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We recently discovered that autonomic dysfunction precedes and predicts arthritis development in subjects at risk of developing seropositive\n                    <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                    . In addition,\n                    <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                    patients with relatively high vagus nerve tone (higher parasympathetic parameters, measured by heart rate variability) respond better to antirheumatic therapies. Together, these data suggest that the ANS may control inflammation in humans. This notion is supported by experimental studies in animal models of\n                    <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                    . We have found that stimulation of the so\u2010called cholinergic anti\u2010inflammatory pathway by efferent electrical vagus nerve stimulation (VNS) or pharmacological activation of the alpha7 subunit of nicotinic acetylcholine receptors (\u03b17n\n                    <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>\n                    hR) improves clinical signs and symptoms of arthritis, reduces cytokine production and protects against progressive joint destruction. Conversely, increased arthritis activity was observed in alpha7n\n                    <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>\n                    hR knockout mice. These studies together with previous work in animal models of sepsis and other forms of inflammation provided the rationale for an experimental clinical trial in patients with\n                    <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                    . We could for the first time show that an implantable vagus nerve stimulator inhibits peripheral blood cytokine production in humans. VNS significantly inhibited\n                    <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20106 production and improved\n                    <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                    disease severity, even in some patients with therapy\u2010resistant disease. This work strongly supports further studies using a bioelectronic approach to treat\n                    <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                    and other IMIDs.\n                  <\/jats:p>","DOI":"10.1111\/joim.12626","type":"journal-article","created":{"date-parts":[[2017,5,26]],"date-time":"2017-05-26T03:18:36Z","timestamp":1495768716000},"page":"64-75","source":"Crossref","is-referenced-by-count":141,"title":["Balancing the autonomic nervous system to reduce inflammation in rheumatoid arthritis"],"prefix":"10.1111","volume":"282","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8622-1319","authenticated-orcid":false,"given":"F. A.","family":"Koopman","sequence":"first","affiliation":[{"name":"Department of Clinical Immunology and Rheumatology Amsterdam Rheumatology and Immunology Center Academic Medical Center\/University of Amsterdam Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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