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Related Experiment Video

Updated: Jun 18, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Published on: December 15, 2011

Antimyenteric neuronal antibodies in scleroderma

S Howe¹, E Y Eaker, J E Sallustio

¹Department of Medicine, University of Florida, Gainesville 32610.

The Journal of Clinical Investigation

|August 1, 1994

Summary

This summary is machine-generated.

Scleroderma patients often have IgG antibodies targeting myenteric neurons, suggesting a neuropathic cause for gastrointestinal dysmotility. This finding was confirmed by immunofluorescence, correlating with Raynaud's phenomenon.

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Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study

Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study

Published on: June 29, 2016

Area of Science:

Gastroenterology
Immunology
Neurology

Background:

Gastrointestinal (GI) dysmotility in scleroderma is poorly understood.
Previous research suggests a neuropathic mechanism.
The role of specific antibodies in this process requires further investigation.

Purpose of the Study:

To investigate the presence of circulating antibodies targeting myenteric neurons in scleroderma patients.
To compare antibody presence in scleroderma with other connective tissue diseases and healthy controls.
To explore the potential neuropathic basis of GI dysmotility in scleroderma.

Main Methods:

Sera from scleroderma patients, other connective tissue disease patients, and normal controls were tested.
Indirect immunofluorescence was used to detect antibodies binding to myenteric neurons in rat intestine.
Sera were absorbed with calf thymus extract to differentiate specific neuronal antibodies from antinuclear antibodies.

Main Results:

19 out of 41 scleroderma patients had high-titer antibodies against myenteric neurons.
Antibodies were not detected in healthy controls or patients with idiopathic GI dysmotility.
After absorption, 15 scleroderma sera retained positive staining, suggesting specific antimyenteric neuronal antibodies, unlike in SLE or MCTD.

Conclusions:

IgG antibodies reacting with myenteric neurons are prevalent in scleroderma patients with GI dysmotility.
The presence of these antibodies supports a neuropathic mechanism in scleroderma-associated GI dysmotility.
Further research is needed to identify the specific neuronal antigen targeted by these antibodies.