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Here's a study suggesting a nasal spray is a potential treatment for CD and
another study comparing tTG and EMA CD screening tests:

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Immunol Lett. 2003 Aug 5;88(2):127-34.

Intranasal administration of a recombinant alpha-gliadin down-regulates the
immune response to wheat gliadin in DQ8 transgenic mice.

Senger S, Luongo D, Maurano F, Mazzeo MF, Siciliano RA, Gianfrani C, David
C, Troncone R, Auricchio S, Rossi M.

Istituto di Scienze dell'Alimentazione, CNR, via Roma 52, 83100, Avellino,
Italy

The mucosal lesion in coeliac disease (CD) is an immune-mediated injury
triggered by gliadin and associated with HLA-DQ2 and HLA-DQ8. In view of
this, an approach that re-induces tolerance to this antigen should be
considered as possible alternative to a strict gluten-free diet in treating
CD. However, T-cell activation to multiple antigens, as a consequence of
the chemical complexity shown by the antigen gliadin, could hamper the
efforts to identify single component(s) useful for tolerance induction. To
address this issue, a recombinant alpha-gliadin was tested in tolerance
experiments in HLA-DQ8 transgenic mice. As tissue transglutaminase (tTG)
treatment of gliadin, previously reported to enhance its stimulatory
activity in CD, did not increase its immunogenicity when parenterally
administered in these mice, untreated gliadin was used as immunogen. A
decrease in systemic T cell responses to the recombinant alpha-gliadin was
found after nasal administration of antigen, reflected by lymphocytes
proliferation assay. Interestingly, while the immunisation protocol induced
transcription of both Th1 (IFN-gamma) and Th2 (IL-4 and IL-10) cytokines,
the tolerisation protocol down-regulated significantly only the IFN-gamma
mRNA expression. More important, the recombinant alpha-gliadin induced a
similar down-regulatory effect in mice immunised with a commercial
preparation of wheat gliadin, that is a mixture of many different gliadin
components. As the Th1 phenotype and the HLA-DQ8 molecule play a role in
the pathogenesis of CD, our data underlined the potential usefulness of
this recombinant protein for the immunomodulation of this disease.

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Ann Clin Biochem. 2003 Jul;40(Pt 4):411-6.

A comparative study of tissue transglutaminase antibodies and endomysium
antibody immunofluorescence in routine clinical laboratory practice.

Sinclair D, Pearce CB, Saas MS, Poller D.

Department of Chemical Pathology, Queen Alexandra Hospital, Portsmouth PO6
3LY, UK.

BACKGROUND: The demand for screening for coeliac disease has grown rapidly
over the last few years. Laboratories depending on immunofluorescence
assays are faced with an increasing workload using a labour-intensive test,
and an alternative to this test has been sought. This study compares tissue
transglutaminase (TTG) and endomysium antibodies (EMA) in a routine
clinical laboratory situation. METHODS: An immunofluorescence IgA EMA test
was compared with a guinea pig TTG antibody ELISA for 816 unselected
requests for gut antibody screening. Discrepant results were investigated
more fully using a variety of human source TTG antigen kits. RESULTS:
Guinea pig TTG ELISA and EMA assays showed agreement for 93.6% of samples.
Four samples were misclassified and 48 samples gave false positive TTG
results. Study of 46 EMA samples (this group included 39 of
the 'discrepant' negative EMA/positive guinea pig TTG group) using three
different human purified and/or recombinant TTG sources showed that 42
patients had no TTG antibodies using human sources, three were
misclassified and one patient had negative EMA and positive TTG results
that could not be readily explained. Further study of 32 EMA positive
samples showed almost complete agreement between the human source TTG kits.
CONCLUSIONS: We can recommend the replacement of EMA with ELISA for TTG
antibodies for the routine screening for coeliac disease, but all positive
TTG antibodies should still be followed up with IgA EMA and samples should
be screened for IgA deficiency.

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