Critical role of synovial tissue–resident macrophage niche in joint homeostasis and suppression of chronic inflammation-Reference-Cited by-同舟云学术

Critical role of synovial tissue–resident macrophage niche in joint homeostasis and suppression of chronic inflammation

Published:2021-01-06 Issue:2 Volume:7 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Huang Qi-Quan¹^ORCID,Doyle Renee¹,Chen Shang-Yang¹^ORCID,Sheng Qicong¹^ORCID,Misharin Alexander V.²^ORCID,Mao Qinwen³^ORCID,Winter Deborah R.¹^ORCID,Pope Richard M.¹^ORCID

Affiliation:

1. Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

2. Division of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

3. Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Abstract

Using a novel model of rheumatoid arthritis, we identified a critical role for reduced tissue-resident macrophages.

Funder

U.S. Department of Defense

NIH Office of the Director

American College of Rheumatology Research and Education Foundation

American Federation for Aging Research

American Heart Association

Scleroderma Foundation

American Lung Association

National Research Foundation

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference45 articles.

1. Recognition of Amino Acid Motifs, Rather Than Specific Proteins, by Human Plasma Cell–Derived Monoclonal Antibodies to Posttranslationally Modified Proteins in Rheumatoid Arthritis

2. Rheumatoid arthritis

3. Absence of changes in the number of synovial sublining macrophages after ineffective treatment for rheumatoid arthritis: Implications for use of synovial sublining macrophages as a biomarker

4. Genetics of rheumatoid arthritis contributes to biology and drug discovery

5. Rheumatoid arthritis synovial macrophages express the Fas-associated death domain-like interleukin-1?-converting enzyme-inhibitory protein and are refractory to Fas-mediated apoptosis

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