T-cell and B-cell immunity in celiac disease

Pré, M. Fleur du; Sollid, Ludvig M.

doi:10.1016/j.bpg.2015.04.001

Cited by 70 publications

(67 citation statements)

References 87 publications

(90 reference statements)

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“…Du Pré and Sollid (19) have also shown that within the small-bowel mucosa, gluten epitopes are presented to CD4+T cells through HLA-DQ2 and HLA-DQ8, thus leading to gliadin-induced T-cell activation. While there is growing evidence that the commensal bacteria in the gastrointestinal tract (i.e., the gut microbiota) influence the development of autoimmunity in rodent models, little is known about the interaction of helminthic diseases of the liver and the small bowel in human immune-mediated diseases (4).…”

Section: Discussionmentioning

confidence: 99%

Celiac disease prevalence in patients with hydatid cyst

Poyrazoglu¹,

Dönder²,

Dülger³

et al. 2017

J Turgut Ozal Med Cent

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Aim: Hydatid cyst (HC), which is localized in the liver and lungs in most cases, has been associated with a variety of hematologic and biochemical manifestations. Celiac disease (CD) is a small-intestinal malabsorption syndrome caused by hypersensitivity to gluten in subjects who carry the HLA haplotypes HLA DQ2 and DQ8. This study has attempted to show the connection between CD and HC. Material and Methods: We prospectively analyzed data from 211 HC patients, 62 of whom had extrahepatic involvement of HC; in addition, we also classified the patients' hydatid cysts by their radiologic features. All patients tested positive for HC by ELISA. Sera from the study population were also analyzed for IgA and IgG with ELISA using human recombinant tTG (AESKU. Diagnostics, Germany); the data were then analyzed statistically. Results: Twelve cases of seropositivity of TTG IgA were found among patients with HC. In the control group, the rate of TTG IgG seropositivity was only 2 out of 211 patients (~2%), which was lower than those with HC. In patients with HC, the mean WBC level was higher in patients with TTG IgA seropositivity compared with those without TTG IgA seropositivity. Younger ages were independently associated with TTG IgA seropositivity in the HC group. Conclusion: This study furthers the understanding of CD risk in HC. If confirmed by future studies, the study's data will assist in developing optimal strategies for the detection of CD in patients with HC. Understanding the infectious factors involved in CD is important for identifying new approaches to the early detection of CD.

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Section: Discussionmentioning

confidence: 99%

Celiac disease prevalence in patients with hydatid cyst

Poyrazoglu¹,

Dönder²,

Dülger³

et al. 2017

J Turgut Ozal Med Cent

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“…In addition to deamidating gliadin peptides, TG2 is also capable of cross-linking peptides to itself [131], and the presence of such complexes is thought to provide an explanation for the celiac disease-specific TG2 autoantibodies. It has been suggested that TG2-specific B cells could take up TG2-gliadin peptide complexes and present the gliadin peptide after being released from TG2 to a gluten-specific CD4-positive cell in the context of an HLA DQ2 or DQ8 molecule [132]. In this way, the gluten-specific CD4-positive cells would also provide help to the TG2-specific B cells (Fig.…”

Section: Biology Underlying Celiac Disease Adaptive and Innate Immunementioning

confidence: 97%

“…This would imply that the deamidation of gliadin peptides could occur during their contact with the intestinal epithelial cells in permissive conditions. Alternatively, the crucial enzymatic reactions of TG2 could also occur outside the small bowel, for instance in lymphoid tissue, as suggested [132], where TG2 is also abundantly expressed [137].…”

Section: Biology Underlying Celiac Disease Adaptive and Innate Immunementioning

confidence: 97%

Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review

Rauhavirta

Hietikko

Salmi

et al. 2016

Clinic Rev Allerg Immunol

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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.

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“…Im Rahmen der Antigenpräsentation aktiviert der Proteinkomplex aus HLA-DQ2 bzw. -DQ8 und den Gliadinepitopen CD4-positive T-Zellen [10]. T-Zell-seitig bedarf es hierzu des TZell-Rezeptors (TCR), der aus einem Repertoire von vielen Millionen TCR auf der Basis einer hoch affinen Bindung an den genannten Proteinkomplex selektioniert wird.…”

Section: Hla-dq2-und -Dq8-moleküleunclassified

“…Dabei sieht das aktuelle Erkrankungsmodell der Zöliakie eine Funktion der B-Zellen jenseits der ausschließlichen Antikörperprodukti-on vor. Vielmehr sind B-Zellen in der Lage, den T-Zellen über den Haupthistokompatibilitätkomplex(MHC)-II natives Antigen (in diesem Fall unprozessierte Gliadinsequenzen) zu präsentieren [10].…”

Section: Rolle Der B-zellenunclassified