Could naltrexone uncouple the autoimmunity caused by cross-targeting by blocking tlr-4? is tlr-4 the issue?

Cross-targeting is when 2 infections in the same place triggers autoimmune disease. A virus marking the inside of the target and an infection like a bacteria, mycobacteria, fungus, or mycoplasma marking the outside of the target. This is my hypothesis and I am looking into how this would involve tlr-4. ( this may not be the only overlap )

tlr-4 increased and involved with MG
http://www.ncbi.nlm.nih.gov/pubmed/24397961

murine diabetes blocked by tlr-4 suppression
http://www.ncbi.nlm.nih.gov/pubmed/23340441

Dendritic cells sample environment using tlr then talk to both t and b cells (antigen presenting)
http://en.wikipedia.org/wiki/Dendritic_cell

tlr-4 is involved in early steps of pathogen recognition
http://www.ncbi.nlm.nih.gov/pubmed/22240038

tlr-4 & gram negative bacteria
http://en.wikipedia.org/wiki/TLR_4
gram negative bacterias
sutterella
e.coli

strep is gram positive...but strep pyogenes involves tlr-4  (the autoimmune triggering strep)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3067360/

tlr-4 and viruses
http://www.ncbi.nlm.nih.gov/pubmed/23997950
(specifically the flu)
http://www.jimmunol.org/content/178/4/2448.full 

tlr-4 and inflammation/autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/21664961
www.ncbi.nlm.nih.gov/pubmed/17763416
http://link.springer.com/article/10.1007/s12016-013-8402-y

Naltrexone is an antagonist of tlr-4
http://www.ncbi.nlm.nih.gov/pubmed/23062774


Naltrexone is now being used to suppress autoimmune disease
References to be posted. This page is still under construction.
http://www.ncbi.nlm.nih.gov/pubmed/21918649
http://www.ncbi.nlm.nih.gov/pubmed/21256121

http://www.ncbi.nlm.nih.gov/pubmed/21174518
ms
http://www.ncbi.nlm.nih.gov/pubmed/20695007
http://www.ncbi.nlm.nih.gov/pubmed/19041189

cytokine storm and autoimmune? does the overlap of infections cause some degree of this?

cytokine storm and flu
http://www.birdfluhealth.com/taxonomy/term/38


TLR-4 activates 2 pathways the myD88 which leads to inflammation cytokines and the TRIF-dependent side.
The TRIF-dependent side is involved with E.coli infections. 
Note that the Bird (avian) flu involves the myD88 pathway. 

If they are both going though the same TLR-4 the response could be amplified.  At what point does the immune system lose control? here?