Title:
Autoimmune Cross-targeting Hypothesis. The "ins and outs" of the immune system.
Abstract:
The trigger of autoimmunity has remained elusive. Genetic susceptibility and infections contribute to the development of autoimmunity but the pathogenesis has not been clear. This Cross-targeting hypothesis suggests that simultaneous infections on one target triggers autoimmunity. One infection exists on the outside and one infection exists on the inside.
Introduction:
Paul Ehrlich called the immune system attack on self tissue Horror autotoxicus; today it is called autoimmunity. Under normal healthy conditions our immune system does not attack self tissue because the immune system has built up a tolerance to self proteins by educating it's B cells and T cells. T cells are educated to recognize the inside of cells while B cells are educated to recognize the outside of our own cells. Both of these "educations" must be compromised for the immune system to attack self. Both the inside and the outside of a tissue must be infected.
Hypothesis:
In order for autoimmune disease to occur two different infections must be attacking the same target tissue. Cross-targeting is a military term for when a target is attacked from 2 different platforms. The 2 branches of the immune system attacking at the same time on the same target but from different systems fits. Those immune cells attacking the outside of a cell to kill large infections and those attacking viruses on the inside. It is this state of both B cell and T cell educations uncoupling and attacking at the same time that causes autoimmunity. There is nothing to hold the immune system back from killing the entire cell thus autoimmunity develops.
Evaluation of Hypothesis:
Dr. Oliver in 1918 dealt with a cluster of encephalitis lethargia patients who seemed to mysteriously freeze following a flu epidemic. In 1993 Dr. Andrew Church found himself with another Encephalitis cluster. Dr. Andrew Church discovered that 2 infections were present. Dr. Andrew discovered that a high number of his patients had a rare form of strep called Diplococcus along with the Spanish flu. He has spent a life time trying to piece together this disease. In 2011 Dr. Andrew and Dr. Russel came out with a paper proving Encephalitis lethargia was an autoimmune disease with antibodies directed at the Basal Ganglia. This is possibly the first paper supporting cross-targeting as the trigger for autoimmune disease.
The concept of the simultaneous activation of the immune system's inside and outside pathways triggering autoimmune disease and not the infections themselves becomes obvious with this autoimmune disease mouse model, NOD. The NOD, non obese diabetic, mouse model has now been shown to be caused by a mutation in the TCR, the T cell receptor. The TCR activates when it encounters an infected cell's HLA mailbox with foreign, typically viral, pieces in it.
Normal, real life not model, autoimmune disease would be the result of simultaneous infections inside and outside.
Most autoimmune diseases have dual infections triggering them and they don't have specific time tables until looked at in terms of cross-targeting infections. Typically the larger infection takes hold first and for some reason has not been eradicated before the second viral infection appears. The autoimmune disease is not triggered unless infections are marking both the inside and the outside at the same time. Which virus does not matter. Which outer infections does not matter. It is the mere coincidence of layered infections on one target. This inside-outside pattern can be found in all autoimmune diseases.
The collection of genetic susceptibilities of autoimmune diseases, specifically the HLAs, can identify which viral infections are involved. Each HLA mailbox is responsible for a specific zone within the cell. Viruses infect specific zones and often match up with a particular HLA mailbox. HLA-A is the mailbox for the nucleus, HLA-B is the mailbox for the mitochondria, HLA-C is the endoplasmic reticulum mailbox, and HLA-D is the cytosolic mailbox. Since susceptibility data using HLAs has been collected for each autoimmune disease we can use them to not only verify the virus we suspect but we can use them to understand the variations found within one type of autoimmune disease. When a virus enters a host cell it uses a receptor with known pathways. These receptor pathways create the variations we see for one type of autoimmune disease. Beyond location of the virus in the cell and what pathways are triggered, the HLAs can be even be matched up with specific viruses revealing suspects in autoimmune diseases we have not even identified yet. The collection of HLA genetic susceptibilities are extremely informative for the inner viral infections.
The environment and a person's medical history will help reveal the larger outer infections especially when different autoimmune diseases are found associated together. The overlapping of autoimmune diseases can reveal which larger infections have taken hold first. There will only be one common suspect. Further the quorum of these larger infections create distinctive problems for the hosts' health which can also be found linked to the autoimmune diseases. Once we establish which large infection we are looking at the autoimmune disease family associations make sense.
