Pancreatic Autoantibodies and Autoantibodies Against Goblet Cells in Pediatric Patients With Inflammatory Bowel Disease

Kovács, Márta; Lakatos, László; Papp, Mária; Jacobsen, Silvia; Nemes, Éva; Polgár, Marianne; Sólyom, Enikő; Bódi, Piroska; Horváth, Ágnes; Müller, Katalin Eszter; Molnár, Kálmán; Szabó, Dolóresz; Aron, C; Dezsőfi, Antal; Arató, András; Veres, Gábor

doi:10.1097/mpg.0b013e318256b516

Cited by 35 publications

(31 citation statements)

References 41 publications

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“…A recent study based on a cohort of 103 Hungarian children with CrD did not demonstrate any association of PAB with clinical features of disease [33]. These data could support the notion that pediatric IBD are probably distinct entities compared to the adult forms of the disease.…”

Section: Autoimmunity In Crohn's Diseasesupporting

confidence: 73%

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Roggenbuck¹,

Reinhold

Schierack

et al. 2014

Clinical Chemistry and Laboratory Medicine

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Crohn's disease (CrD) and ulcerative colitis (UC) are the main inflammatory bowel diseases (IBD). IBDspecific humoral markers of autoimmunity in the form of autoantibodies have been reported first in the late 1950s by demonstrating the occurrence of autoimmunity in UC, while humoral autoimmunity in CrD can be traced back to the 1970s. Ever since, the pathophysiological role of autoimmune responses in IBDs has remained poorly understood. Notwithstanding, autoreactive responses play a major role in inflammation leading to overt IBD. In CrD, approximately 40% of patients and < 20% of patients with UC demonstrate loss of tolerance to antigens of the exocrine pancreas. Glycoprotein 2 (GP2) has been identified as a major autoantigenic target of the so-called pancreatic antibodies. The previously unsolved contradiction of pancreatic autoreactivity and intestinal inflammation in IBD was elucidated by demonstrating the expression of GP2 at the site thereof. Intriguingly, GP2 has been reported to be a receptor on microfold cells of intestinal Peyer's patches, which are believed to represent the origin of CrD inflammation. The development of immunoassays for the detection of antibodies to GP2 has paved the way to investigate the association of such antibodies with the clinical phenotype in CrD. Given the recently discovered immunomodulating role of GP2 in innate and adaptive intestinal immunity, this association can shed further light on the pathophysiology of IBD. In this context, the association of anti-GP2 autoantibodies as novel CrD-specific markers with the clinical phenotype in CrD will be discussed in this review.

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Section: Autoimmunity In Crohn's Diseasesupporting

confidence: 73%

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Roggenbuck¹,

Reinhold

Schierack

et al. 2014

Clinical Chemistry and Laboratory Medicine

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“…The necessity for ileal inflammation in order for anti-GP2 antibodies to be developed can also explain why only a minority of patients with UC have shown autoantibody reactivity against this antigen [12, 17–19, 21–23]. In our study, fewer than 7% of 225 patients with UC have shown anti-GP2 antibodies.…”

Section: Discussionmentioning

confidence: 56%

“…Pancreatic antibodies directed against GP2 have been considered serological markers of CD, being present in approximately 20–36% of patients with IBD [12, 17–19, 21–23]. Why GP2 becomes an autoantigenic target in CD is unclear [12, 13, 24].…”

Section: Discussionmentioning

confidence: 99%

Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease

Pavlidis

Romanidou

Roggenbuck

et al. 2012

Clinical and Developmental Immunology

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Why zymogen glycoprotein 2 (GP2), the Crohn's disease (CD)-specific pancreatic autoantigen, is the major target of humoral autoimmunity in inflammatory bowel diseases (IBD) is uknown. Recent evidence demonstrates that GP2 is also present on the apical surface of microfold (M) intestinal cells. As the colon lacks GP2-rich M cells, we assumed that patients with colonic CD are seronegative for anti-GP2. Anti-GP2 antibodies were tested in 225 CDs, including 45 patients with colonic location (L2), 45 with terminal ileum (L1) and 135 with ileocolonic involvement; 225 patients with ulcerative colitis (UC) were also tested. Anti-GP2 reactivity was detected in 59 (26.2%) CDs and 15 (6.7%) UCs (P < 0.001). Only 5 CDs with L2 had anti-GP2 antibodies, compared to 54/180 (30.0%, P = 0.0128) of the CDs with L1 and L3. Anti-GP2 antibody positive CD patients had higher ASCA titres compared to seronegative cases. Amongst the 128 CD patients with previous surgical intervention, 45 (35.0%) were anti-GP2 antibody positive compared to 14/97 (14.0%) without surgical (P < 0.001). Our data support the assumption that ileal inflammation is required for the development of anti-GP2 antibodies in CD, and suggest that the intestine rather than the pancreatic juice is the antigenic source required for the initiation of anti-GP2 antibodies.

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“…For example, anti-Saccharomyces cerevisiae antibodies (ASCA) are widely accepted markers for CD, whereas goblet cell antibodies and anti-neutrophil cytoplasmic antibodies (P-ANCA) support the diagnosis of UC. 4,5 Additional antibodies that demonstrate a high specificity for CD are autoantibodies against glycoproteins of the pancreatic acini (PABs). 6 They occur in 27% to 39% of patients with CD and 0% to 5% of patients with UC.…”

mentioning

confidence: 99%

Pancreatic Autoantibodies Against CUZD1 and GP2 Are Associated with Distinct Clinical Phenotypes of Crohnʼs Disease

Michaels

Jendrek

Korf

et al. 2015

Inflammatory Bowel Diseases

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Pancreatic Autoantibodies and Autoantibodies Against Goblet Cells in Pediatric Patients With Inflammatory Bowel Disease

Cited by 35 publications

References 41 publications

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Crohn’s disease specific pancreatic antibodies: clinical and pathophysiological challenges

Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease

Pancreatic Autoantibodies Against CUZD1 and GP2 Are Associated with Distinct Clinical Phenotypes of Crohnʼs Disease

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