Why is Celiac Disease a Type IV Hypersensitivity Reaction?

[Ronin786]

According to Pathoma it is due to circulating Antibodies against the small bowel villi. Wouldn't that make it a Type II Hypersensitivity? Most sources have it listed as Type IV but without any real explanation.

Wiki is saying it is T-Cell Mediated, but then why do we see Anti-Gliadin and Anti-Tissue Transglutaminase Antibodies?

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[Ronin786]

So I continued the video and he explained that the deaminated gliadin is presented by APCs and MHC Class II and then you get T Helper Cell damage haha.

Now my question is, where do the antibodies come from?

 

[Boardz]

remember in celiac's you have a lymphocytic infiltrate. Same with diabetes type 1, hashimoto's, guillain barre, etc. That helps me remember that a) they're all type IV hypersensitivity, and 2) histologic description

also, notice they all have associated antibodies.

 

[ijn]

In Hashimoto's antibodies are a marker of the disease process, but it's the WBCs that are doing the damage to the thyroid cells. I presume the same phenomenon is going on in Celiac disease. As you blow up normal cells, their guts are released into the environment and I guess the immune system starts developing antibodies to these new antigens (such as tissue transglutaminase, gliadin, etc) but the antibodies aren't actually causing damage.

 

[ThisGuy911]

I know this is long dead, but it was on the top of the search list when I was looking for Celiac Disease and hypersensitivity. I just thought I would throw a quick post up so nobody gets the wrong idea. But I am looking at three sources right now which say that Celiac Disease is a type III hypersensitivity.

 

[Transposony]

I am looking at three sources right now which say that Celiac Disease is a type III hypersensitivity.

Which three sources?
This is what Harrison says;

An immunologic component in the pathogenesis of celiac disease is critical and involves both adaptive and innate immune responses. Serum antibodies—IgA antigliadin, IgA antiendomysial, and IgA anti-tTG antibodies—are present, but it is not known whether such antibodies are primary or secondary to the tissue damage. The antiendomysial antibody has 90–95% sensitivity and 90–95% specificity; the antigen recognized by the antiendomysial antibody is tTG, which deaminates gliadin, which is presented to HLA-DQ2 or HLA-DQ8. Antibody studies are frequently used to identify patients with celiac disease; patients with these antibodies should undergo duodenal biopsy. This autoantibody has not been linked to a pathogenetic mechanism (or mechanisms) responsible for celiac disease. Nonetheless, this antibody is useful in establishing the true prevalence of celiac disease in the general population. A 4-week treatment with prednisolone of a patient with celiac disease who continues to eat gluten will induce a remission and convert the “flat” abnormal duodenal biopsy to a more normal-appearing one. In addition, gliadin peptides interact with gliadin-specific T cells that mediate tissue injury and induce the release of one or more cytokines (e.g., IFN-γ) that cause tissue injury.

 

[aspiringmd1015]

that + whenever you have th0 cells, if they become th2, secrete il 4 and 5, you get class switch so yeah, that and the fact that you destroy the enterocytes, which then releases masked antigens, so two reasons why youd get antibodies.