Sorting IgG antibodies: Does IgG3 match up with organelle infections while IgG2a appears alone (no IgG2b) with cytosol infections?

IgG1 is the dominant antibody with high FC receptor affinity

IgG2a and IgG2b are strong complement antibodies (mice, humans only have IgG2)

IgG2c Fc receptor "clean up antibody" only macrophage pick up not complement

IgG3 is seen less often with some viral infections

Flu a cytosol virus triggers IgG1 and IgG2a
http://cvi.asm.org/content/13/9/981.full

Herpes virus, organelle virus, triggers IgG1 and IgG3
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC271254/

strep a visible bacteria : IgG1, IgG2a, IgG2b
https://www.ncbi.nlm.nih.gov/pubmed/15232177

IgG2c against amyloid (self protein outside of the cell)
https://www.ncbi.nlm.nih.gov/pubmed/12565127

IgG2c against tumors
http://www.jimmunol.org/content/jimmunol/172/2/929.full.pdf

IgG2c does not activate complement
https://www.researchgate.net/post/how_different_are_the_functions_of_IgG2a_and_IgG2c

campylobacteria is hidden in the host's cytosol (bacteria in vacuoles) IgG1 and IgG2a
https://www.sciencedirect.com/science/article/pii/S1877282X15000089

HPV, organelle (nucleus) virus, triggers IgG1 and IgG3
https://www.ncbi.nlm.nih.gov/pubmed/24058629

antibody review
http://absoluteantibody.com/antibody-resources/antibody-overview/antibody-isotypes-subtypes/

note IgG4 appears with autoimmunity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2897107/

IgG4 inhibits compliment
https://www.sciencedirect.com/science/article/pii/B9780323069472100094

IgG2 triggers complement

IgG4 and IgG2 have the same non classical disulfide bond structure
https://www.researchgate.net/publication/221825860_Disulfide_bond_structures_of_IgG_molecules

Disulfide bonds in IgG
IgG1 has 2
IgG2 has 4
IgG3 has 11

why does IgG3 have 11 disulfide bonds? is it because it interacts with DNA?

DNA and disulfide bonds
https://www.sciencedirect.com/science/article/pii/S0014579399000599

IgG3 and anti-DNA

https://books.google.com/books?id=tj9JR3IITy8C&pg=PA455&lpg=PA455&dq=IgG3+anti+DNA&source=bl&ots=nnbaHQAhrL&sig=P7Vin_57g7Wqt1QwZZ4C4WNbqrc&hl=en&sa=X&ved=0ahUKEwjt4rO7hYPZAhUG02MKHVzPCmY4ChDoAQg2MAM#v=onepage&q=IgG3%20anti%20DNA&f=false

IFN cytokines and pore cytokines ?

IFNbeta and IFN alpha cause monocytes to infiltrate into tissue
https://www.ncbi.nlm.nih.gov/pubmed/12044977

IFN beta

IFN beta and the cytosol infections
https://www.ncbi.nlm.nih.gov/pubmed/18771559

IFN alpha (the nucleus and the mitochondria)

IFN alpha 2B
https://www.ncbi.nlm.nih.gov/pubmed/11426550

Is IFNalphaA the mitochondria while IFNalphaB the nucleus?

IFNalphaA induces apoptosis by the mitochondria
https://www.ncbi.nlm.nih.gov/pubmed/11850845
http://europepmc.org/abstract/med/17158029

IFNalpha2B has been shown to call cancer remission
https://www.hindawi.com/journals/scientifica/2014/970315/

IFNalpha2B and behcet (a nucleus disorder)
http://europepmc.org/abstract/med/7932420
https://www.ncbi.nlm.nih.gov/pubmed/22541781

IFN gamma

IFNgamma....tends to be made more by natural killer cells.  TLR8 which when triggered makes IFNgamma often never gets through.  This is the condition of a viral or foreign infection of the endoplasmic reticulum which means the HLAs may never make it to the surface.

IFN lambda

Is IFN lambda the golgi and is set off by poxvirus????
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424062/

IFN lambda is in the family of il-19
https://www.ncbi.nlm.nih.gov/pubmed/17027511

IFN lambda 1,2,3 suppresses TH2 and pushes fight against viral infection
http://www.jimmunol.org/content/178/1_Supplement/S180.5
http://www.bloodjournal.org/content/113/23/5829?sso-checked=true

influenza A and IFN lambda
https://www.ncbi.nlm.nih.gov/pubmed/18787692

influenza and the golgi
http://onlinelibrary.wiley.com/store/10.1016/0014-5793(89)80668-4/asset/feb20014579389806684.pdf?v=1&t=ja44i6aj&s=23d27958562f6e827b09e685bbc6c08206fdcab6

il-20 and lfn-lamda have short hydrophobic regions and il-24 uses the il-20 receptor....are these all golgi cytokines?