Often these larger infectious suspects appear in each of the autoimmune diseases but the viral trigger companions are different. Viruses use specific receptors as doorknobs to enter cells. These receptor doorknobs vary with different cell types. Viruses do not infect all cells. Only the ones with their receptor. Thus when a larger infection has established itself on several organs and a virus appears it is only the organ where they both, virus and large infection, are infecting that develops autoimmunity. Hence explaining the lack of order to autoimmune disease family development. One autoimmune disease does not lead specifically to another. It is random chance which virus is encountered next. Autoimmune disease development is random upon viral exposure once the larger infection has taken hold.
Analysis of the autoimmune diseases:
Rheumatoid arthritis
Autoimmune disease of the tendons.
Mycoplasmas have long been suspected and HLA-DR4 suggests the flu. Other viruses might trigger RA but the most common appears to be HLA-DR4.
Narcolepsy
Narcolepsy is caused by an autoimmune attack on hypocretin cells.
Similar to Encephalitis lethargia, Narcolepsy has been associated with both a flu virus and strep but in this case inducing an autoimmune attack on the the hypocretin cells of the hypothalamus.
A group of children in England developed narcolepsy after receiving vaccinations against the flu H1N1 suggesting that it is not the virus directly rather the immune system itself causing the narcolepsy. In other words, a section of the virus although not active still goes to and binds the target tissue bringing the immune system and triggering the autoimmune disease just like a live virus. Foreign is foreign to the immune system wether or not the virus is active or not active.
All the children who developed narcolepsy after the vaccine had recently had a strep infection supporting the notion of an autoimmune cross-targeting event triggering the narcolepsy.
The HLA associated with Narcolepsy is HLA-DR2. The HLA-DR is a mailbox for the cytosol of the cell. HLA-DR2 specifically has strong correlations with flu virus H1N1.
Rheumatic fever
Rheumatic fever can trigger an autoimmune attack on the heart by cross-targeting on myocytes.
There is a high incidence of co-infection in Rheumatic fever. Coxsackie B virus antibodies have been found along side streptococcus antibodies in children with rheumatic fever.
The strongest HLA for rheumatic fever is HLA-DR7. HLA-DR7 has strong associations with blood group antigen binding bacterias. Strep recognizes blood group antigens.
Patients with rheumatic fever were also more likely to have HLA-DR3. HLA-DR3 has associations with the coxsackie virus.
In this case the antibodies that cross-react with strep lead the immune system to the heart marking the outside of the organ. When the coxsackie virus infects the heart cells, myocytes, an autoimmune reaction results.
Parkinson's disease has been associated with psoriasis' mycobacteria and nocardia. These mycobacterias are capable of crossing the blood brain barrier.
There are 3 major types of parkinson's and 3 different virus families associated.
Idopathic, late onset parkinson's disease has been connected to flaviviruses like west nile and hepatitis C. HLA-DR15 (odor impaired group because of melanocortin receptors used by flaviviruses)
Vascular, postencephalitic parkinson's is linked to the flu H1N1 and frontal lobe issues. HLA-DR2? (task switching impaired group because of frontal lobe)
The parkinsonism that appears to be linked with Alzheimer's suggests a connection to herpes viruses. HLA-B (memory impaired)
All 3 virus families can trigger parkinson's disease by cross-targeting with the mycobacteria. The type of parkinson's seems to vary depending on the virus. (maybe viruses and the receptors they use do influence the autoimmune disease somewhat)
The collection of genetic susceptibilities of autoimmune diseases, specifically the HLAs, can identify which viral infections are involved. Each HLA mailbox is responsible for a specific zone within the cell. Viruses infect specific zones and often match up with a particular HLA mailbox. HLA-A is the mailbox for the nucleus, HLA-B is the mailbox for the mitochondria, HLA-C is the endoplasmic reticulum mailbox, and HLA-D is the cytosolic mailbox. Since susceptibility data using HLAs has been collected for each autoimmune disease we can use them to not only verify the virus we suspect but we can use them to understand the variations found within one type of autoimmune disease. When a virus enters a host cell it uses a receptor with known pathways. These receptor pathways create the variations we see for one type of autoimmune disease. Beyond location of the virus in the cell and what pathways are triggered, the HLAs can be even be matched up with specific viruses revealing suspects in autoimmune diseases we have not even identified yet. The collection of HLA genetic susceptibilities are extremely informative for the inner viral infections.
