IgG4 antibodies and shutting down outer pathways...considered again.

IgG4 are the autoimmune antibodies which shut down the outer pathway so the immune system can focus on the inside pathway.

Autoimmune hypothesis: Two infections on one target triggers autoimmune disease. One infection inside and one infection outside of the cell.

Does the B cell that gets pulled from outside antigen pathways to inside antigen pathways become the IgG4 producing B cell with the goal of shutting down the outside pathways?

This would mean that the IgG4 would be similar based on the large infection and the pathway stopped if the autoimmune diseases share the same large infection.    For example, all mycobacteria triggered autoimmune diseases would have the same IgG4 against aquaporins.

IgG4 antibodies represent a down-regulatory response
https://www.ncbi.nlm.nih.gov/pubmed?term=24111912

IgG4 made by Bcells that produce il-10
https://www.jacionline.org/article/S0091-6749(13)00150-4/pdf

Br1 up regulate the plasma cells to become IgG4 producing
https://www.jacionline.org/article/S0091-6749(16)30722-9/pdf

Anti-gangliosides

Involves vacuole bacteria

Guillian-barre and anti-gangliosides
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422685/

http://www.neurologyindia.com/article.asp?issn=0028-3886;year=2018;volume=66;issue=5;spage=1324;epage=1331;aulast=Baskar

https://www.researchgate.net/publication/325884578_Anti-ganglioside_Antibodies_in_Peripheral_Nerve_Pathology


il-15 and gangliosides
https://www.ncbi.nlm.nih.gov/pubmed/16116192

gangliosides in autism
https://www.ncbi.nlm.nih.gov/pubmed/9766735

sutterella and autism spectrum disorder
https://molecularautism.biomedcentral.com/articles/10.1186/2040-2392-4-42


Anti-ANCA / anti-ANA

involves golgi infections and neutrophils 

salmonella and anti-ANCA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1905360/

reactive arthritis and salmonella
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195798/

anti-ANCA bind the neutrophil traps
https://www.frontiersin.org/articles/10.3389/fimmu.2017.00439/full

Anti-ANCA and Rheumatoid
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552688/

anti-nuclear in strep with tourettes
https://www.ncbi.nlm.nih.gov/pubmed/12699862

TLR8 and strep
http://www.jimmunol.org/content/195/3/1092

TLR8 is the Tcell mailbox for the Endoplasmic reticulum

polyarthritis and strep
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803937/

Anti-CCP

involves ER infections (by mycoplasmas) and the neutrophils

autophagy and ER stress
https://www.ncbi.nlm.nih.gov/pubmed/26391548

autophagy generates citrullinated proteins
https://www.ncbi.nlm.nih.gov/pubmed/27074807

neutrophils and citrullinated proteins in RA
https://www.nature.com/articles/s41598-018-33385-z

some how this antibody stops the neutrophils from coming for mycoplasmas?


Anti-leiomodin

Nodding disease is triggered by the parasitic worm and what virus? The IgG4 was found against leiomodin-1.  Nodding disease is autoimmune disease of the skin where the autoantigen attacks the brain?

Autoimmune cross-targeting hypothesis: two infections on one tissue. The reaction is at the skin but then the antibody attacks the brain?

 For these worms how does this work? The Leiomodin-1 antibody bound the worms...but they were IgG4?

When exposed to cold temperatures or food the children nod their heads uncontrollably. The hippocampus of the brain is responsible for body temperature sensations and hunger urges.

The worm is not in the hippocampus but the autoantibody shows up there.
https://www.ncbi.nlm.nih.gov/pubmed/28202777

Which virus at the skin has co-infected and caused the IgG4?

