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Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
Published on: December 15, 2011
[Sclerosing mesenteritis: can it be a IgG4 dysimmune disease?]
Hicham Belghiti1, Dominique Cazals-Hatem, Anne Couvelard
1Service d'anatomie-pathologique, hôpital Beaujon, AP-HP, 92118 Clichy cedex, France.
Inflammatory mesenteric diseases show heterogeneous histological features, with significant plasma cell, eosinophil, and TCD8+ lymphocyte components. These findings suggest a dysimmune pathogenesis distinct from hyper-IgG4 diseases.
Area of Science:
- Gastroenterology
- Pathology
- Immunology
Background:
- Mesenteric panniculitis (MP), sclerotic mesenteritis (SM), and mesenteric lipodystrophy (ML) are rare inflammatory mesenteric diseases with unknown pathogenesis.
- A dysimmune disorder is hypothesized as the underlying cause.
Purpose of the Study:
- To investigate the histological basis for a dysimmune disorder in inflammatory mesenteric diseases.
- To analyze the cellular components and immunohistochemical markers in MP, SM, and ML.
Main Methods:
- Histological analysis and systematic immunostaining (IgG4, CD3, CD8) were performed on patient samples.
- Dysimmune features were defined by specific thresholds for plasma cells, eosinophils, TCD8/CD3 ratio, and IgG4+ plasma cells.
- Cases were classified into MP, SM, or ML based on predominant histological components.
Main Results:
- Thirteen patients with inflammatory mesenteric disease were analyzed; paraffin blocks were available for ten.
- Histological analysis revealed plasma cell and eosinophil components in 46% and 23% of cases, respectively.
- Immunohistochemistry showed numerous TCD8+ cells in 80% of cases, but numerous IgG4+ plasma cells in only 31%.
Conclusions:
- Inflammatory mesenteric diseases exhibit significant heterogeneity in plasma cell, eosinophil, and TCD8+ lymphocyte infiltration.
- Eosinophils were predominantly observed in sclerotic mesenteric disease forms.
- The limited presence of IgG4+ plasma cells suggests a pathogenesis distinct from typical hyper-IgG4 related disorders.
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