Anti-gliadin antibodies
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| Antibody(s) | |
|---|---|
| Anti-glaidin | |
| Common Antibody characteristics | |
| Biological Source | Triticum aestivum |
| Isoform specific | |
| antibody characteristics | |
| Antigen Isoform |
α/β-gliadin |
| Antigen Gene | Gli-X2 |
| Affected Organ(s) | Intestine (Small) |
| Affected Tissue(s) | Villi |
| Affected Cells(s) | Epithelial |
| Also Affected | Epithelial extracellular matrix |
| Associated Disease(s) |
Coeliac disease |
| Antibody class | IgA, IgG |
| DQ2.5 | |
| HLA associations | DQ8 |
| DQ2.2/DQ7.5 | |
| Antigen Isoform |
γ-gliadin |
| Antigen Gene | Gli-X3 |
| Affected Organ(s) | (See α/β-gliadin) |
| Associated Disease(s) |
Coeliac disease |
| Antibody class | IgA, IgG |
| DQ2.5 | |
| HLA associations | DQ8 |
| DQ2.2/DQ7.5 | |
| Antigen Isoform |
ω-gliadin |
| Biological source | & Aegilops speltoides |
| Antigen Gene | Gli-B1 |
| Affected Organ(s) | Vascular, Respiratory |
| Affected Tissue(s) | Serum |
| Affected Cells(s) | Mast Cells, Eosinophiles |
| Associated Disease(s) |
Exercise-induced anaphylaxis, Baker's Allergy |
| Antibody class | IgE |
Anti-gliadin antibodies are produced in response to gliadin, a prolamin found in the wheat. In bread wheat it is encoded by three different genomes, AA, BB, and DD. These genomes can produce slight different gliadins, which can cause the body to produce different antibodies. Some of these antibodies can detect proteins in specific grass taxa such as Triticeae (Triticeae glutens), while others react sporadically across with certain species in those taxa, or over many taxonomically defined grass tribes.
Contents |
[edit] Anti-gliadin IgA
This antibody is found in ~80% of patients with coeliac disease.[1][2] It is directed against the alpha/beta and gamma (α,β,γ) gliadins.[3] It is also found in a number of patients who are not enteropathic. Some of these patients may have neuropathies that respond favorably to gluten elimination diet. This is referred to as gluten-sensitive idiopathic neuropathy.[4] Clinically these antibodies and IgG antibodies to gliadin are abbreviated as AGA.
[edit] Anti-gliadin IgG
IgG antibodies is similar to AGA IgA, but is found at higher levels in patients with the IgA-less phenotype. It is also associated with coeliac disease and idiopathic gluten sensitivity.[5][6][7] and IgA-less is associated with Coeliac disease. Anti-gliadin antibodies are frequently found with anti-transglutaminase antibodies
[edit] Anti-gliadin IgE
The IgE antibodies are more typically found in allergy-related conditions such as urticaria, asthma, and wheat-dependent exercise-induced anaphylaxis. The target of the most allergenic antibodies are ω-5 gliadin,[8] that is encoded by the Gli-1B gene found on the B haplome (Aegilops speltoides derived) of wheat.[9]
[edit] Anti-gliadin antibodies and the gluten-free diet
| Days on GF diet | AGA | |
| 0 | 203 | |
| 7 (1 wk) | 195 | |
| 30 (1 mo.) | 171 | |
| 61 (2 mo.) | 144 | |
| 91 (3 mo) | 121 | |
| 122 (4 mo) | 101 | |
| 183 (6 mo) | 72 | |
| 274 (9 mo) | 44 | |
| 365 (1 yr) | 27 | |
| 548 (18 mo) | 11 | |
| 730 (2 yr) | 6 | |
| AGA values below 10 (black) are normal | ||
What is the relationship of gluten and anti-gliadin antibodies?. In gluten-sensitive individuals AGA testing is a routinely used blood test for possible presence of coeliac disease, allergies or idiopathic phenomena. The measurement of AGA is done with ELISA or radioimmunoassay. Such test measure the level of AGA relative to a standard, such as a level of 10 = point in which 85% of normal population falls below. Greater than 10 equals disease and a value of 3 is expected (mean).
