Celiac disease future or investigational therapies: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Celiac disease}} | {{Celiac disease}} | ||
{{CMG}} | {{CMG}}; {{AE}} {{Anmol}} | ||
==Overview== | ==Overview== | ||
== | Various approaches are being studied that would reduce the need of dietary modification ([[gluten-free diet]]). Most of them are still under development and include [[genetically engineered]] wheat species, [[enzymes]], [[gluten]] [[vaccination]], [[biological agents]], and inhibition of endogenous signaling protein. | ||
Various other approaches are being studied that would reduce the need of | |||
* [[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. | ==Future or investigational therapies== | ||
* A combination of [[enzyme]]s | 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><ref name="pmid25219527">{{cite journal |vauthors=Mooney PD, Hadjivassiliou M, Sanders DS |title=Emerging drugs for coeliac disease |journal=Expert Opin Emerg Drugs |volume=19 |issue=4 |pages=533–44 |year=2014 |pmid=25219527 |doi=10.1517/14728214.2014.959490 |url=}}</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> | * [[Genetic engineering|Genetically engineered]] wheat species, or wheat species that have been selectively bred to be minimally [[Immunogenicity|immunogenic]]. This, however, could interfere with the effects that [[gliadin]] has on the quality of dough. | ||
* Other treatments aimed at other well-understood steps in the pathogenesis of | * [[Enzymes]]: | ||
** Glutenases: Glutenases 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 celiac 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 of gluten: 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> | |||
*Induction of oral tolerance by "gluten vaccination" | |||
*Use of [[Biological agent|biological agents]] modulating pro-inflammatory intestinal [[Cytokine|cytokines]]. | |||
* Other treatments aimed at other well-understood steps in the pathogenesis of celiac disease include: | |||
**Blocking antigen-presenting [[HLA-DQ2]] (-DQ8) | |||
**[[Tissue transglutaminase]] and the MICA/NKG2D interaction that may be involved in the killing of [[enterocyte]]s (bowel lining cells). | |||
**Use of specific [[transglutaminase]] 2 blockers to inhibit [[transglutaminase]] 2 | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Gastroenterology]] | |||
[[Category:Rheumatology]] | |||
[[Category:Autoimmune diseases]] | |||
[[Category:Genetic disorders]] | |||
[[Category:Malnutrition]] | |||
[[Category:Pediatrics]] | |||
[[Category:Dermatology]] | |||
[[Category:Up-To-Date]] | |||
Latest revision as of 20:50, 29 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]
Overview
Various approaches are being studied that would reduce the need of dietary modification (gluten-free diet). Most of them are still under development and include genetically engineered wheat species, enzymes, gluten vaccination, biological agents, and inhibition of endogenous signaling protein.
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][2]
- 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.
- Enzymes:
- Glutenases: Glutenases 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 celiac disease patients to consume gluten-containing products.[3]
- Drugs that lowers the interstinal permeablity of gluten: 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.[4]
- Induction of oral tolerance by "gluten vaccination"
- Use of biological agents modulating pro-inflammatory intestinal cytokines.
- Other treatments aimed at other well-understood steps in the pathogenesis of celiac disease include:
- Blocking antigen-presenting HLA-DQ2 (-DQ8)
- Tissue transglutaminase and the MICA/NKG2D interaction that may be involved in the killing of enterocytes (bowel lining cells).
- Use of specific transglutaminase 2 blockers to inhibit transglutaminase 2
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.
- ↑ Mooney PD, Hadjivassiliou M, Sanders DS (2014). "Emerging drugs for coeliac disease". Expert Opin Emerg Drugs. 19 (4): 533–44. doi:10.1517/14728214.2014.959490. PMID 25219527.
- ↑ 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.