Studies on the Significance of the R1 Anti-Reticulin Antibody Associated with Gluten Sensitivity

Abstract

The R1 type anti-reticulin antibody (ARA) is closely associated with gluten-sensitive enteropathy. It disappears from the circulation within a few weeks of starting on a gluten-free diet and often reappears following gluten challenge. It is not clear how gluten ingestion leads to the production of the ARA. We have investigated four possibilities. (1) The ARA is simply a food antibody generated against meats in the diet. (2) The ARA is an anti-gluten antibody which cross-reacts with reticulin. (3) Gluten binds to gut reticulin in vivo rendering reticulin autoimmunogenic. (4) Immune complexes of gluten and anti-gluten antibody bind to reticulin (by virtue of the affinity that gluten has for reticulin) to give the appearance of an ARA in immunofluorescence tests. Our results do not support any of these possible explanations, and the significance of the ARA remains obscure.

B cell epitopes of gliadin

“…The finding that only IgA of EmA‐positive but not of EmA‐negative patients with high AGA titre showed an enhanced recognition of deamidated B cell epitopes cannot be due to cross‐reactivity between AGA and coeliac autoantibodies. Lack of such cross‐reactivity was demonstrated already earlier [30–32]. In accordance with previous results, our experiments indicate that binding to the deamidated epitopes is correlated with AGA but not with EmA ( Table 3).…”

Lack of Antireticulin and IgA Antiendomysium Antibodies in Sera of Patients with Primary IgA Nephropathy Associated with Circulating IgA Antibodies to Gliadin

“…Antireticulin and IgA class antiendomysium antibodies (IgA EmA) are specific immunological markers for CD and DH associated withCD [2,6].The IgA EmAarefound only in gluten-sensitive enteropathy and their formation precedes the development of the pathological gut changes in CD and DH [1]: these autoantibodies become undetec table in CD when the flattening of the gut mucosa disap pears after gluten-free diet [1], Therefore, we looked for antireticulin and IgA EmA in the sera of IgA G N patients with high levels of circulating IgA antigliadin antibodies. We analyzed the sera of 19 untreated patients with IgA GN having permanent proteinuria, according to the usual his tological and immunofluorescence criteria [4], (>1<3 g/24 h; age: mean 41 years, range 24-58).…”

“…All the patients were on a normal diet. The antireticulin and antiendomysium antibodies were studied with indirect immunofluores cence technique with sera tested at the dilutions of one fifth and one tenth; for antireticulin antibodies the sub strates were unfixed frozen sections of rat liver, kidney and gastric mucosa [6] and forantiendomysium antibodies the substrates were frozen sections of monkey esophagus (Zeus-Scientific Inc.) [2], The conjugates were fluores cein-conjugated antibodies to human immunoglobulins (IgG. IgA, IgM : Diagnostic Pasteur,dilution 1/100)and to human «-chain (Dako, dilution 1/20).…”

Extracts of wheat gluten activate complement via the alternative pathway

“…Anti-FIII, anti-f lactoglobulin and anti-ovalbumin titres were quantified by ELISA [ 13]. Note that whilst high titres of IgA and IgG food antibodies typify jejunal villous atrophy, normal individuals also have low titres of 'naturally occurring' IgG food antibodies [13].…”