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

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The adaptive immune response in celiac disease.

Shuo-Wang Qiao¹, Rasmus Iversen, Melinda Ráki

¹Department of Immunology and Centre for Immune Regulation, University of Oslo, Oslo University Hospital-Rikshospitalet, 0027, Oslo, Norway. s.w.qiao@medisin.uio.no

Seminars in Immunopathology

|April 27, 2012

Summary

Celiac disease pathogenesis is well understood due to known gluten triggers and human leukocyte antigen (HLA) associations. Recent research clarifies the roles of T cells, B cells, and antigen-presenting cells in its immune response.

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Area of Science:

Immunology
Gastroenterology

Background:

Celiac disease pathogenesis is better understood than other human leukocyte antigen (HLA)-associated disorders like type 1 diabetes, multiple sclerosis, and rheumatoid arthritis.
The known causative agent (gluten proteins) and specific HLA molecules involved facilitate detailed study.

Purpose of the Study:

To review recent advancements in understanding the immune response in celiac disease.
To highlight the roles of T cells, B cells, and antigen-presenting cells in celiac disease pathogenesis.

Main Methods:

Review of recent scientific literature on celiac disease immunology.
Analysis of adaptive immune responses, including T cell, B cell, and antigen-presenting cell functions.

Main Results:

The specific antigen (gluten) and HLA associations provide clear targets for immune dissection.
Distinct antibody responses to gluten and transglutaminase 2 offer insights into the adaptive immunity.

Conclusions:

Understanding of celiac disease pathogenesis is advanced by defined antigens and HLA associations.
Recent developments offer a comprehensive view of cellular players in the pathogenic immune response.