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Toward protein biomarkers for allergy: CD4+ T cell proteomics in allergic and nonallergic subjects sampled in and out of pollen season.

Authors: Bluggel, M  Spertini, F  Lutter, P  Wassenberg, J  Audran, R  Corthesy, B  Mullner, S  Blum, S  Wattenberg, A  Mercenier, A  Affolter, M  Kussmann, M 
Citation: Bluggel M, etal., J Proteome Res. 2011 Apr 1;10(4):1558-70. Epub 2011 Mar 16.
Pubmed: (View Article at PubMed) PMID:21410266
DOI: Full-text: DOI:10.1021/pr100939g

Allergy is an immunological disorder of the upper airways, lung, skin, and the gut with a growing prevalence over the last decades in Western countries. Atopy, the genetic predisposition for allergy, is strongly dependent on familial inheritance and environmental factors. These observations call for predictive markers of progression from atopy to allergy, a prerequisite to any active intervention in neonates and children (prophylactic interventions/primary prevention) or in adults (immunomodulatory interventions/secondary prevention). In an attempt to identify early biomarkers of the "atopic march" using minimally invasive sampling, CD4+ T cells from 20 adult volunteers (10 healthy and 10 with respiratory allergies) were isolated and quantitatively analyzed and their proteomes were compared in and out of pollen season (+/- antigen exposure). The proteome study based on high-resolution 2D gel electrophoresis revealed three candidate protein markers that distinguish the CD4+ T cell proteomes of normal from allergic individuals when sampled out of pollen season, namely Talin 1, Nipsnap homologue 3A, and Glutamate-cysteine ligase regulatory protein. Three proteins were found differentially expressed between the CD4+ T cell proteomes of normal and allergic subjects when sampled during pollen season: carbonyl reductase, glutathione S-transferase omega 1, and 2,4-dienoyl-CoA reductase. The results were partly validated by Western blotting.


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CRRD Object Information
CRRD ID: 5491008
Created: 2011-09-27
Species: All species
Last Modified: 2011-09-27
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.