autoimmune mechanism

The conundrum of how autoimmune diseases develop can be solved if we have a decent mechanism to work with.  Focusing on celiac disease which is now the most common autoimmune disease effecting 1.5 million Americans and then by looking at the areas of overlap that exists with other autoimmune diseases we can illuminate and then validate a basic core autoimmune mechanism.  The right mechanism will be applicable to all autoimmune diseases.  

The mechanism needs to explain the 2 stages of autoimmunity: the antibody precursor stage and then the viral induced attack stage where self-organs are damaged.

 In the case of celiac disease the proteins gluten and casein have been shown to induce several antibodies. Induced antibodies are against these polypeptides and to various self-proteins, autoantibodies.  Why are antibodies developing?   Removal of said proteins calms the immune system and removes the risk of autoimmune disease development but how could these proteins cause this? The proteins must be acting on something which then elicits an immune response. Our immune system is geared to respond to infection.  Can we reasonable place an infection between these proteins and our immune system?

There is a considerably high association between urinary tract infections and patients with celiac disease. Most urinary tract infections, 80%, are caused by E.coli.   The strain B of e.coli has a filamentous form and a rod form.  The filamentous form of this e.coli can be triggered by casein hydrolysate. In other words, casein induces a morphological change in e.coli.   The enzyme in E.coli responsible for the morphology change was named LONG or LON for short. It is a serine protease which has been shown to interact with casein. Is it not feasible that our immune system could be reacting to the morphology change of e.coli? Could gluten which has such a similar protein structure to casein act on LON and also cause a morphology change?

With an infection changing morphology it seems possible that some people’s immune system might become confused. Their immune system could have the genetic predisposition to grab too quickly the triggers gluten and casein while the infection evades detection disappearing only then later to reappear on their immune system radar.   The HLA of genetic predisposition is the t-cell mailbox which has been shown to have a high affinity for gluten and casein.  Their immune systems are acting too quickly and missing the real culprit E.coli.  The resulting situation is an infection in hiding and a hyper looking immune system. 

The second stage is the viral provoker.  It has long been a mystery, why some people develop an autoimmune disease after a viral infection while others do not. George Eisenbarth showed that before the virus the vulnerable patients already had autoantibodies. In the case of type one diabetes antibodies existed against insulin long before the development of the disease. Insulin is normally made by our pancreas.  

If e.coli has something that could cause the molecular mimicry of insulin this could make sense. Celiac patients often progress to type one diabetes.

Then the virus, like the flu virus which inflames and incubates in the pancreas itself could cause a crosstalk target. In other words the immune system which is already looking for a hidden infection is given a second reason to attack the pancreas by the virus.  Cross targeting of the viral and bacterial settings of the immune system could be the key to the development of autoimmune disease. Pandemics of flu are often followed by new cases of type one diabetes. Coxsackie virus also causes severe pancreatitis which could also cause the cross targeting. 

Let us consider autoimmune liver disease which also overlaps celiac disease.  E.coli when it gets into the blood stream and breaks down red blood cells produces bilirubin much like our liver.  If antibodies exist against bilirubin and then hepatitis C infects the liver the immune system would have cross targeting or 2 reasons to attack the liver.   Not everyone who has celiac disease has autoimmune liver disease and not everyone has autoimmune liver disease after Hepatitis but some do.  The cross targeting could be reason. 

Perhaps we should consider something similar to celiac disease but drastically different, autism.  Autism has been associated with gluten and casein proteins and the MMR vaccine.  Very recently autism has also been associated with the sutterella bacteria.  If you put sutterella in the middle you find that sutterella is dimorphic which means it could change morphology much like E.coli. Sutterella was distinguished from Campylobacter by a distinctive cell wall. Sutterella has long chain fatty acids in it’s cell wall much like our nerves myelin sheath.  I phrase it in this way because it is well documented that the measles vaccine produces antibodies against myelin sheath protein.  Cross targeting could be occurring. The herpes simplex virus has been shown to produce similar nerve antibodies and could also cause the same reaction.  

Neither autism nor psoriasis which have the gluten and casein sensitivity seem to be associated with type one diabetes. These infections must not drop or have something that could be confused with insulin. Candida albicans has been associate with type one and must have something that would induce antibodies toward the pancreas.  Candida does have more than one morphology: a mold and a yeast form.

 ......any thoughts? anyone out there understand me?