Is scleroderma an autoimmune disease caused by cross-targeting?

Cross-targeting of the immune system triggers autoimmunity by layering immune system attacks onto one target.  One viral marking the inside of the target and one visible marking the outside of the target...like a fungus or bacteria.

Epstein barr virus and scleroderma
http://www.ncbi.nlm.nih.gov/pubmed/24164500
http://www.ncbi.nlm.nih.gov/pubmed/24129067

Cryptococcus neoformans and scleroderma
http://www.ncbi.nlm.nih.gov/pubmed/23496879
http://www.ncbi.nlm.nih.gov/pubmed/22381693
this is the fungus found in the droppings of wild birds

Crest syndrome (connective tissue is the target?)
http://en.wikipedia.org/wiki/CREST_syndrome
http://www.ncbi.nlm.nih.gov/pubmed/21956352

What would cause the hardened skin? cryptococcus secretes Mucopolysaccharidoses

https://books.google.com/books?id=eLHQAgAAQBAJ&pg=PA807&lpg=PA807&dq=Cryptococcus+secretes&source=bl&ots=LTAfTTSaQg&sig=5199n_brNSVOVS0e66h6Q_PM7Bs&hl=en&sa=X&ved=0ahUKEwiax62J24TNAhVVO1IKHZ4sDOcQ6AEITjAG#v=onepage&q=Cryptococcus%20secretes&f=false

Mucopolysaccharides are also called glucosaminoglycans and are also found in the fluids that lubricate joints. Glucosaminoglycans are major components of connective tissue like tendons.  Glucosaminoglycans: dermatan sulfate and chondroitin sulfate associate with the collagen of the tendon.

Glucosaminoglycans are increased in scleroderma
http://www.sciencedirect.com/science/article/pii/S0022202X15481126

I had previously connected sjogern's to candida infections and Hashimoto's thyroid.
Here is a personal post from someone who has hashimoto's with scleroderma. Do they have cryptococcus?
http://www.inspire.com/groups/autoimmune-diseases/discussion/hashimotos-rheumatoid-arthritis-scleroderma-i/

I am also looking at nickel allergy and it's relationship to crytococcosis:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3697809/
allergy and scleroderma
http://www.inspire.com/groups/scleroderma-foundation/discussion/nickle-exposure-and-scleroderma/

note that cyrptococcus gatti infects the lungs, the skin, the lymph nodes, bones, and joints
while the epstein barr virus (mono) infects primarily lymphatic cells....this could the the area of overlap.

here are posts of people with scleroderma and swollen lymph nodes
http://treato.com/Scleroderma,Swollen+Lymph+Nodes/?a=s 

the lymphatic system and scleroderma
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2829123/

Epstein barr can infect any cell with an estrogen receptor so it could be infecting the connective tissue directly too

Tendons and estrogen receptors
http://www.ncbi.nlm.nih.gov/pubmed/20073985

Does this make sense to anyone else out there? Can anyone see what i see?

Myasthenia Gravis Autoimmune disease starts in the thymus

This is an autoimmunity hypothesis for Myasthenia gravis:

Cross-targeting of the immune system triggers autoimmunity by layering immune system attacks on one target. In this case an infection of the thymus overlaps a viral infection of the thymus.  Raising the level of tlr-4 too high?

Possible viral triggers are:

West nile virus and MG
http://www.ncbi.nlm.nih.gov/pubmed/23559196
http://cdn.f1000.com/posters/docs/250566628

epstein-barr and MG
http://www.ncbi.nlm.nih.gov/pubmed/21961056 
http://www.ncbi.nlm.nih.gov/pubmed/20517934

coxsackie and MG?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC514990/

Note these viral infections must infect the target or generate antibodies toward the target.

MG has been associated with RA, lupus and type 1 diabetes so I am looking into mycoplasmas as the infection which may have taken up residence in the thymus (non viral)

specifically M.fermentans
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC415086/

and C. pneumoniae (detected in thymus)
http://www.ncbi.nlm.nih.gov/pubmed/9593019

Tlr-4 and MG
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1603452/

note that this is slightly different then Graves.

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?

Can Autism's sutterella cross the blood brain barrier?

If autism is caused by autoimmune cross-targeting and the target is the brain, how do the antibodies get past the blood brain barrier? note that this is not always the case because antibodies against the brain have been found in pregnant mothers crossing the blood brain barrier. I am just trying to figure out if it is just antibody driven as an autoimmune disease or if the infection can move there.