The environment and a person's medical history will help reveal the larger outer infections especially when different autoimmune diseases are found associated together. The overlapping of autoimmune diseases can reveal which larger infections have taken hold first. There will only be one common suspect. Further the quorum of these larger infections create distinctive problems for the hosts' health which can also be found linked to the autoimmune diseases. Once we establish which large infection we are looking at the autoimmune disease family associations make sense.
Often these larger infectious suspects appear in each of the autoimmune diseases but the viral trigger companions are different. Viruses use specific receptors as doorknobs to enter cells. These receptor doorknobs vary with different cell types. Viruses do not infect all cells. Only the ones with their receptor. Thus when a larger infection has established itself on several organs and a virus appears it is only the organ where they both, virus and large infection, are infecting that develops autoimmunity. Hence explaining the lack of order to autoimmune disease family development. One autoimmune disease does not lead specifically to another. It is random chance which virus is encountered next. Autoimmune disease development is random upon viral exposure once the larger infection has taken hold.
Analysis of the autoimmune diseases:
Rheumatoid arthritis
Autoimmune disease of the tendons.
Mycoplasmas have long been suspected and HLA-DR4 suggests the flu. Other viruses might trigger RA but the most common appears to be HLA-DR4.
Narcolepsy
Narcolepsy is caused by an autoimmune attack on hypocretin cells.
Similar to Encephalitis lethargia, Narcolepsy has been associated with both a flu virus and strep but in this case inducing an autoimmune attack on the the hypocretin cells of the hypothalamus.
A group of children in England developed narcolepsy after receiving vaccinations against the flu H1N1 suggesting that it is not the virus directly rather the immune system itself causing the narcolepsy. In other words, a section of the virus although not active still goes to and binds the target tissue bringing the immune system and triggering the autoimmune disease just like a live virus. Foreign is foreign to the immune system wether or not the virus is active or not active.
All the children who developed narcolepsy after the vaccine had recently had a strep infection supporting the notion of an autoimmune cross-targeting event triggering the narcolepsy.
The HLA associated with Narcolepsy is HLA-DR2. The HLA-DR is a mailbox for the cytosol of the cell. HLA-DR2 specifically has strong correlations with flu virus H1N1.
Rheumatic fever
Rheumatic fever can trigger an autoimmune attack on the heart by cross-targeting on myocytes.
There is a high incidence of co-infection in Rheumatic fever. Coxsackie B virus antibodies have been found along side streptococcus antibodies in children with rheumatic fever.
The strongest HLA for rheumatic fever is HLA-DR7. HLA-DR7 has strong associations with blood group antigen binding bacterias. Strep recognizes blood group antigens.
Patients with rheumatic fever were also more likely to have HLA-DR3. HLA-DR3 has associations with the coxsackie virus.
In this case the antibodies that cross-react with strep lead the immune system to the heart marking the outside of the organ. When the coxsackie virus infects the heart cells, myocytes, an autoimmune reaction results.
Parkinson’s
Parkinson's is an autoimmune disease of the Basal ganglia's substantia nigra.
Parkinson's disease has been associated with psoriasis' mycobacteria and nocardia. These mycobacterias are capable of crossing the blood brain barrier.
There are 3 major types of parkinson's and 3 different virus families associated.
Idopathic, late onset parkinson's disease has been connected to flaviviruses like west nile and hepatitis C. HLA-DR15 (odor impaired group because of melanocortin receptors used by flaviviruses)
Vascular, postencephalitic parkinson's is linked to the flu H1N1 and frontal lobe issues. HLA-DR2? (task switching impaired group because of frontal lobe)
The parkinsonism that appears to be linked with Alzheimer's suggests a connection to herpes viruses. HLA-B (memory impaired)
All 3 virus families can trigger parkinson's disease by cross-targeting with the mycobacteria. The type of parkinson's seems to vary depending on the virus. (maybe viruses and the receptors they use do influence the autoimmune disease somewhat)
Type 1 diabetes
In type one diabetes the immune system has decided to attack the pancreas. Two viruses have been associated with the development of type one diabetes the Coxsackie virus (an enterovirus) and the Flu viruses. Both of these viruses can and do replicate inside of pancreatic cells but it only takes one virus to mark the inside.
Larger infections have been found infecting pancreatic cells from the outside: mycoplasmas, e.coli, campylobactera, and candida. So which infection is responsible for the development of autoimmune type one diabetes? All of them and yet only one of them on the outside at a time is needed to trigger type one diabetes.
