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 antibodies are found in high titres in Sjögren syndrome,3 4 remarking the absence of a connective tissue disease control group in the study by Kawaguchi et al.1

Howe et al5 have previously shown the presence of circulating antibodies to myenteric neurons in SSc, with a positive correlation with the presence of Raynaud’s phenomenon but not with gastrointestinal involvement. Moreover, Eaker et al6 have injected antimyenteric neuronal antibodies separated from SSc serum into an immunosuppressed rat model (with chronic indwelling intestinal electrodes to measure intestinal myoelectric activity) to observe the effects on intestinal motility. A prolongation in activity front duration and interval and a disruption were seen after SSc antibody injections. The authors hypothesised that these antibodies could account for the gastrointestinal …