Strep and E.coli infections are able to get past the blood brain barrier and the intestinal barrier.

Invasion of the brain by strep by receptor-ligand
http://www.ncbi.nlm.nih.gov/pubmed/9393798

Invasion of brain by e.coli by receptor-ligand
http://www.ncbi.nlm.nih.gov/pubmed/10496943

Mycobacteria can also break the blood-brain barrier causing a hole by cytoskeleton alterations but it does not use a receptor to get into the host cell. (this reference is a review paper by Kim)
http://www.ncbi.nlm.nih.gov/pubmed/16542662

Here is just Kim's table of what can transverse the blood brain barrier:
http://www.nature.com/nrmicro/journal/v6/n8/fig_tab/nrmicro1952_T1.html

Does sutterella have the ability to cross in the same way?  by receptor- ligands?  It has been found in brain abcesses.....does it know how to cross the barriers?

I am looking for this "ligand" in the genetic code but it doesn't even appear to be elucidated in Strep. They think it is choline related because with out choline virulence is lost.
http://www.ncbi.nlm.nih.gov/pubmed/19433549
Choline immediately makes me think of neurons.....how foreboding.

Once sutterella is infecting the neurons would a measles shot cause them to be targeted?  The cross-targeting would cause the brain cells to be attacked by the immune system seeing not just the infections as the issue but the brain's neurons?

This is based on a ton of assumptions.  First that sutterella is a culprit because it is found in half of autistic kids indicating it's involvement.

This page is still under construction.

I am wondering if:
Classic autism is the maternal antibody driven kind
Childhood disintegrative disorder is the sutterella driven kind.

Lon enzyme has involvement in virulence, morphology, and is stimulated by casein...gluten too?

This hypothesis was disproven. T.gondii and strep are not dimorphic. See newer gluten posts.

LON is the enzyme I am attempting to associate with gluten and casein for the dimorphic switching of infections...causing our immune systems to develop sensitivity to them.

NEWER post: http://angelabiggs.blogspot.com/2014/03/lon1-and-dimorphic-switching-caused-by.html

lon enzyme
http://www.ncbi.nlm.nih.gov/pubmed/15501647 

E.coli Lon and morphology (changes between rod and filament forms)
http://www.ncbi.nlm.nih.gov/pubmed/23391222

Campylobactor (lon protein contributes to virulence)
http://www.ncbi.nlm.nih.gov/pubmed/17933920

Mycobacteria Lon
 casein sensitive
http://www.ncbi.nlm.nih.gov/pubmed/11045626  
http://www.ncbi.nlm.nih.gov/pubmed/9698372

Mycobacteria are dimorphic (changes morphology like e.coli does with LON into a cording form)
http://mic.sgmjournals.org/content/26/1/97

T.gondii and proteases and virulence ? (it might not be t.gondii but mycobacteria with this form of  schizophrenia )
http://www.ncbi.nlm.nih.gov/pubmed/22202120

not sure how this fits:  HU is involved with t.gondii virulence ( mutated in e.coli HU causes filamentation)
http://ec.asm.org/content/11/7/905.full
lon protease degrades HU...so would this explain gluten/casein and t.gondii?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC298136/

or there is more than one type of schizophrenia which is the most logical conclusion given that Tuberculosis has a risk of schizophrenia
http://www.biomedcentral.com/1471-2334/13/351

parkinson's, olfactory dysfunction, and mycobacterias of the sinus? or h. pylori!

Trying to determine which, if any, mycobacterias are the culprits for Parkinson's disease and how this fits with the cross-targeting.

Tuberculous has been connected to parkinson's through a protein called Parkin
http://medicalxpress.com/news/2013-09-tuberculosis-parkinson-disease-linked-unique.html
to dispose of mitochondria....parkin is involved.  Parkin disposes of mycobacterias too.

(note that our mitochondria maybe have in our evolutionary past evolved from something like a mycobacteria)  If we are infected with Mycobacteria could we have too much parkin in our systems which could damage us? or could parkin be something we have autoantibodes against triggering parkinson's?

Parkinson's does have autoantibodies:
http://www.ncbi.nlm.nih.gov/pubmed/21234712

How can we connect parkinson's to mycobacteria? the olfactory ?

