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Sci Immunol. 2018 Mar 30;3(21). pii: eaar3701. doi: 10.1126/sciimmunol.aar3701.

Response to comment on "Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis".

Author information

1
Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin, National Institutes of Health, Bethesda, MD 20892, USA.
2
Department of Chemistry, Middle Tennessee State University, Murfreesboro, TN 37132, USA.
3
Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
4
Translational Research Program, Benaroya Research Institute at Virginia Mason, Seattle, WA 98101, USA.
5
VA Palo Alto Health Care System, Palo Alto, CA 94304, USA.
6
Division of Rheumatology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
7
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
8
Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin, National Institutes of Health, Bethesda, MD 20892, USA. mariana.kaplan@nih.gov.

Abstract

The citrullinome cargo in neutrophil extracellular traps varies according to disease condition and stimulation conditions.

PMID:
29602804
DOI:
10.1126/sciimmunol.aar3701

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