jats:title> <jats:p>Dead cells accumulating in the tissues may contribute to chronic inflammation. We examined the cause of impaired apoptotic cell clearance in human and murine lupus. Dead cells accumulated in bone marrow from lupus patients but not from nonautoimmune patients undergoing myeloablation, where they were efficiently removed by macrophages (MΦ). Impaired apoptotic cell uptake by MΦ also was seen in mice treated i.p. with pristane (develop lupus) but not mineral oil (MO) (do not develop lupus). The inflammatory response to both pristane and MO rapidly depleted resident (Tim4+) large peritoneal MΦ. The peritoneal exudate of pristane-treated mice contained mainly Ly6Chi inflammatory monocytes; whereas in MO-treated mice, it consisted predominantly of a novel subset of highly phagocytic MΦ resembling small peritoneal MΦ (SPM) that expressed CD138+ and the scavenger receptor Marco. Treatment with anti-Marco–neutralizing Abs and the class A scavenger receptor antagonist polyinosinic acid inhibited phagocytosis of apoptotic cells by CD138+ MΦ. CD138+ MΦ expressed IL-10R, CD206, and CCR2 but little TNF-α or CX3CR1. They also expressed high levels of activated CREB, a transcription factor implicated in generating alternatively activated MΦ. Similar cells were identified in the spleen and lung of MO-treated mice and also were induced by LPS. We conclude that highly phagocytic, CD138+ SPM-like cells with an anti-inflammatory phenotype may promote the resolution of inflammation in lupus and infectious diseases. These SPM-like cells are not restricted to the peritoneum and may help clear apoptotic cells from tissues such as the lung, helping to prevent chronic inflammation.</jats:p> |
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spelling | Han, Shuhong Zhuang, Haoyang Shumyak, Stepan Wu, Jingfan Li, Hui Yang, Li-Jun Reeves, Westley H. 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.1700099 <jats:title>Abstract</jats:title> <jats:p>Dead cells accumulating in the tissues may contribute to chronic inflammation. We examined the cause of impaired apoptotic cell clearance in human and murine lupus. Dead cells accumulated in bone marrow from lupus patients but not from nonautoimmune patients undergoing myeloablation, where they were efficiently removed by macrophages (MΦ). Impaired apoptotic cell uptake by MΦ also was seen in mice treated i.p. with pristane (develop lupus) but not mineral oil (MO) (do not develop lupus). The inflammatory response to both pristane and MO rapidly depleted resident (Tim4+) large peritoneal MΦ. The peritoneal exudate of pristane-treated mice contained mainly Ly6Chi inflammatory monocytes; whereas in MO-treated mice, it consisted predominantly of a novel subset of highly phagocytic MΦ resembling small peritoneal MΦ (SPM) that expressed CD138+ and the scavenger receptor Marco. Treatment with anti-Marco–neutralizing Abs and the class A scavenger receptor antagonist polyinosinic acid inhibited phagocytosis of apoptotic cells by CD138+ MΦ. CD138+ MΦ expressed IL-10R, CD206, and CCR2 but little TNF-α or CX3CR1. They also expressed high levels of activated CREB, a transcription factor implicated in generating alternatively activated MΦ. Similar cells were identified in the spleen and lung of MO-treated mice and also were induced by LPS. We conclude that highly phagocytic, CD138+ SPM-like cells with an anti-inflammatory phenotype may promote the resolution of inflammation in lupus and infectious diseases. These SPM-like cells are not restricted to the peritoneum and may help clear apoptotic cells from tissues such as the lung, helping to prevent chronic inflammation.</jats:p> A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus The Journal of Immunology |
spellingShingle | Han, Shuhong, Zhuang, Haoyang, Shumyak, Stepan, Wu, Jingfan, Li, Hui, Yang, Li-Jun, Reeves, Westley H., The Journal of Immunology, A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus, Immunology, Immunology and Allergy |
title | A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_full | A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_fullStr | A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_full_unstemmed | A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_short | A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
title_sort | a novel subset of anti-inflammatory cd138+ macrophages is deficient in mice with experimental lupus |
title_unstemmed | A Novel Subset of Anti-Inflammatory CD138+ Macrophages Is Deficient in Mice with Experimental Lupus |
topic | Immunology, Immunology and Allergy |
url | http://dx.doi.org/10.4049/jimmunol.1700099 |