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Updated: Feb 14, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
Published on: December 15, 2011
Immunoexpression of IgA receptors (CD89, CD71) in dermatitis herpetiformis
Justyna Gornowicz-Porowska1, Agnieszka Seraszek-Jaros, Monika Bowszyc-Dmochowska
1Autoimmune Blistering Dermatoses Section, Department of Dermatology, Poznan University of Medical Sciences, Poznan, Poland. justynagornowicz1@poczta.onet.pl.
Introduction:
The role of IgA receptors in dermatitis herpetiformis (DH) pathogenesis is still unknown. CD89 and CD71 may be associated with immune response during DH development. The purpose of this study was to perform semiquantitative analysis of simultaneous immunoexpression of CD89 and CD71 in DH and IgA/neutrophil-mediated non-DH dermatoses (IgAN) in relation to specific IgA autoantibodies/antibodies (tissue and epidermal transglutaminases, nonapeptides of gliadin - eTG/tTG/npG) as well neutrophil activation via the release of neutrophil elastase (NE).
Material And Methods:
In total, 48 patients were studied. The study was conducted on skin lesions and sera obtained from DH and IgAN patients. DH and IgAN served as mutually positive control groups. We used immunohistochemical technique with semiquantitative digital morphometry and ELISA to measure serum levels of anti-eTG/tTG/npG IgA.
Results:
CD89 showed a significantly higher expression in DH than in IgAN. CD71 was overexpressed in DH and IgAN. CD89 immunoexpression correlated negatively with CD71 in IgAN. A positive correlation was revealed between CD89 immunoexpression and anti-npG IgA in DH. No statistically significant correlations were found in DH between the CD89/CD71 and NE immunoexpression, between CD71 immunoexpression and anti-tTG/eTG/npG IgA, or between CD89 immunoexpression and anti-eTG/tTG IgA serum levels.
Conclusions:
CD89 is probably a key IgA Fc receptor in DH development, where it is associated with immune response to gluten. CD71 may be linked with inflammation in DH and IgAN. We suggest that interaction between CD89 and CD71 can modulate the inflammation in IgAN.
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