Autoimmunity to Pancreatic Juice in Crohn's Disease Results of an Autoantibody Screening in Patients with Chronic Inflammatory Bowel Disease

Stöcker, W.; Otte, M.; Ulrich, Sebastian; Normann, D.; Finkbeiner, H; Stöcker, K.; Jantschek, G.; Scriba, P. C.

doi:10.3109/00365528709089774

Cited by 118 publications

(74 citation statements)

References 29 publications

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“…Walker described a possible diagnostic test for CrD by the use of buccal mucosa as a substrate in indirect immunofluorescence (IIF) for the detection of respective autoantibodies [13]. Loss of immunological tolerance observed in CrD and UC has been reported mainly for exocrine pancreatic, neutrophilic, and intestinal goblet cellular antigens [14][15][16].…”

Section: Autoimmunity In Crohn's Diseasementioning

confidence: 99%

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 Diseasementioning

confidence: 99%

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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“…This realization led to a growing interest in Abs to carbohydrate (glycan)-based Ags, as cellular and humoral immune responses rely heavily on interactions between glycans and specific glycan-binding proteins (4). One such glycan-directed, CD-specific serological marker is pancreatic autoantibody (PAB), first described more than two decades ago (5). However, its antigenic epitope was unknown until recently.…”

mentioning

confidence: 99%

Identification of Pancreatic Glycoprotein 2 as an Endogenous Immunomodulator of Innate and Adaptive Immune Responses

Werner

Paclik

Fritz

et al. 2012

The Journal of Immunology

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Pancreatic autoantibodies are Crohn disease-specific serologic markers. The function and immunological role of their recently identified autoantigen, glycoprotein 2 (GP2), are unknown. We therefore investigated the impact of GP2 on modulation of innate and adaptive immune responses to evaluate its potential therapeutic use in mucosal inflammation. Our data indicate a previously unknown function for GP2 as an immunomodulator. GP2 was ubiquitously expressed on cells vital to mucosal immune responses. The expression of GP2 was upregulated on activated human T cells, and it was further influenced by pharmaceutical TNF-α inhibitors. Recombinant GP2 significantly decreased human intestinal epithelial cells, mucosal and peripheral T cell proliferation, apoptosis, and activation, and it distinctly modulated cytokine secretion. Furthermore, intestinal epithelial cells stimulated with GP2 potently attracted T cells. In conclusion, we demonstrate a novel role for GP2 in immune regulation that could provide a platform for new therapeutic interventions in the treatment of Crohn disease.

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“…In case of Crohn's disease, the presence of papilledema secondary to inflammation of the duodenal mucosa may increase the risk of acute pancreatitis, however, this theory could not be mentioned in ulcerative colitis [3,14]. A study of Stokers et al showed an elevated auto antibodies directed against the pancreas in 40% of patients with Crohn's disease and a high prevalence of these autoantibodies in first-degree relatives of patients with chronic inflammatory bowel disease [15]. Our patient had no significant medical history, presented no risk factor for acute pancreatitis and had no history of recent drug taking including those described above.…”

Section: Discussionmentioning

confidence: 99%

Acute pancreatitis revealing ulcerative colitis—A case report

Bousfiha¹,

Charif²,

Abkari³

et al. 2014

OJGas

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The association of acute pancreatitis with ulcerative colitis [UC] has been described in the literature. It is usually induced by drugs, but sometimes it may be idiopathic. This association remains rare. We report the case of a patient who was treated in our department. Medical observation: Mr. KA, a 60-year-old man, was admitted in our unit for management of acute epigastric. The clinical examination at the admission was normal. After eliminating a cardiac or surgical cause, the diagnosis of acute pancreatitis was made on the basis of the presence of a serum lipase up to 5 times the normal level and pain intensity. An abdominal scanner tomography was performed for the assessment of the pancreatitis. It has shown a pancreatitis stage C associated with a thick rectosigmoidien that was discovered incidentally. Symptomatology was enriched 10 days after by the occurrence of rectal bleeding. A lower endoscopy was performed after the improvement of the pancreatitis and had shown an ulcerative colitis on pancolitis which was confirmed by biopsy. In order to search other causes of this pancreatitis, other tests were made [a biliary IRM, endoscopic ultrasonography, autoimmune tests] and the results were negative. We concluded an idiopathic pancreatitis. The ulcerative colitis was classified as moderate and the patient was put on oral corticosteroids with degression. The evolution was marked by a clinical and biological improvement of pancreatitis and colitis. Conclusion: The association of idiopathic pancreatitis with ulcerative colitis is rare. The case of our patient is the first case reported in our series with 400 cases of ulcerative colitis diagnosed in our service.

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Autoimmunity to Pancreatic Juice in Crohn's Disease Results of an Autoantibody Screening in Patients with Chronic Inflammatory Bowel Disease

Cited by 118 publications

References 29 publications

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

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

Identification of Pancreatic Glycoprotein 2 as an Endogenous Immunomodulator of Innate and Adaptive Immune Responses

Acute pancreatitis revealing ulcerative colitis—A case report

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