Note that the e.coli and campylobacter infections attach to intestinal cells using the blood type antigens. Like the epithelial tissues, the pancreas has expressed the blood type antigens which means that E.coli or campylobacter will be drawn to this organ if they cross from the intestine into the body.
How do you know which infection could possibly be infecting the pancreas? E.coli is involved with bladder infections and intestinal infections. Fungal infections tend to trigger Hashimoto's thyroid disease. (how is unknown) Mycoplasmas have been linked to rheumatoid arthritis. You only need one of these to infect the outside of the pancreas.
Note that the e.coli and campylobacter infections attach to intestinal cells using the blood type antigens. Like the epithelial tissues, the pancreas has expressed the blood type antigens which means that E.coli or campylobacter will be drawn to this organ if they cross from the intestine into the body.
How do you know which infection could possibly be infecting the pancreas? E.coli is involved with bladder infections and intestinal infections. Fungal infections tend to trigger Hashimoto's thyroid disease. (how is unknown) Mycoplasmas have been linked to rheumatoid arthritis. You only need one of these to infect the outside of the pancreas.
As for the virus that marks the inside of the pancreatic cells either the flu or the coxsackie enterovirus can trigger the autoimmune disease but because they use different receptors to enter the pancreatic cell they may create two different variants of type one diabetes.
Dopamine receptors inhibit insulin secretion which means that a flu virus using the dopamine receptor to enter the cell would create a fast progression to diabetes compared to enteroviruses which use acetylcholine receptors. Acetylcholine receptors increase insulin secretion so the development of diabetes would appear to be slower. This prediction of fast and slow progression fits with the HLA mailboxes associated with diabetes: HLA-DR4 and HLA-DR3. The HLA-DR 3 has been linked to a slower progression to type one diabetes. HLA-DR3 is linked to enteroviruses, like coxsackie, while HLA-DR4 is linked to the flu viruses.
Dopamine receptors inhibit insulin secretion which means that a flu virus using the dopamine receptor to enter the cell would create a fast progression to diabetes compared to enteroviruses which use acetylcholine receptors. Acetylcholine receptors increase insulin secretion so the development of diabetes would appear to be slower. This prediction of fast and slow progression fits with the HLA mailboxes associated with diabetes: HLA-DR4 and HLA-DR3. The HLA-DR 3 has been linked to a slower progression to type one diabetes. HLA-DR3 is linked to enteroviruses, like coxsackie, while HLA-DR4 is linked to the flu viruses.
Multiple sclerosis and the myelin of nerves
Mycobacteria and multiple sclerosis connections
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5437105/
https://www.sciencedaily.com/releases/2010/02/100226084007.htm
Mycobacteria and multiple sclerosis connections
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5437105/
https://www.sciencedaily.com/releases/2010/02/100226084007.htm
People with psoriasis have higher rates of multiple sclerosis but not everyone with psoriasis gets it. Now put into place the cross-targeting hypothesis. Mycobacterias have been closely tied to psoriasis. If the mycobacterias mark the outside of the myelin then the virus must mark the inside of the myelin.
HLA-B, HLA-C, and HLA-DR have been linked to multiple sclerosis.
HLA-B is Shingles is the herpes zoster virus that would mark the inside of the myelin because the oligodendrocytes and schwann cells have estrogen receptors, the receptors used by the herpes virus to infect. Because the herpes-viruses come and go this form could the relapsing remitting form of multiple sclerosis.
The immune system would be triggered to destroy all myelin. Are people who have shingles while they have mycobacterial infections the ones at risk for multiple sclerosis?
HLA-C has been linked to polyomavirues like hepatitis B. A hepatitis B vaccine triggered several multiple sclerosis cases in France. Because polyomaviruses use vitamin D receptors this form of Multiple sclerosis might have the most change with Vit D.
HLA-DR15 which binds Flaviviruses has also been linked to multiple sclerosis. This form could the the secondary progressive type. Because this virus likes the optic nerve this may be the form of MS with vision issues.
These are guesses:
HLA-B: Herpes-alpha (zoster): Relapsing remitting
HLA-DR15 : Flavivirus (hepatitis C/dengue ) :Secondary progressive
HLA-A: Herpes-gamma (epstein barr): progressive relapsing
HLA-C: Polyomavirus (hepatitis B/ JC, BK) / enteroviruses? (coxsackie, polio): primary progressive
HLA-B, HLA-C, and HLA-DR have been linked to multiple sclerosis.