Does this mean that leiomodin-1 is involved with eosinophils degranulation attack? Since eosinophils at the main cell type attacking the worms how would this work?

eosinophils and smooth muscles
https://www.ncbi.nlm.nih.gov/pubmed/23180361

NEW

Natural killer cells anti-TRR

JIA IgG4 antibody to TRR
https://www.sciencedaily.com/releases/2016/02/160225101100.htm

TTR is a serum cerebrospinal fluid carrier of thyroid hormone thyroxine T4
https://www.acrobiosystems.com/L-514.html?utm_source=google&utm_medium=keywords&utm_campaign=US-proteinno-core-PC&utm_content=hhhis&utm_term=Transthyretin&gclid=Cj0KCQjw2K3rBRDiARIsAOFSW_7MhivjRGdtDNRxMtjDu6ncdwisF-Hr002WWJBfblMQl-yYluCc8ZsaAqbEEALw_wcB

Natural killer cells and Thyroid hormones
https://www.ncbi.nlm.nih.gov/pubmed/21745103

Do mycoplasmas which infect the endoplasma reticulum trigger NK cells but then in the autoimmune cross-targeting event the NK need to be "turned off"?

thyorid and nk cells associated in women with reproductive failure
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5806729/

TTR and arthritis
https://www.researchgate.net/figure/TTR-expressions-were-examined-in-other-joint-disease-and-autoimmune-disease-such-as-OA_fig4_261515697

nk and rheumatoid arthritis
https://www.ncbi.nlm.nih.gov/pubmed/30718650

Eosinophils and degranulation

anti-fab IgG4
https://link.springer.com/article/10.1007/BF00269196

FAB is the part of the antibody bound to the FC receptor by cells like Eosinophils

RA and FAB
https://www.ncbi.nlm.nih.gov/pubmed/3928684

Anti-myelin for mycobacteria in cytosol and eosinophils 

anti-myelin for lyme
https://www.ncbi.nlm.nih.gov/pubmed/11987581

Aquaporin and Eosinophils (phagocytosis)

Anti-Aquaporin (from old post)

Mycobacteria and other bacterial cytosol / nuclear infections which involve eosinophils and macrophages in a phagocytosis method appear to develop anti-AQP ( aquaporin antibodies)

aquaporins move eosoinophils
https://www.ncbi.nlm.nih.gov/pubmed/18510218

anti-aquaporin4 and multiple sclerosis
https://www.ncbi.nlm.nih.gov/pubmed/20705110

mycobacteria and multiple sclerosis
https://www.sciencedaily.com/releases/2010/02/100226084007.htm

idiopathic demyelination and anti-AQP4
https://www.hindawi.com/journals/msi/2017/1359761/

anti-aquaporin4 in neuromyelitis
https://www.ncbi.nlm.nih.gov/pubmed/18808744

salivary glands and parkinson's disease
https://www.michaeljfox.org/foundation/grant-detail.php?grant_id=838

salivary gland and psoriasis
https://www.ncbi.nlm.nih.gov/pubmed/7165375

salivary glands and aquaporins
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783900/

parkinson's and mycobacteria
https://www.ncbi.nlm.nih.gov/pubmed/25459140

psoriasis and mycobacteria
https://www.ncbi.nlm.nih.gov/pubmed/9657322

aquaporin and psoriasis
https://www.ncbi.nlm.nih.gov/pubmed/21400035

(Candida also has portions move to the cytosol)

SJ and salivary
https://www.ncbi.nlm.nih.gov/pubmed/1055974

Candida and SJ
https://www.ncbi.nlm.nih.gov/pubmed/12973284

SJ and MS because of salivary
https://www.jwatch.org/jn200112200000006/2001/12/20/possible-association-between-sjogrens-syndrome

Anti-TPO

How would anti-TPO stop TH17 cells which combat fungal infections

TPO increases the numbers of TH17
https://www.ncbi.nlm.nih.gov/pubmed/26836805

TH17 and fungal infections
https://www.ncbi.nlm.nih.gov/pubmed/19283705

quorum of fungus: farnesol
https://www.ingentaconnect.com/contentone/govi/pharmaz/2017/00000072/00000006/art00001?crawler=true&mimetype=application/pdf

Does farnesol stimulate the thyroid to produce TPO?  Is TPO used by TH17 cells?

Would blocking TPO stop TH17 cells?

original post
I have looked at these pathways before https://angelabiggs.blogspot.com/2019/05/igg4-antibodies.html