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Subject:
From:
Roy Jamron <[log in to unmask]>
Reply To:
Roy Jamron <[log in to unmask]>
Date:
Mon, 17 Oct 2005 17:48:18 -0500
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<<Disclaimer: Verify this information before applying it to your situation.>>

In the latest October Gastroenterology, Khosla, Gray, and Sollid respond to
the research paper published earlier in Gastroenterology by Matysiak-
Budnik, Cerf-Bensussan, and Heymann concerning the efficacy of prolyl
endopeptidase (PEP) for digesting and detoxifying gliadin peptides.  The
jury is still out on the question of the "pill".  The text of this
correspondence and reply are free.  Also in the latest Gastroenterology is
a free article, "Celiac Disease: Caught Between a Rock and a Hard Place."
See:

http://journals.elsevierhealth.com/periodicals/ygast/current

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Gastroenterology Volume 129, Issue 4, Pages 1362-1363 (October 2005)

Putative Efficacy and Dosage of Prolyl Endopeptidase for Digesting and
Detoxifying Gliadin Peptides

Chaitan Khosla, Gary M. Gray, Ludvig M. Sollid

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Gastroenterology Volume 129, Issue 4, Page 1363 (October 2005)

Reply

Tamara Matysiak-Budnik, Nadine Cerf-Bensussan, Martine Heymann

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Gastroenterology Volume 129, Issue 4, Pages 1294-1301 (October 2005)

Celiac Disease: Caught Between a Rock and a Hard Place

Frits Koning

Department of Immunohematology and Blood Transfusion, Leiden University
Medical Centre, Leiden, The Netherlands

Celiac disease (CD) is an intestinal disorder caused by an intolerance to
gluten, proteins in wheat. CD is an HLA-associated disease: virtually all
patients express HLA-DQ2 or HLA-DQ8. Recent work has shown that these
disease-predisposing HLA-DQ molecules bind enzymatically modified gluten
peptides and these HLA-DQ peptide complexes trigger inflammatory T-cell
responses in the small intestine that lead to disease. In addition, gluten
induces innate immune responses that contribute to the tissue damage that
is characteristic for CD. Thus, CD patients are caught between a rock and a
hard place: the disease is caused by a combination of adaptive and innate
immune responses that both are triggered by gluten. These findings explain
the disease-inducing properties of gluten and provide valuable clues for
the development of alternative treatment modalities for patients. They also
may be of relevance for our understanding of other multifactorial disorders
including IBD and HLA-associated autoimmune diseases.

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