Autoimmune cross-targeting hypothesis: when two infections are on one target typically the immune attack on the larger infection is stopped. This "stopping" action can trigger autoimmune disease.
Autoimmune antibody in Rheumatoid Arthritis is anti-ccp or cyclic citrullinated peptide
HLA-C allele confers risk for RA and cyclic citrullinated peptide antibodies
https://www.ncbi.nlm.nih.gov/m/pubmed/23901134/
HLA-C is the T cell mailbox for ER proteins
mycoplasmas infect the ER
https://www.ncbi.nlm.nih.gov/pubmed/4844719
Natural killer cells are responsible for ER and golgi infections (HLA-C and HLA-E). When infections occur in these areas no proteins make it to the surface of cells and they often appear naked.
It is possible that anti-CCP are to stop Natural killer cells from binding the HLA-Cs.
Like the case with aquaporin and ER viral infections the ER mycoplasma infection is halted but this time through HLA-C.
Mycoplasmas and RA
http://www.ncbi.nlm.nih.gov/pubmed/24097830
http://www.ncbi.nlm.nih.gov/pubmed/10618069 (infection found in synovial fluid)
http://www.ncbi.nlm.nih.gov/pubmed/17122006
Not a new idea 1971...mycoplasmas and RA
http://www.ncbi.nlm.nih.gov/pubmed/5165178
Synovial membrane antibodies and RA
http://www.ncbi.nlm.nih.gov/pubmed/16184347
Virus: epstein barr and RA (nuclear virus)
https://www.ncbi.nlm.nih.gov/pubmed/28499895
http://www.ncbi.nlm.nih.gov/pubmed/25407647
The Rheumatoid arthritis group that has negative anti-CCP has conferred risk with HLA-DR3 : a cytosolic mailbox.
https://www.ncbi.nlm.nih.gov/pubmed/16200610
Type 1 diabetes is closely tied to HLA-DR4 and HLADR3
HLA-DR3 and coxsackie
https://www.ncbi.nlm.nih.gov/pubmed/12941542
https://www.ncbi.nlm.nih.gov/pubmed/9498628
https://www.ncbi.nlm.nih.gov/pubmed/12845430
HLA-DR3 and Hepatitis C
https://www.ncbi.nlm.nih.gov/pubmed/9490691
These viruses infect the Golgi
HLA-G (the golgi mailbox) has also been linked to RA
https://www.ncbi.nlm.nih.gov/pubmed/16916651?dopt=AbstractPlus
hepatitis C and the golgi
http://www.pnas.org/content/114/17/E3462
coxsackie and the golgi
https://jvi.asm.org/content/81/13/6785
This form of rheumatoid arthritis could be connected to gangliosides
https://www.ncbi.nlm.nih.gov/pubmed/8761183
since viral infections ten to create "naked cells" and this is the only way NK can bind
This form of RA can develop neuropathy
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026612/
In this case the large infection could be mycobacterias
http://www.rheumatologynetwork.com/arthritis/latent-tuberculosis-infection-ra-disease-and-diagnosis
nodular vasculitis and mycobacteria
https://www.ncbi.nlm.nih.gov/pubmed/20666819
This mycobacteria form of RA would involve Basophils. They would take the MHC2 from the TH1 and then the basophils would present to the TH2. Basophils are the liaisons to TH2 cells. They do this when there are parasites or mycobacterias hiding in the cytosol.
Autoimmune antibody in Rheumatoid Arthritis is anti-ccp or cyclic citrullinated peptide
HLA-C allele confers risk for RA and cyclic citrullinated peptide antibodies
https://www.ncbi.nlm.nih.gov/m/pubmed/23901134/
HLA-C is the T cell mailbox for ER proteins
mycoplasmas infect the ER
https://www.ncbi.nlm.nih.gov/pubmed/4844719
Natural killer cells are responsible for ER and golgi infections (HLA-C and HLA-E). When infections occur in these areas no proteins make it to the surface of cells and they often appear naked.
It is possible that anti-CCP are to stop Natural killer cells from binding the HLA-Cs.
Like the case with aquaporin and ER viral infections the ER mycoplasma infection is halted but this time through HLA-C.
Mycoplasmas and RA
http://www.ncbi.nlm.nih.gov/pubmed/24097830
http://www.ncbi.nlm.nih.gov/pubmed/10618069 (infection found in synovial fluid)
http://www.ncbi.nlm.nih.gov/pubmed/17122006
Not a new idea 1971...mycoplasmas and RA
http://www.ncbi.nlm.nih.gov/pubmed/5165178
Synovial membrane antibodies and RA
http://www.ncbi.nlm.nih.gov/pubmed/16184347
Virus: epstein barr and RA (nuclear virus)
https://www.ncbi.nlm.nih.gov/pubmed/28499895
http://www.ncbi.nlm.nih.gov/pubmed/25407647
The Rheumatoid arthritis group that has negative anti-CCP has conferred risk with HLA-DR3 : a cytosolic mailbox.
https://www.ncbi.nlm.nih.gov/pubmed/16200610
Type 1 diabetes is closely tied to HLA-DR4 and HLADR3
HLA-DR3 and coxsackie
https://www.ncbi.nlm.nih.gov/pubmed/12941542
https://www.ncbi.nlm.nih.gov/pubmed/9498628
https://www.ncbi.nlm.nih.gov/pubmed/12845430
HLA-DR3 and Hepatitis C
https://www.ncbi.nlm.nih.gov/pubmed/9490691
These viruses infect the Golgi
HLA-G (the golgi mailbox) has also been linked to RA
https://www.ncbi.nlm.nih.gov/pubmed/16916651?dopt=AbstractPlus
hepatitis C and the golgi
http://www.pnas.org/content/114/17/E3462
coxsackie and the golgi
https://jvi.asm.org/content/81/13/6785
This form of rheumatoid arthritis could be connected to gangliosides
https://www.ncbi.nlm.nih.gov/pubmed/8761183
since viral infections ten to create "naked cells" and this is the only way NK can bind
This form of RA can develop neuropathy
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026612/
In this case the large infection could be mycobacterias
http://www.rheumatologynetwork.com/arthritis/latent-tuberculosis-infection-ra-disease-and-diagnosis
nodular vasculitis and mycobacteria
https://www.ncbi.nlm.nih.gov/pubmed/20666819
This mycobacteria form of RA would involve Basophils. They would take the MHC2 from the TH1 and then the basophils would present to the TH2. Basophils are the liaisons to TH2 cells. They do this when there are parasites or mycobacterias hiding in the cytosol.
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