I just thought I'd stick this down as it's minor and it will get forgotten if I don't say something. There are grades/types of inflammatory bowel disease. The really easy one to treat is coeliac disease, where gluten avoidance is all that is required. There are also a host of problems which are responsive to gluten avoidance which do not come up positive on antibody test or have "typical" coeliac gut biopsy results.
I stumbled across this paper which grabbed me because my wife works with Natural Killer (NK) cells and has pointed out their relevance to surviving diseases before antibodies kick in. I was lucky to get the full text.
This is from the introduction, before it discusses coeliac disease, which is the second disease it covers (rheumatoid arthritis is the first):
"MIC A/B are stress-induced molecules acting as danger signals to alert NK cells and CD8 T lymphocytes through engagement of the NKG2D activating receptor . At variance with classical MHC class I molecules, MIC are specialized for reporting stress without the requirement for peptide (or other ligand) binding and can direct NK and T cells to kill transformed or infected cells."
This translates as:
Gluten stresses your gut cells. They scream on the molecular level. NK cells cells get in there and put them out of their misery. This is (auto) immunity. It does NOT REQUIRE antibody production.
Antibody production appears to be an add on to the immune system, a memory storage facility for preventing future re infection with a previous encountered bug. The acute survival of an infection, like influenza, relies on the innate immune system, based around NK cells. If you had to wait 10 days for your lymphocytes to get around to antibody production before you recovered, all viruses would be lethal. NK cells are non specific and use molecules like MIC as markers that something is seriously wrong with a cell and it's time to get killin'. MIC is a like a large target sign painted on a cell and NK cells are equipped an AK47 looking for that target. Usually a cell expressing MIC is infected, but gluten appears to do as much "stressing" as a viral infection.
Gluten reactions do not need antibody production. It is perfectly possible to have serious on going gut damage without a positive antibody test. Statistically it is quite probable that you WILL get a positve antibody test. There is so much damage going in that battlefield which is your gut under the influence of gluten that there is a trauma "soup". All you need is for an "antigen presenting cell" (APC) to collect some gluten from this soup, give it to your lymphocytes and tell them "we want this stuff recognised by an antibody, get producing". Of course the APC may pick up tissue transaminase, endomysial protein or any of a host of other proteins to push at the lymphocytes (which make the antibodies). But there is a chance you may not get either gluten or transaminase etc presented (ie no antibodies in our current lab tests), so you continue with "psychosomatic" gut problems or get labeled as inflammatory bowel disease, which is not regarded as gluten responsive. Severe IBD requires more than gluten avoidance but this basic step is probably essential.
Antibodies are a consequence, and an amplifier, of gluten toxicity, not a cause. That's intrinsic to gluten, MIC and NK cells. What brought this on?
Did I have psoriasis or Dermatitis Herpetiformis (essentially coeliac disease of the skin)?
Answer: Maybe it's the same parallel as gut problems. WGA certainly gets in to the systemic circulation. I think it's a reasonable assumption gluten does too. It will be landing on vascular and/or dermal cells in the skin. Gluten induced stress here results in MIC expression. NK cells have that AK47, an itchy trigger finger and are seriously looking for MIC. Sometimes there is antibody production, sometimes there isn't. This could easily be the result of receptor subtypes (genetic) on your antigen presenting cells. Different labels, different lab results (if it ever gets that far) but a similar approach is needed. Perhaps there are a host of immune mediated problems triggered by gluten that are not antibody producing.