PMID- 27263022
OWN - NLM
STAT- MEDLINE
DCOM- 20191211
LR  - 20220801
IS  - 1559-0267 (Electronic)
IS  - 1080-0549 (Linking)
VI  - 57
IP  - 1
DP  - 2019 Aug
TI  - Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a 
      Review.
PG  - 23-38
LID - 10.1007/s12016-016-8557-4 [doi]
AB  - Celiac disease is a common inflammatory disorder with a prevalence of 1-2 % in 
      which a distinct dietary wheat, rye, and barley component, gluten, induces 
      small-bowel mucosal villous atrophy, crypt hyperplasia, and inflammation. The 
      small-bowel mucosal damage can be reversed by a strict lifelong gluten-free diet, 
      which is currently the only effective treatment for the condition. A key player 
      in the pathogenetic process leading to the enteropathy is played by a protein 
      called transglutaminase 2 (TG2), which is able to enzymatically modify 
      gluten-derived gliadin peptides. The TG2-catalyzed deamidation of the gliadin 
      peptides results in their increased binding affinity to the disease-predisposing 
      human leukocyte antigen (HLA) DQ2 and DQ8 molecules, thus enabling a strong 
      immune response to be launched. Blocking the enzymatic activity of TG2 has thus 
      been suggested as a suitable novel pharmacological approach to treat celiac 
      disease. By virtue of its transamidation capacity, TG2 is also able to cross-link 
      gliadin peptides to itself, this resulting in the generation of TG2-gliadin 
      peptide complexes whose presence might provide an explanation for the generation 
      of the TG2 autoantibodies characteristic of celiac disease. Due to their 
      excellent specificity for the disorder, the TG2-targeted autoantibodies are 
      widely used in the diagnostics as a first-line test to select patients for 
      gastrointestinal endoscopy. More recently, it has come to be appreciated that 
      these autoantibodies and also the TG2-specific B cells might play an active role 
      in the disease pathogenesis. In this review, we assess the role of TG2, 
      TG2-specific B cells, and autoantibodies in celiac disease.
FAU - Rauhavirta, Tiina
AU  - Rauhavirta T
AD  - Pediatric Research Center, University of Tampere and Tampere University Hospital, 
      Finn Medi 3, 33520, Tampere, Finland.
FAU - Hietikko, Minna
AU  - Hietikko M
AD  - Pediatric Research Center, University of Tampere and Tampere University Hospital, 
      Finn Medi 3, 33520, Tampere, Finland.
FAU - Salmi, Teea
AU  - Salmi T
AD  - School of Medicine, University of Tampere, Tampere, Finland.
AD  - Department of Dermatology, Tampere University Hospital, Tampere, Finland.
FAU - Lindfors, Katri
AU  - Lindfors K
AD  - Pediatric Research Center, University of Tampere and Tampere University Hospital, 
      Finn Medi 3, 33520, Tampere, Finland. katri.lindfors@uta.fi.
LA  - eng
GR  - 9T058/Competitive State Research Financing of the Expert Responsibility Areas of 
      Tampere University Hospital/
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Clin Rev Allergy Immunol
JT  - Clinical reviews in allergy & immunology
JID - 9504368
RN  - 0 (Autoantibodies)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DQ2 antigen)
RN  - 0 (HLA-DQ8 antigen)
RN  - 9007-90-3 (Gliadin)
RN  - EC 2.3.2.13 (Protein Glutamine gamma Glutamyltransferase 2)
RN  - EC 2.3.2.13 (Transglutaminases)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
SB  - IM
MH  - Adult
MH  - Animals
MH  - Autoantibodies/*immunology
MH  - Autoimmune Diseases
MH  - B-Lymphocytes/immunology
MH  - Celiac Disease/diagnosis/*epidemiology/*immunology
MH  - Child
MH  - Diet, Gluten-Free
MH  - Female
MH  - GTP-Binding Proteins/*immunology/metabolism
MH  - Gliadin/metabolism
MH  - HLA-DQ Antigens/metabolism
MH  - Humans
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Prevalence
MH  - Protein Glutamine gamma Glutamyltransferase 2
MH  - Risk Factors
MH  - Transglutaminases/*immunology/metabolism
OTO - NOTNLM
OT  - Celiac disease
OT  - Transglutaminase 2
OT  - Transglutaminase 2 autoantibodies
EDAT- 2016/06/06 06:00
MHDA- 2019/12/18 06:00
CRDT- 2016/06/06 06:00
PHST- 2016/06/06 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2016/06/06 06:00 [entrez]
AID - 10.1007/s12016-016-8557-4 [pii]
AID - 10.1007/s12016-016-8557-4 [doi]
PST - ppublish
SO  - Clin Rev Allergy Immunol. 2019 Aug;57(1):23-38. doi: 10.1007/s12016-016-8557-4.