Individuals who have coeliac disease may have values in excess of 200. There is the common expectation that removal of gluten results in the loss of AGA, however since gluten is the target of the antibodies, that which would deplete them from the body, removal of gluten results in the benign circulation of antibodies. The half life of these antibodies is typically 120 days. Given an expected normal of 3 and assuming that the individual starts with a score of 203 we can predict the levels of AGA at various future time points. Based on these initial numbers, patients with very high AGA values may take 2 years to return to the normal range.
Refractory coeliac diease (RCD). RCD or non-strict gluten-free diet can be two cause of failure of AGA to return to normality on the GF diet. The first instance lymphocytes may remain stimulated even though the antigen that originally stimulated them was removed from the diet.
[edit] Diagnostic serology
Anti-gliadin antibodies were one of the first serological markers for coeliac disease. Problematic with AGA is the typical sensitivity and specificity was about 85%. Gliadin peptides which are senthesized as the deamidated form have much higher sensitivity and specificity, creating 2 serological tests for CD that approach biopsy diagnostic in performance.[10][11]
[edit] References
| This article is part of the Gluten sensitivity series. |
| Coeliac disease |
| Wheat allergy |
| Gluten-sensitive idiopathic neuropathies |
| Triticeae glutens |
| Gluten-free diet |
| GSE associated conditions |
| Anti-gliadin antibodies |
| Anti-transglutaminase antibodies |
| HLA-DQ2, HLA-DQ8 |
- ^ Volta U, Cassani F, De Franchis R, et al (1984). "Antibodies to gliadin in adult coeliac disease and dermatitis herpetiformis". Digestion 30 (4): 263–70. PMID 6391982.
- ^ Volta U, Lenzi M, Lazzari R, et al (1985). "Antibodies to gliadin detected by immunofluorescence and a micro-ELISA method: markers of active childhood and adult coeliac disease". Gut 26 (7): 667–71. PMID 3894169.
- ^ Bateman EA, Ferry BL, Hall A, Misbah SA, Anderson R, and Kelleher P. (2004). "IgA antibodies of coeliac disease patients recognise a dominant T cell epitope of A-gliadin.". Gut. 53 (9): 1274–1278. doi:. PMID 15306584.
- ^ Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A (1996). "Does cryptic gluten sensitivity play a part in neurological illness?". Lancet 347 (8998): 369–71. PMID 8598704.
- ^ Crabbé P, Heremans J (1967). "Selective IgA deficiency with steatorrhea. A new syndrome". Am J Med 42 (2): 319–26. doi:. PMID 4959869.
- ^ Tucker NT, Barghuthy FS, Prihoda TJ, Kumar V, Lerner A, Lebenthal E (1988). "Antigliadin antibodies detected by enzyme-linked immunosorbent assay as a marker of childhood celiac disease". J. Pediatr. 113 (2): 286–9. PMID 3397791.
- ^ Collin P, Mäki M, Keyriläinen O, Hällström O, Reunala T, Pasternack A (1992). "Selective IgA deficiency and coeliac disease". Scand J Gastroenterol 27 (5): 367–71. doi:. PMID 1529270.
- ^ Matsuo H, Morita E, Tatham AS, Morimoto K, Horikawa T, Osuna H, Ikezawa Z, Kaneko S, Kohno K, and Dekio S. (2004). "Identification of the IgE-binding epitope in omega-5 gliadin, a major allergen in wheat-dependent exercise-induced anaphylaxis.". J Biol Chem. 279 (13): 12135–12140. doi:. PMID 14699123.
- ^ Denery-Papini S, Lauriére M, Branlard G, et al (2007). "Influence of the allelic variants encoded at the Gli-B1 locus, responsible for a major allergen of wheat, on IgE reactivity for patients suffering from food allergy to wheat". J. Agric. Food Chem. 55 (3): 799–805. doi:. PMID 17263477.
- ^ Agardh D (November 2007). "Antibodies against synthetic deamidated gliadin peptides and tissue transglutaminase for the identification of childhood celiac disease". Clin. Gastroenterol. Hepatol. 5 (11): 1276–81. doi:. PMID 17683995.
- ^ Antibody Recognition against Native and Selectively Deamidated Gliadin Peptides