HLA-B is Shingles is the herpes zoster virus that would mark the inside of the myelin because the oligodendrocytes and schwann cells have estrogen receptors, the receptors used by the herpes virus to infect. Because the herpes-viruses come and go this form could the relapsing remitting form of multiple sclerosis.
The immune system would be triggered to destroy all myelin. Are people who have shingles while they have mycobacterial infections the ones at risk for multiple sclerosis?
HLA-C has been linked to polyomavirues like hepatitis B. A hepatitis B vaccine triggered several multiple sclerosis cases in France. Because polyomaviruses use vitamin D receptors this form of Multiple sclerosis might have the most change with Vit D.
HLA-DR15 which binds Flaviviruses has also been linked to multiple sclerosis. This form could the the secondary progressive type. Because this virus likes the optic nerve this may be the form of MS with vision issues.
These are guesses:
HLA-B: Herpes-alpha (zoster): Relapsing remitting
HLA-DR15 : Flavivirus (hepatitis C/dengue ) :Secondary progressive
HLA-A: Herpes-gamma (epstein barr): progressive relapsing
HLA-C: Polyomavirus (hepatitis B/ JC, BK) / enteroviruses? (coxsackie, polio): primary progressive
Autism the 3 types (not including asperger's or ADD)
Autism is an autoimmune attack of the brain's cerebellum, frontal lobe, and temporal lobe. Not damage from vaccines or infections alone but from one's own immune system; autism is an autoimmune disease.
Autism is an autoimmune attack of the brain's cerebellum, frontal lobe, and temporal lobe. Not damage from vaccines or infections alone but from one's own immune system; autism is an autoimmune disease.
What about the vaccine induced autoimmunity? This cross-targeting hypothesis can be applied to vaccine reactions. Looking at the list of what has been accused of causing autism then listing the targets they infect reveals patterns which reflect distinctively different forms of autism. Autism appears to be an autoimmune disease.
The DTP vaccine has three bacterial infections that it inoculates for : diphtheria, pertussis, and tetanus. Only one of these bacterial infections exists in the temporal lobe of the brain and that is tetanus. When the vaccine is given even if the disease is prevented a small amount of antibodies would end up at the temporal lobe because some of those bacterial pieces bind there. Why pick tetanus out of this list ? Some autism patients have HHV6 with the neural autoantibodies. This 6th disease known for it’s rash Roseola is a virus that replicates in the temporal lobe of the brain. Applying the cross-targeting hypothesis on the temporal lobe suggest that if a child with 6th disease gets the dtp vaccine they could develop an autoimmune attack of the temporal lobe thus developing an autism disease of this part of the brain. The CMV herpes virus could be implicated here too. C. tetanus has been found in the guts of some children with autism. These kids may have developed autism not because of a vaccine rather from catching a herpes virus while dealing with the C. tetanus in their system. The key autism feature of the temporal lobe is the involvement of the senses. Visual and hearing decoding including dyslexia has been associated with the temporal lobe.
What about the infamous MMR vaccine? Autoantibodies for the measles part of that vaccine have been seen in a group of autistic kids and the measles virus pieces migrate to the cerebellum. Clusters of autistic kids have been found to have sutterella bacteria in their system too. Sutterella is closely related to campylobacteria which can infect the cerebellum. Does the cross-targeting of the measles vaccine and sutterella cause an autoimmune attack of the cerebellum? Is this possible? Does campylobacteria do the same thing? Can the coxsackie virus replace the measles virus because it too infects the cerebellum?
What about the children born with autism that were not induced by vaccines? Pregnant women with Rheumatoid arthritis are more likely to have autistic children. Women who catch the flu during pregnancy are more likely to have autistic kids. If we apply the cross-targeting hypothesis and look for a specific target we find the frontal lobe in this form of autism. Antibodies to the frontal lobe have been found in mother's with rheumatoid arthritis. The flu (H1N1) when it has infected the brain of the young children has been found in the frontal lobe region. It is possible that an unborn fetus develops an autoimmune form of autism on the frontal lobe when both of these infections occur at the same time in a pregnant woman.
Acute Flaccid Paralysis
There are at least 3 types of acute flaccid paralysis: two types of Guillain Barre (GB) of the peripheral nerves and Acute inflammatory demyelinating polymeuropathy (AIDP) of the anterior nerves.
