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The immune system acts in strange ways, and clearly science is far 
from fully understanding the ways in which our bodies decide to 
tolerate or attack any foreign entity which crosses its borders.  
Previous experiments using non-obese diabetic (NOD) mice have 
demonstrated that a gluten-free diet dramatically reduces the onset of 
type 1 diabetes in these mice.  A new study sought to show that a 
high-gluten diet would further increase the incidence of diabetes in 
NOD mice.  However, the study showed exactly the OPPOSITE occurs!  
The incidence of diabetes in NOD mice fed a high-gluten diet is as 
equally low as in NOD mice fed a gluten-free diet when compared to 
NOD mice fed a standard diet!

What does this mean for celiac disease?  Could a diet high in gluten 
introduced to genetically susceptible human infants at the right time 
actually prevent the onset of celiac disease?  Scientists know that 
celiac disease can occur in one identical twin and not the other, but 
has yet to explain why.  The immune system decides whether to 
tolerate or attack an antigen, such as a gluten peptide, when a 
dendritic or antigen-presenting cell presents the antigen to a T cell 
receptor.  The presence and involvement of various immune signaling 
chemicals and receptors determines whether or not the antigen will be 
tolerated.  It does not seem likely that a gluten peptide alone has the 
ability to initiate signals to cause intolerance.  I have previously 
proposed and written that a gluten-ingesting bacteria may be an 
intermediary which produces the immune signals that "switch-on" 
gluten-intolerance when a dendritic cell processes both the bacteria 
and its ingested gluten peptide contents and then, in turn, presents 
the gluten peptide to a T cell which mistakes the gluten peptide for a 
component of a harmful bacteria.

Now what if a genetically susceptable human infant were first 
introduced to gluten via a diet highly enriched with gluten?  If it is 
assumed that a gluten-ingesting bacteria is involved in celiac disease 
pathogenesis, a diet high in gluten would mean there would likely be 
many more free gluten peptides floating around the body and 
gastrointestinal tract than gluten-ingesting bacteria.  When dendritic 
cells present free gluten peptides to T cells, a tolerant response to 
gluten is likely learned as opposed to an intolerant response learned 
when bacteria-ingested-gluten peptides are presented to T cells.  
Having many, many more free gluten peptides around to overwhelm 
the numbers of bacteria-ingested-gluten peptides might then cause 
the immune system to learn to become tolerant to gluten rather than 
intolerant preventing the onset of celiac disease.

NOD mice make good models for studying the pathogenesis of 
diabetes.  Unfortunately, there do not seem to be any good equivalent 
mouse models for studying celiac disease.  Scientists cannot readily 
just stuff human infants full of gluten and see what happens.  So the 
answer to the question of whether a high-gluten diet fed to infants at 
the right time can prevent celiac disease may remain elusive and 
intriguing.

----------
Diabetes Metab Res Rev. 2007 Jul 2; [Epub ahead of print]
Gluten-free but also gluten-enriched (gluten+) diet prevent diabetes in 
NOD mice; the gluten enigma in type 1 diabetes.
Funda DP, Kaas A, Tlaskalova-Hogenova H, Buschard K.

< http://dx.doi.org/10.1002/dmrr.748 >

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