EDITORIAL
Immune–endothelial–nerve interaction: an explanation for the failure of the gastrointestinal system in systemic sclerosis?
1 Department of Biomedicine, Division of Rheumatology AOUC, Denothe Centre, University of Florence, Florence, Italy
2 Department of Immunology and Rheumatology, Clinical Center, University of Pécs, Pécs, Hungary
Correspondence to:
Dr Marco Matucci Cerinic, Department of Biomedicine, Division of Rheumatology AOUC, Villa Monna Tessa, Viale Pieraccini 18, I-50139 Florence, Italy; cerinic@unifi.it
Accepted 19 February 2009
| The first 150 words of the full text of this article appear below. |
In this issue, Kawaguchi et al1 (see page 710) report the occurrence of antimuscarinic 3 receptor (M3R) antibodies correlating with gastrointestinal involvement and severe dysmotility in systemic sclerosis (SSc). Contractility of the gastrointestinal system is controlled, in the myenteric plexus, by the autonomic nervous systems—sympathetic and parasympathetic—that are both essentially sustained by cholinergic transmission. The data reported by Kawaguchi et al1 might suggest that these antibodies impair enteric cholinergic neurotransmission, thus fostering enteric dysmotility in SSc. Clearly, this report focuses interest on the role that the immune system, with the production of autoantibodies, may play in generating the dysmotility of the gastrointestinal system in SSc. It is also important to focus attention on the technical details. It is well known that the technique for antibody detection is critical and may lead to controversial results, as already shown in Sjögren syndrome.2 This aspect is even more important because these
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Ann Rheum Dis 2009 68: 710-714.[Abstract] [Full Text] [PDF]
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