The pore cytokines: il-19, il-22, il-26

il-19 and il-22 have long hydrophobic regions similar to il-26 which is a pore forming cytokine
Are these for fighting infections? Are they pore forming for the nucleus and the mitochondria (il-19) while il-26 pops the plasma membrane? Hypothesis...unclear

il-26 pore: against bacteria and our own cells
http://www.the-rheumatologist.org/article/il-26-plays-antimicrobial-role-in-immune-response/

Autism and cytokines ?

Cytokines

il-4 is a gamma chain cytokine responsible for triggering B cells and T helper cells

il-6 is a GP130 cytokine which increases neutrophils and macrophages

il-8 is also known as the neutrophil chemotactic factor

il-2 is a gamma cytokine triggering T cytotoxic cells (viral infections)

il-1 family cytokines trigger cells to cytokine rain. This produces massive amounts of chemokines. (attractants)

il-1 also induces the expression of adhesion proteins so the arriving immune system knows where to stick.

Th17 (the second popping T helper cells) secrete il-17a (just means the infections are inside host cells  not outside or the virus is in organelles)

il-1 with il-23 at th17 causes them to secrete il-8 which calls the neutrophils

il-22 seems linked to cytosolic bacteria infections and the initiation of Th17

il-23  seem linked to bacterias that move into vacuoles

il-24 seems linked to golgi bacterias

il-26 is a PORE which helps break things down, second popping involving organelles etc.

type 1
Babies born with autism were the result of an autoimmune cross-targeting of the flu and mycoplasmas on the frontal lobe.

key cytokines: IFN gamma and il-4 Because the ER is infected by mycoplasmas, the mother had RA

http://cmr.asm.org/content/17/4/697.full


type 2: Cerebellum Autism: sutterella and the measles vaccine
(is this the regressive form?)

Key cytokine: il-23 because sutterella moves into vacuoles

type 3: temporal lobe autism: HHV6/CMV and tetanus

Key cytokine: IFNalpha a because the herpes viruses involved move into the nucleus
(causes deafness and high pain tolerance?)

measured levels of cytokines comparison of no-regression and regression autism
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991432/table/T2/

neonatal autism cytokine profiles: High il-4
https://www.ncbi.nlm.nih.gov/pubmed/26392128

suggesting an infection is present in the newborns

postmortem autism il-6
https://www.ncbi.nlm.nih.gov/pubmed/23994594
https://vaccinepapers.org/wp-content/uploads/Brain-IL-6-and-autism.pdf

il-17a and severe autism
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410815/
https://www.ncbi.nlm.nih.gov/pubmed/28455196

Hypotheses: 3 types of autism: frontal lobe, temporal lobe, and cerebellum

type 1
Babies born with autism were the result of an autoimmune cross-targeting of the flu and mycoplasmas on the frontal lobe.

il-4 levels are high in neonatal autism supporting the notion that an infection is present.

il-8 and newborns with autism?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080514/

il-8 and mycoplasmas
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146377

il-17a and mycoplasmas
https://www.nature.com/articles/s41598-017-13292-5

TH17 cells are called for a second popping when infections hide inside of cells' organelles

????? Are mycoplasmas so small they are treated like viruses?

mycoplasmas move into cells and nest into the endoplasmic reticulum which should trigger IFN gamma

IFN gamma is higher in mothers of autistic babies in the second trimester
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3554862/

Mycoplasmas are linked to RA which is why I started with them.

Autism babies and mothers with RA: possible increased risk
https://www.ncbi.nlm.nih.gov/pubmed/28319657
http://jaacap.org/article/S0890-8567(17)31766-5/fulltext

What about the TNF alpha?

TNF-alpha and autism
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5669898/

TNF-alpha means that macrophages or dendritic cells or B cells are themselves infected

Is the flu infecting the immune system of autistic children?  Previous blog matched the flu viruses up with dopamine receptors.

dopamine receptors on B cells and RA
https://www.ncbi.nlm.nih.gov/pubmed/25468566

flu shot triggering RA
https://www.hindawi.com/journals/crirh/2012/785028/

Flu virus uses dopamine receptors and the piece of the virus that binds the receptor is still there in the vaccine. The flu is a cytosolic virus. So pieces would go the receptor only to float around in the cytosol.

flu infects NK cells
http://jvi.asm.org/content/83/18/9215.full

dopamine receptors modulate NK cells
https://www.ncbi.nlm.nih.gov/pubmed/23799052



type 2: Cerebellum Autism: sutterella and the measles vaccine
(is this the regressive form?)