The first and major type is the Guillain Barre form that has strong associations with Campylobacteria Jejuni and Sutterella. These infections begin in the gut but can trigger the autoimmune paralysis of the legs by triggering autoimmune cross-targeting of the peripheral nervous system after it has moved into the body from the intestine and taken residence with the nerves. HLA-DR7 has been found in Guillain Barre.
The HLA-DR7 has a strong association with blood type antigens which the c.jejuni binds.
The second type of Guillain Barre involves Mycoplasmas. This form of Guillain Barre typically occurs with rheumatoid arthritis and can be triggered by ciprofloxacin not just viruses.
AIDP has strong associations with staph, asthma, and eczema. Several children with severe staph died when they contracted d68. Since staph has often been found in eczema lets assume this is the larger infection.
The viral infections for all 3 acute flaccid paralysis may overlap. All the viruses that infect nerves are involved: herpes viruses, flaviviruses, and enteroviruses.
Zika and west nile have both been shown to trigger both Guillian barre and AIDP. D68 and the polio virus have been known to trigger AIDP. The herpes viruses have also been suspected of trigger some Guillain barre cases.
What is interesting is that the HLAs seem to validate these specific viral suspects as the triggers.
Zika and west nile have both been shown to trigger both Guillian barre and AIDP. D68 and the polio virus have been known to trigger AIDP. The herpes viruses have also been suspected of trigger some Guillain barre cases.
What is interesting is that the HLAs seem to validate these specific viral suspects as the triggers.
Flavivirus : HLA-DR33 or HLA-DR15
Herpes Zoster: HLA-B15
Enterovirus: HLA-DR3, HLA-A33 (enterovirus 71)
Enterovirus: HLA-DR3, HLA-A33 (enterovirus 71)
Bell's palsy
Four HLAs have been found in Bell's Palsy patients.
HLA-DR2 and HLA-DR-4 are linked to the Flu virus. Bell's palsy has been known to appear after both episodes of flu and vaccine forms of the flu.
2 types of Myasthenia gravis
There are two types of Myasthenia gravis and based on the viruses involved drastically different symptoms along with the thymus autoimmune attack.
One involves the conjunctivitis and ACTH antibodies. This type is associated with flaviviruses like west nile which use ACTH receptors. The late type of MG has been associated with HLA-DR15. HLA-15 has been associated with flaviviruses.
Early onset MG has been associated with HLA-DR3. HLA-DR3 has been connected to coxsackie and other enteroviruses. This type of myasthenia gravis has muscle weakness of the arms and legs. The enteroviruses, the polio family viruses, use acetylcholine receptors.
Close association of MG with rheumatoid arthritis suggests that the outer infections are the mycoplasmas.
Alopecia
Alopecia is the autoimmune cross-targeting attack of hair follicles.
HLA-DQ : Reovirus : Areata Alopecia
HLA-C : Polyomavirus: Universalis Alopecia
HLA-DR : Flu : Totalis Alopecia
Is vitiligo associated with Alopecia more often because some type of skin infection is one of the triggers? Trichophyton violaceum has been associated with discord lupus and vitiligo. If trichophyton makes tyrosol as it's quorum that could explain the pigment loss. Tyrosol inhibits tyrosinase a step in melanogenesis. Note that autoimmune antibodies to tyrosine have been found in vitiligo patients.
Rheumatoid arthritis also has a strong association with alopecia. The infection involved with Rheumatoid arthritis could be mycoplasmas which is further supported by those who have hair loss following mycoplasma pneumonia.
Nodding disease and epilepsy
Nodding disease and epilepsy are closely related.
Nodding disease, the zombie like state of those in Africa that has been connected to the black fly blindness from Trypanosoma brucei. The africans feel that polio or even the live polio vaccine triggers the nodding disease. What may actually be occurring is cross-targeting of the T.brucei and the enterovirus causing an autoimmune disease which is the nodding disease.
Epilepsy has an strong link with schizophrenia a T.gondii disease. Epilepsy could similarly be autoimmune cross-targeting of t.gondii, t.cruzi, or malaria with enteroviruses. The pattern here is trypanosoma and enterovirus at the medial temporal lobe. Epilepsy has been linked to HLA-DR3 which is known to be connected to enteroviruses. Polio is a type of enterovirus.
Kikuchi-Fujimoto
Alopecia is the autoimmune cross-targeting attack of hair follicles.
HLA-DQ : Reovirus : Areata Alopecia
HLA-C : Polyomavirus: Universalis Alopecia
HLA-DR : Flu : Totalis Alopecia
Rheumatoid arthritis also has a strong association with alopecia. The infection involved with Rheumatoid arthritis could be mycoplasmas which is further supported by those who have hair loss following mycoplasma pneumonia.
