Autoimmune Cross-targeting hypothesis summary

   The triggers of autoimmunity have been evasive.  A virus will only trigger autoimmunity in a small number of cases and we have not been able to predict who is vulnerable.  This autoimmune hypothesis is an attempt to put forth a reasonable mechanism that allows not just prediction but also an explanation as to why more than one virus can trigger autoimmunity and why not all the time.

   Genetic susceptibility to infections can play a role in the development of autoimmunity, for example the HLA gene of celiac disease is a mailbox protein for Tcells.   Autoimmunity may run in families but this is a shared genetic weakness to infections hence explaining also why there seems to be no specific age of autoimmune development.  Genetic susceptibility is not required to develop an autoimmune disease.

   My autoimmune cross-targeting hypothesis suggests that the development of autoimmune disease is triggered when 2 infections coexist in the target or make the immune system attack the same target through antibodies.  Cross-targeting literally means attacking from different platforms.  This hypothesis is that  the immune system attacks large infections on the outside of cells while simultaneously attacking the inside because of viral infections and in the process removes the self education.  Nothing stops the destruction of the entire target cell.

   Viruses enter host cells through receptors.  Not all cells have the same receptors so a virus can only trigger autoimmunity in cells they have access to.  Consider Type one diabetes as an example, the flu virus replicates in  pancreas cells and when the flu moves through a population more cases of type 1 diabetes appear.  Not everyone who gets the flu gets diabetes only a small percent that have an outer pancreatic infection do.

   My cross targeting hypothesis suggests that another infection exists in the pancreas in order to trigger the autoimmunity.  Rheumatoid arthritis has been linked with mycoplasmas and mycoplasmas can very easily infect a pancreas.  Note that other infections can replace the mycoplasmas.  Bladder infections and celiac disease have also been linked to type one diabetes.  If e.coli which is often the cause of bladder infection is the culprit here it could not only infect the pancreas but make anti- insulin antibodies because e.coli produces insulin like proteins.  Please note that  I can not prove that these second infections exist but based on the associations I think we should look for them.  It seems logical that if the inside and the outside of the host's pancreatic cells were marked for destruction at the same time that this could set off autoimmunity.  Also note that the coxsackie virus also infects the pancreas and could replace the flu virus in this scenario.

This autoimmune-cross targeting hypothesis can be applied to other diseases.  This blog has been gathering references to test the notion that this happens in all cases. The difference is which host cells are infected.  For example multiple sclerosis patients tend to have skin issues like psoriasis which has mycobacteria associations.  Interestingly multiple sclerosis appears after shingles in some patients.   Could this be the marking of the inside and outside of a nerve?  Any thoughts out there ?