Key cytokine: il-23

il-23 and autism
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5038352/

il-23 could be linked to infections hiding in vacuoles

sutterella does move into vacuoles

But sutterella should be part of the regressive form of autism?  regressive appeared to have normal il-23 compared to low il-23 in early onset.

campylobactera (which is similar to sutterella ) and it's cytokines: il-23
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936335/

ASD autism spectrum disorder and il-8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991432/

il-8 and thyroid stimulating hormone in autism
https://www.ncbi.nlm.nih.gov/pubmed/28577577 

sutterella wadsworthensis and il-8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5080374/

measle virus pieces could possible move into cells and attach to the ER

measles were identified in ER by electron microscope images
https://www.researchgate.net/publication/278787836_Histopathology_of_Measles_Report_of_2_Cases_With_New_Findings

So would the vaccine pieces trigger any cytokines?

measles vaccine and cytokines : il-2
https://www.ncbi.nlm.nih.gov/pubmed/12922130

il-2 is a gamma cytokine triggering Tcells (which makes sense because the body thinks a virus is there)

measles vaccine and IFNgamma
https://www.ncbi.nlm.nih.gov/pubmed/9285547

IFN gamma matches up with the ER


type 3: temporal lobe autism: HHV6/CMV and tetanus

Key cytokine: IFNalpha a

previous post
http://angelabiggs.blogspot.com/2015/04/roseola-6th-disease-and-autoimmune.html
it is not proven that HHV6 causes this form of autism and I am still questioning it myself

I just highly suspect that these kids with HHV6 got their vaccine while still sick.

temporal lobe autism group and seizures
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4820486/ 

temporal lobe and HHV6
https://www.ncbi.nlm.nih.gov/pubmed/26933580
https://www.ncbi.nlm.nih.gov/pubmed/17535102
https://www.ncbi.nlm.nih.gov/pubmed/8012736

CMV and autism
https://www.ncbi.nlm.nih.gov/pubmed/17974154

CMV and seizures
https://www.ncbi.nlm.nih.gov/pubmed/18215482

CMV and infant seizures
https://www.ncbi.nlm.nih.gov/pubmed/17718825

HHV6 and seizures
https://hhv-6foundation.org/associated-conditions/hhv-6-seizures

does prenatal exposures of il-6 cause seizures?
https://www.ncbi.nlm.nih.gov/pubmed/26103532

after a seizure il-6 rapidly increases
http://www.sciencedirect.com/science/article/pii/S1059131110003122

HHV6 and lowers il-6 ?
https://hhv-6foundation.org/hiv-aids-progression/hhv-6-shedding-correlates-negatively-with-il-6-and-other-inflammatory-cytokines-in-hiv-patients

Beta-herpes viruses: CMV, HHV6, HHV7 :  Estrogen-related receptors (CMV binding confirmed)

HHV6 TLR9
https://www.hindawi.com/journals/isrn/2013/834890/

HHV6 and CMV infect the nucleus: IFNalpha

IFN alpha and autism?
https://link.springer.com/article/10.1007%2FBF02178169

IFN alpha can cause hearing loss
https://www.ncbi.nlm.nih.gov/pubmed/8561688

autism and hearing loss
https://www.ncbi.nlm.nih.gov/pubmed/10587881

autism and high pain tolerance/sensory issues
http://www.sciencedirect.com/science/article/pii/S0021755717307659

IFN alpha and pain tolerance
https://www.ncbi.nlm.nih.gov/pubmed/10676852

only 30 children tested for HHV6 antibodies...only half had autism and no correlation with autism was found for hhv6 or hhv8
http://iv.iiarjournals.org/content/27/6/843.full

is it CMV?

But I contest that this is a small percent of autism kids anyway and the odds of it showing up  would not be likely...unless their autism kids happened to be of the hear loss kind


Confusion with il-23

Tetanus is a bacteria that would secrete a toxin and move into vacuoles which I have linked to il-23

il-23 is the early onset but not regressive ? (should be both?)
https://www.ncbi.nlm.nih.gov/pubmed/27688738
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5038352/

DTap (with the tetanus) is given at 2 months of age
https://www.webmd.com/children/vaccines/tc/tetanus-topic-overview#1

Does Tetanus trigger il-23???

Early and late epilepsy in autism

"The most frequent type of epilepsy was temporal lobe epilepsy and West syndrome in the early-onset epilepsy group (42.9% and 33.3%, respectively) and temporal lobe epilepsy, frontal lobe epilepsy and other symptomatic generalized epilepsy in the late-onset epilepsy group (each 31.6%). "
https://www.omicsonline.org/open-access/early-and-lateonset-epilepsy-in-autism-high-rate-of-secondarily-generalized-seizures-2165-7890.1000130.php?aid=26012

il-25 aka il-17E is a parastic endoplasmic reticulum cytokine

Hypothesis: the il-25 cytokine appears to be linked to parasites, large infections, that infect/stress the endoplasmic reticulum and stimulates ER growth/repair.

il-17 types (il-17a  is similar to il-25)
https://www.nature.com/articles/emi201358

il-25 and mammary tumors
https://www.nature.com/articles/ncomms11311

increased ER in mammary glands
https://www.ncbi.nlm.nih.gov/pubmed/21920588

is il-25 the growth cytokine for the ER?