Nodding disease and epilepsy
Nodding disease and epilepsy are closely related.
Nodding disease, the zombie like state of those in Africa that has been connected to the black fly blindness from Trypanosoma brucei. The africans feel that polio or even the live polio vaccine triggers the nodding disease. What may actually be occurring is cross-targeting of the T.brucei and the enterovirus causing an autoimmune disease which is the nodding disease.
Epilepsy has an strong link with schizophrenia a T.gondii disease. Epilepsy could similarly be autoimmune cross-targeting of t.gondii, t.cruzi, or malaria with enteroviruses. The pattern here is trypanosoma and enterovirus at the medial temporal lobe. Epilepsy has been linked to HLA-DR3 which is known to be connected to enteroviruses. Polio is a type of enterovirus.
Kikuchi-Fujimoto
Kikuchi-Fujimoto disease is an autoimmune disease of the lymph nodes. In Japan Aspergillus oryzae is used for making miso, soy sauce, and sake. Exposure rates for aspergillus are high there. The key here is that only one virus and not a specific virus can trigger the autoimmune attack as long as the virus infects the lymph glands. Herpes viruses and parvoviruses have been suspected but large case studies have failed to prove a direct connection. It is suspicious that the rare acute disseminated encephalitis, an autoimmune disease of brain and spinal cord, has been known to overlap Kikuchi-fujimoto. Unlike multiple sclerosis this autoimmune attack on the nerves does not wax and wane, perhaps it is triggered by the parvoviruse B19.
Hashimoto's thyroid
Hashimoto's thyroid disease has antibodies to thyroid peroxidase (TPO). All fungal infections secrete peroxidases in order to digest their surroundings. Logically antibody cross-reactivity can occur between the fungal peroxidase and the thyroid's peroxidase. Sjoren's has strong associations with candida and Hashimoto's. Discord lupus and vitiligo has strong associations with trichophyton and Hashimoto's. If these autoantigens to the thyroid are started by fungal infections then the inside of the thyroid still needs to be marked as foreign. Multiple viruses have been linked to triggering thyroid disease. Any of the viruses that infect a thyroid can trigger the autoimmune attack. Flaviviruses, enteroviruses, and even parvoviruses can infect thyroid cells. The key to autoimmune cross-targeting is that the inside and the outside must be simultaneously marked as foreign to trigger the immune system to attack and destroy self tissue.
Graves thyroid
Graves disease is not an autoimmune cross-targeting disease; the tissue is not attacked. Antibodies generated by yersinia infections cross react, bind, and activate the TSH receptors. The thyroid activity is stimulated. The thyroid tissue is not attacked by the immune system. Now Graves can turn into an autoimmune variety through cross-targeting but the antibody binding the receptor is not on the cells surface very long and a virus or medication must also be marking the inside as foreign. The window of opportunity for graves disease to become autoimmune is small because the antibody quicky cycles in with the receptor and doesn't have much of a chance to do it's job.
Celiac disease
Celiac disease is an autoimmune disease of the intestine. Patients tend to have histories of bladder infections or Dermatitis Herpetiformis both of which are associated with e.coli infections. Campylobacteria was also found in high concentrations in celiac patients. Either of these infections could be the larger mark on the outside of intestinal cells.
Astroviruses have been isolated from newly diagnosed celiac disease patients. Other intestinal lining viruses could logically trigger the cross-targeting of e.coli feathered intestinal cells. Hepatitis B was once considered and so was rotavirus. The specific virus is not as important as the layering of inside and outside infections. The HLA-DQ suggests a cytosolic unencapsulated virus.
Gluten sensitivity occurs because e.coli is a membrane barrier crosser like T.gondii. The hole created in the intestine allows gluten to pass through and heighten the immune response. Celiac disease is an autoimmune cross-targeting on top of a membrane crossing which is why gluten seems to inflame the situation. Gluten does not cause the autoimmune cross-targeting. It has guilt by association with e.coli.