Parkinson's and mycobacteria/ and similar infections
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC228573/

Mycobacterium leprae which causes leprosy also causes the olfactory bulb to shrink
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431526

non tuberculous mycobacteria in sinus from water and soil (plumbing)
http://www.ncbi.nlm.nih.gov/pubmed/23017381

Mycobacterium avium (most non tuberculous infections)  
http://www.ncbi.nlm.nih.gov/pubmed/23460008

 The person to person mycobacteria is Mycobacterium tuberculosis

psoriasis and tuberculous
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331879

crohn's and mycobacteria
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031217


Mycobacteria breaks the blood brain barrier: BBB allowing any  virus/ immune system cells to cross

H1n1  then causing the cross-targeting on the brain?

This could explain this recent outbreak
http://www.mumbaimirror.com/mumbai/others/2nd-wave-H1N1-stumps-docs/articleshow/16029319.cms
where the flu seemed to have a second wave of attack moving beyond the lungs and infecting the nerves, spine, and in some cases the brain...the brain may have been those with mycobactera infections? This puts the virus infecting the nerves inside and mycobacteria would infect the outside of nerves.   (cross targeting the immune system on these nerves)

Did the Micheal J. Fox parkinson's cluster in Canada have the flu or tuberculous?

Lots of possibilities here.  This page is still under construction and may change.

Here is the older post I had looking at il-6 and the bird flu
 http://angelabiggs.blogspot.com/2013/04/parkinsons-disease.html

added FEB /2014
Here is the other mystery: H.pylori
Some parkinson's patients have H.pylori infections causing ulcers and reflux and when it is treated have their symptoms improve.

H.pylori and parkinson's?
http://www.ncbi.nlm.nih.gov/pubmed/24117797
http://www.ncbi.nlm.nih.gov/pubmed/22071847

Is there a relationship between h.pylori and mycobacteria? how similar are they? do the same drugs kill them? do they coexist? i didn't think h.pylori existed outside of the digestive track.  Could this infection do the same thing?

coexist?
http://www.ncbi.nlm.nih.gov/pubmed/12613749?dopt=Abstract&otool=stanford
H.pylori can be in the sinus! (nasal polyps)
http://www.ncbi.nlm.nih.gov/pubmed/22926364
olfactory? the infection of h.pylori can alter taste and smell!
http://www.ncbi.nlm.nih.gov/pubmed/23845559
wow...h.pylori can even raise il-6
http://www.ncbi.nlm.nih.gov/pubmed/24453409

So Parkinson's could be caused by mycobacteria or h.pylori....cross targeting with the virus? Can H.pylori break the BBB? blood brain barrier.   if they infect the same areas the target might match...would they infect the dopamine neurons? does mycobacteria?

Heliobacteria pylori (h.pylori) used to be called Campylocateria pylori. We know that Campylobacteria Jejuni infects the peripheral nerves which could trigger Guillianbarre syndrome.  Realizing that h.pylori is a relative of  C. jejuni...it is extremely likely that it could infect neurons.

So we have a puzzle: mycobacterias have the ability to cross the BBB.  H.pylori does not.  which one is the culprit or are they both?

susac syndrome and cross-targeting autoimmunity

Cross-targeting:  the layering of 2 different infections on one target causing autoimmune disease.  A viral infection marking the inside. A larger infection marking the outside. In this case the target would be the small blood vessels.

 Autoimmune Triad: encephalopathy, hearing loss and microangiopathy of the retina (can be mixed up with MS)....autoimmune attack of the endothelial cells at the smallest blood vessels of the brain ?

antibodies and endothelial in susac's
http://www.ncbi.nlm.nih.gov/pubmed/19643446

the same antibodies are in lupus and sjogren's
http://www.ncbi.nlm.nih.gov/pubmed/9256310

anti-phospholipids lupus or sjogren's overlap?
http://www.ncbi.nlm.nih.gov/pubmed/15462492

could sjogren's tinnitus, itchy ear overlap with the hearing loss of Susac?  I have candida possibly linked to sjogren's which would grow on the blood vessel walls.  Do fungal infections cause itchy ears?

virus triggers : hepatits C or HIV?
HIV and susac
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766273
hepatits C and susac
http://www.researchgate.net/publication/38079571_Susac_syndrome_a_case_report_and_PET_imaging_findings 
Hepatitis makes sense because it can make antibodies that mark the small blood vessels!
http://www.webmd.com/hepatitis/hepc-guide/conditions-associated-with-hepatitis-c

Edothelial cells, blood brain barrier, MS
http://www.ncbi.nlm.nih.gov/pubmed/19442163