Do other infections that move into the ER trigger il-25?

il-17E aka il-25 has been linked to parasite infections ?

il-17E and parasites (il-17 review)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3811766/
https://www.ncbi.nlm.nih.gov/pubmed/22476048
https://www.sciencedirect.com/topics/immunology-and-microbiology/interleukin-17-receptor

trichinella spiralis and ER stress/apoptosis
https://www.ncbi.nlm.nih.gov/pubmed/24996067

trichinella spiralis and il-25
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3811766/

ER and round worms
https://www.ncbi.nlm.nih.gov/pubmed/24996067

Trichinella spiralis uses the host cells a nursery. Specifically the SR of muscles grow the larva
https://link.springer.com/article/10.1007/s004360050494 (electron microscope pictures)

note that il-25 triggers apoptosis in breast cancer cells expressing the il-25R receptor
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199022/

ER stress and cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204165/

Note that this infection is different from viral or mycoplasma infection of the ER which would trigger IFNgamma. In those cases it would be very hard for the immune system to identify an infection was in the cell because of the ER malfunction causing a lack of surface proteins....in the case of worms...a large worm is sitting outside of the host cell. 

TH17 cells second popping cytokines: il-17A, il-17-F, il-17C, and il-17D

6 members of the cytokine 17 family

IL-17A (commonly referred to as IL-17), IL-17B, IL-17C, IL-17D, IL-17E (also known as IL-25) and IL-17F.

https://www.nature.com/articles/emi201358

il-17A has homology to il-17F

il-17F strong associations to mycobacteria (infection that moves into the cytosol)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663007/

TLR3 and mycobacteria
https://www.sciencedirect.com/science/article/pii/S0898656814000345

TLR3 (cytosol) and il-17F
http://www.fasebj.org/doi/10.1096/fasebj.30.1_supplement.966.7

il-17A with mycoplasmas/viruses (infections that move inside of the organelles..vacuoles etc)
https://www.nature.com/articles/s41598-017-13292-5

TLR9 (mitochondria) and il-17A
https://www.hindawi.com/journals/mi/2016/3296307/

TLR7/8 (nuclear or ER) trigger il-17A
https://www.ncbi.nlm.nih.gov/pubmed/19265114

il-17A and the starvation of fungal cells ?
https://www.nature.com/articles/ncomms1685

il-17C fungal infections
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0122807

il-17C is very high in the colon when does this appear? is this made to stick to the outside of infections like fungus? not involved with second popping? made to help kill infections that are large but not as large as worms?

TLR3 and il-17C ?
https://www.ncbi.nlm.nih.gov/pubmed/23944933

does this try to stick to mycobacteria before they move into the cell's cytosol?

note that psoriasis and IBS which are both connected to mycobacteria also both have high il-17

TLR3 cytosol RNA virus (like the flu )
TLR9 mitochondrial DNA virus (herpes zoster)
TLR7 nuclear DNA virus (hpv, epstein barr)
TLR8 endoplasmic reticulum RNA virus (polyomavirus)

the switching to il-17F indicates mycobacteria

il-17 inhibition made IBS and psoriasis worse 
https://www.ncbi.nlm.nih.gov/pubmed/28521565

TB mycobacteria is TLR2 dependent triggering il-17 ? 
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004099

TLR2 and TLR5 triggers il-17C in the mucosa

TLR1 peptidoglycan (found on almost all bacterias and yeasts)
TLR2 modulins (compounds bacterias use to alter or  modulate our cells cytokine messages)
TLR4 lipopolysaccharides (found on gram negative bacteria like e.coli and mycobacteria)
TLR5 flagellins (bacteria tails)/ fungus
TLR6 diacyl lipoproteins (found on gram positive bacteria..like strep)

il-17C and bacteria tails and fungus?

TLR5 and fungus
https://www.ncbi.nlm.nih.gov/pubmed/21067314

il-17D is the ancient cytokine also found in sea lamprey
https://www.ncbi.nlm.nih.gov/pubmed/26491201

il-17D triggers the cytokines il-6 (increases activation of neutrophils/macrophages) il-8 (neutrophil chemotactic factor) and gm-csf (beta side chain that favors myeloid side of development creating macrophages)

asks the immune system to come eat the infection without popping?

il-17E is il-25 which is used against parasitic infections
https://www.ncbi.nlm.nih.gov/pubmed/22476048