Autoimmune cross-targeting and Treg confusion ?

My Hypothesis:
Cross-targeting:  the layering of 2 different infections on one target causes autoimmune disease.  A viral infection marking the inside of the target then a bacterial, or fungal, or mycobacteria..etc.. infection marking the outside.

Tregs are T regulating cells with the "just right" goldilock's medium touch for looking into cells using the MHC mailboxes. The mailboxes hold up one piece at a time from inside. Tregs are not too weak or too strong when looking into the cells they spend just the right amount of time looking at the MHCs and they are conditioned to know all interior self proteins.

 Specifically Tregs look into cells to see if they are infected with viruses or to protect any antibody labeled cells which are healthy and fine on the inside from being mistakenly killed as bacteria.

In suppressive mode the Tregs secrete il-10 creating tolerance.  Il-10 is a cytokine that halts immune system attack.  It is interesting to note that some viruses have developed evil il-10 homologs in order to stop the immune system from attacking.  However under normal conditions the Treg expresses il-10  for tolerance when cross-reacting antibodies have marked a new area falsely because of molecular mimicry or the bad luck of a shared protein.

For example if e.coli breaks down red blood cells it creates bilirubin.  The liver also breaks down red blood cells creating bilirubin.  If antibodies against bilirubin show up as the immune system patrols your body the Treg would halt any attack on your liver by first checking the health of the marked liver cells and then secreting il-10.

Now considering cross-targeting: what if when the Treg arrives at the liver it finds that the liver cells are infected by a virus like betaretrovirus or hepatitis.   The infection generating the antibodies bringing it here was actually from e.coli but now your treg won't secrete il-10.  You have an overlap of infections causing autoimmunity because of confused Tregs. The Tregs have no idea what mode to go into.  Is this possible?

Let us consider another example: George Eisenbarth found a latent period of type 1 diabetes where he could first see anti-islet antibodies until something triggered the rapid progression into autoimmunity.  The flu and coxsackie are viruses that replicate in the pancreas. Both viruses have been implicated in diabetes because new cases of type 1 diabetes appear during outbreaks.  Could these viruses be the rapid trigger Eisenbarth was looking for? Could this be cross-targeting and Treg confusion?

Celiac and treg
http://www.ncbi.nlm.nih.gov/pubmed/23874626

type 1 diabetes and treg
http://www.jimmunol.org/content/181/7/4516.full.pdf

Rheumatoid arthritis and treg
http://deepblue.lib.umich.edu/bitstream/handle/2027.42/55983/22415_ftp.pdf?sequence=1

Autoimmune liver disease and treg
http://www.hindawi.com/journals/jir/2013/607073/

e.coli and the liver primary biliary cirrhosis
http://www.ncbi.nlm.nih.gov/pubmed/24128311

betaretrovirus and primary biliary cirrhosis
http://www.pnas.org/content/100/14/8454

il-2 and tregs
http://www.jimmunol.org/content/172/7/3983.full

treg cells are antigen dependent
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784904/

Fox and Treg
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008159/