Celiac disease future or investigational therapies: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
Line 5: | Line 5: | ||
==Overview== | ==Overview== | ||
==Future or investigational therapies== | ==Future or investigational therapies== | ||
Various other approaches are being studied that would reduce the need of | Various other approaches are being studied that would reduce the need of dietary modification (gluten-free diet). All are still under development and potential approach include:<ref name="pmid24355936">{{cite journal |vauthors=Schuppan D, Zimmer KP |title=The diagnosis and treatment of celiac disease |journal=Dtsch Arztebl Int |volume=110 |issue=49 |pages=835–46 |year=2013 |pmid=24355936 |pmc=3884535 |doi=10.3238/arztebl.2013.0835 |url=}}</ref> | ||
* [[Genetic engineering|Genetically engineered]] wheat species, or wheat species that have been selectively bred to be minimally immunogenic. This, however, could interfere with the effects that gliadin has on the quality of dough. | * [[Genetic engineering|Genetically engineered]] wheat species, or wheat species that have been selectively bred to be minimally immunogenic. This, however, could interfere with the effects that gliadin has on the quality of dough. | ||
* A combination of [[enzyme]]s ([[prolyl endopeptidase]] and a barley glutamine-specific [[cysteine endopeptidase]] (EP-B2)) | * Synthetic enzymes: | ||
** Glutaneses: Glutaneses degrades immune-dominant gluten peptides which do not not undergo proteolytic degradation in the intestinal lumen. | |||
**A combination of [[enzyme]]s ([[prolyl endopeptidase]] and a barley glutamine-specific [[cysteine endopeptidase]] (EP-B2)): These enzymes degrade the putative 33-mer peptide in the [[duodenum]]. This combination would enable coeliac disease patients to consume gluten-containing products.<ref>{{cite journal | author = Siegel M, Bethune M, Gass J, Ehren J, Xia J, Johannsen A, Stuge T, Gray G, Lee P, Khosla C | title = Rational design of combination enzyme therapy for celiac sprue | journal = Chem Biol | volume = 13 | issue = 6 | pages = 649-58 | year = 2006 | id = PMID 16793522}}</ref> | |||
*Drugs that lowers the interstinal permeablity to gluten | |||
*Induction of oral tolerance by 'gluten vaccination' | |||
*Use of biological agents modulating pro-inflammatory intestinal cytokines. | |||
* Inhibition of [[zonulin]], an endogenous signaling protein linked to increased permeability of the bowel wall and hence increased presentation of gliadin to the immune system.<ref>{{cite journal | author = Fasano A, Not T, Wang W, Uzzau S, Berti I, Tommasini A, Goldblum S | title = Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease | journal = Lancet | volume = 355 | issue = 9214 | pages = 1518–9 | year = 2000 | id = PMID 10801176}}</ref> | * Inhibition of [[zonulin]], an endogenous signaling protein linked to increased permeability of the bowel wall and hence increased presentation of gliadin to the immune system.<ref>{{cite journal | author = Fasano A, Not T, Wang W, Uzzau S, Berti I, Tommasini A, Goldblum S | title = Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease | journal = Lancet | volume = 355 | issue = 9214 | pages = 1518–9 | year = 2000 | id = PMID 10801176}}</ref> | ||
* Other treatments aimed at other well-understood steps in the pathogenesis of | * Other treatments aimed at other well-understood steps in the pathogenesis of celiac disease include: | ||
**the action of HLA-DQ2 (blocking antigen-presenting HLA-DQ2 i.e.-DQ8) | |||
**tissue transglutaminase(use of specific transglutaminase 2 blockers to inhibit transglutaminase 2) and the MICA/NKG2D interaction that may be involved in the killing of [[enterocyte]]s (bowel lining cells). | |||
==References== | ==References== |
Revision as of 19:47, 12 September 2017
Celiac disease Microchapters |
Diagnosis |
---|
Treatment |
Medical Therapy |
Case Studies |
Celiac disease future or investigational therapies On the Web |
American Roentgen Ray Society Images of Celiac disease future or investigational therapies |
Celiac disease future or investigational therapies in the news |
Risk calculators and risk factors for Celiac disease future or investigational therapies |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Future or investigational therapies
Various other approaches are being studied that would reduce the need of dietary modification (gluten-free diet). All are still under development and potential approach include:[1]
- Genetically engineered wheat species, or wheat species that have been selectively bred to be minimally immunogenic. This, however, could interfere with the effects that gliadin has on the quality of dough.
- Synthetic enzymes:
- Glutaneses: Glutaneses degrades immune-dominant gluten peptides which do not not undergo proteolytic degradation in the intestinal lumen.
- A combination of enzymes (prolyl endopeptidase and a barley glutamine-specific cysteine endopeptidase (EP-B2)): These enzymes degrade the putative 33-mer peptide in the duodenum. This combination would enable coeliac disease patients to consume gluten-containing products.[2]
- Drugs that lowers the interstinal permeablity to gluten
- Induction of oral tolerance by 'gluten vaccination'
- Use of biological agents modulating pro-inflammatory intestinal cytokines.
- Inhibition of zonulin, an endogenous signaling protein linked to increased permeability of the bowel wall and hence increased presentation of gliadin to the immune system.[3]
- Other treatments aimed at other well-understood steps in the pathogenesis of celiac disease include:
- the action of HLA-DQ2 (blocking antigen-presenting HLA-DQ2 i.e.-DQ8)
- tissue transglutaminase(use of specific transglutaminase 2 blockers to inhibit transglutaminase 2) and the MICA/NKG2D interaction that may be involved in the killing of enterocytes (bowel lining cells).
References
- ↑ Schuppan D, Zimmer KP (2013). "The diagnosis and treatment of celiac disease". Dtsch Arztebl Int. 110 (49): 835–46. doi:10.3238/arztebl.2013.0835. PMC 3884535. PMID 24355936.
- ↑ Siegel M, Bethune M, Gass J, Ehren J, Xia J, Johannsen A, Stuge T, Gray G, Lee P, Khosla C (2006). "Rational design of combination enzyme therapy for celiac sprue". Chem Biol. 13 (6): 649–58. PMID 16793522.
- ↑ Fasano A, Not T, Wang W, Uzzau S, Berti I, Tommasini A, Goldblum S (2000). "Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease". Lancet. 355 (9214): 1518–9. PMID 10801176.