Hashimoto's thyroid
Hashimoto's thyroid disease has antibodies to thyroid peroxidase (TPO). All fungal infections secrete peroxidases in order to digest their surroundings. Logically antibody cross-reactivity can occur between the fungal peroxidase and the thyroid's peroxidase. Sjoren's has strong associations with candida and Hashimoto's. Discord lupus and vitiligo has strong associations with trichophyton and Hashimoto's. If these autoantigens to the thyroid are started by fungal infections then the inside of the thyroid still needs to be marked as foreign. Multiple viruses have been linked to triggering thyroid disease. Any of the viruses that infect a thyroid can trigger the autoimmune attack. Flaviviruses, enteroviruses, and even parvoviruses can infect thyroid cells. The key to autoimmune cross-targeting is that the inside and the outside must be simultaneously marked as foreign to trigger the immune system to attack and destroy self tissue.
Graves thyroid
Graves disease is not an autoimmune cross-targeting disease; the tissue is not attacked. Antibodies generated by yersinia infections cross react, bind, and activate the TSH receptors. The thyroid activity is stimulated. The thyroid tissue is not attacked by the immune system. Now Graves can turn into an autoimmune variety through cross-targeting but the antibody binding the receptor is not on the cells surface very long and a virus or medication must also be marking the inside as foreign. The window of opportunity for graves disease to become autoimmune is small because the antibody quicky cycles in with the receptor and doesn't have much of a chance to do it's job.
Celiac disease
Celiac disease is an autoimmune disease of the intestine. Patients tend to have histories of bladder infections or Dermatitis Herpetiformis both of which are associated with e.coli infections. Campylobacteria was also found in high concentrations in celiac patients. Either of these infections could be the larger mark on the outside of intestinal cells.
Astroviruses have been isolated from newly diagnosed celiac disease patients. Other intestinal lining viruses could logically trigger the cross-targeting of e.coli feathered intestinal cells. Hepatitis B was once considered and so was rotavirus. The specific virus is not as important as the layering of inside and outside infections. The HLA-DQ suggests a cytosolic unencapsulated virus.
Gluten sensitivity occurs because e.coli is a membrane barrier crosser like T.gondii. The hole created in the intestine allows gluten to pass through and heighten the immune response. Celiac disease is an autoimmune cross-targeting on top of a membrane crossing which is why gluten seems to inflame the situation. Gluten does not cause the autoimmune cross-targeting. It has guilt by association with e.coli.
Drug induced
The exception to this infection driven hypothesis is the drug-induced autoimmunity. Cross-targeting is still occurring triggering when drugs are triggering the immune system but a drug replaces an infection.
Drug induced lupus can be triggered by monocycline and hydralazine. Hydralazine is a muscle relaxer and works inside the muscles cells. Monocycline which is an acne medication is known to penetrate muscles and cause severe muscle cramping. Either of these drugs could replace the viral infection which marks the inside of the cell. A patient with autoimmune liver disease makes anti-muscle antibodies which would mark the outside of muscle cells. They are the vulnerable group. If the outside and the inside of the muscle appears marked or foreign to the immune system cross-targeting autoimmunity could result.
Halothane hepatitis could be caused by cross-targeting too. The Halothane would replace the virus on the inside of liver cells. A child with a pre-existing issues of e.coli might have the liver already marked on the outside. A young girl developed hepatitis after using the anesthetic. This particular girl also went on to develop type one diabetes. Does the girl have celiac too? Is celiac a risk factor for halothane hepatitis?
The reverse scenario can also occur. Hemolytic anemia is triggered when a drug like penicillin coats the outside of the red blood cells. Normally this would not be an issue but if the person had recently had the RSV virus which replicates in bone marrow or had chronic hepatitis C which might try to infect red blood cells and the virus was still visible in the red blood cells thus it might trigger autoimmunity.
This leads us to the next autoimmune issue of recognizing and diagnosing what you are infected with. People who host parasites like t.gondii, yeasts, mycobacterias or mycoplasmas will find this hard to accept and it is still hard to diagnose. Very little is known about the good verse the bad microbes in our digestive system but we must learn what is there in the body and what they can do.
Conclusion:
The pathogenesis of autoimmune disease can be elucidated if autoimmune diseases are analyzed as targets and infections. The overlapping characteristics are key to understanding what we are really looking at, which infections we are looking at. Think of the immune system cross-targeting on one target as the trigger for autoimmune disease. What infections are shared among autoimmune disease families, what is the target tissue, and what these infections have in common can give us not just insight into how autoimmune disease is triggered but how to prevent them and maybe even cure them.
I need to respectfully identify Dr. Andrew Church and Dr. Russel Dale who work on Encephalitis Lethargia as the first to recognize the coexistance of two infections.
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