Monday, January 22, 2018

IFN cytokines and pore cytokines ?

IFNbeta and IFN alpha cause monocytes to infiltrate into tissue

IFN beta

IFN beta and the cytosol infections

IFN alpha (the nucleus and the mitochondria)

IFN alpha 2B

Is IFNalphaA the mitochondria while IFNalphaB the nucleus?

IFNalphaA induces apoptosis by the mitochondria

IFNalpha2B has been shown to call cancer remission

IFNalpha2B and behcet (a nucleus disorder)

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????

IFN lambda is in the family of il-19

IFN lambda 1,2,3 suppresses TH2 and pushes fight against viral infection

influenza A and IFN lambda

influenza and the golgi

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(il-19) and the mitochondria (il-22) while il-26 pops the plasma membrane? Hypothesis...unclear

il-22 rescued cells from acetaminophen liver damage

is il-22 a pore for the mitochondria? Does it stop the mitochondria from swelling?

acetaminophen caused mitochondria in liver to swell
which was rescued by the drug cyclosporine A which binds the mitochondria transition pore

il-19 appears in cancers which could involve nuclear swelling
the expression of il-19 might allow cancer cells to live when they would have otherwise burst

il-26 pore: against bacteria and our own cells

note that some mycoplasmas infect the nucleus not just the ER

This could explain why some cases of RA have il-19
some RA would be caused by mycoplasmas hominis with proteins penetrating the nucleus?

The cytokines would still interact with receptors but the action as a pore would explain the other characteristics.

Thursday, January 18, 2018

Autism and 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

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

neonatal autism cytokine profiles: High il-4

suggesting an infection is present in the newborns

postmortem autism il-6

il-17a and severe autism

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?

il-8 and mycoplasmas

il-17a and mycoplasmas

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

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

Autism babies and mothers with RA: possible increased risk

What about the TNF alpha?

TNF-alpha and autism

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

flu shot triggering RA

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

dopamine receptors modulate NK cells

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

Key cytokine: il-23

il-23 and autism

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

ASD autism spectrum disorder and il-8

il-8 and thyroid stimulating hormone in autism 

sutterella wadsworthensis and il-8

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

measles were identified in ER by electron microscope images

So would the vaccine pieces trigger any cytokines?

measles vaccine and cytokines : il-2

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

measles vaccine and IFNgamma

IFN gamma matches up with the ER

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

Key cytokine: IFNalpha a

previous post
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 

temporal lobe and HHV6

CMV and autism

CMV and seizures

CMV and infant seizures

HHV6 and seizures

does prenatal exposures of il-6 cause seizures?

after a seizure il-6 rapidly increases

HHV6 and lowers il-6 ?

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


HHV6 and CMV infect the nucleus: IFNalpha

IFN alpha and autism?

IFN alpha can cause hearing loss

autism and hearing loss

autism and high pain tolerance/sensory issues

IFN alpha and pain tolerance

only 30 children tested for HHV6 antibodies...only half had autism and no correlation with autism was found for hhv6 or hhv8

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?)

DTap (with the tetanus) is given at 2 months of age

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%). "

Wednesday, January 17, 2018

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)

il-25 and mammary tumors

increased ER in mammary glands

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)

trichinella spiralis and ER stress/apoptosis

trichinella spiralis and il-25

Trichinella spiralis uses the host cells a nursery. Specifically the SR of muscles grow the larva (electron microscope pictures)

note that il-25 triggers apoptosis in breast cancer cells expressing the il-25R receptor

ER stress and cancer

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 the case of worms...a large worm is sitting outside of the host cell. 

Tuesday, January 16, 2018

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.

il-17A has homology to il-17F

il-17F strong associations to mycobacteria (infection that moves into the cytosol)

TLR3 and mycobacteria

TLR3 (cytosol) and il-17F

il-17A with mycoplasmas/viruses (infections that move inside of the organelles..vacuoles etc)

TLR9 (mitochondria) and il-17A

TLR7/8 (nuclear or ER) trigger il-17A

il-17A and the starvation of fungal cells ?

il-17C fungal infections

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 ?

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

TB mycobacteria is TLR2 dependent triggering il-17 ?

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 strep)

il-17C and bacteria tails and fungus?

TLR5 and fungus

il-17D is the ancient cytokine also found in sea lamprey

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

Sunday, December 24, 2017

Hypothesis: When a second popping is needed when fighting an infection Th17 and Tc17 are created

Bacterial infections can move inside of host cells and hide. Viral infections can further hide inside of organelles. When these states occur a second popping must occur in order to expose the infections.

Two types of 17 cells exist.

Th17 (the hiding bacteria)

dendritic cells produce il-23 when calling macrophages

Bcells produce il-12 to stimulate Th1, il-6 to stimulate Th17, and il-15 to stimulate Tc

il-23 together with il-6 activate Th17 cells

Th17 cells produce il-17F/F and il-17A/F

Hypothesis: mycobacteria triggers il-17F by hiding in the cytosol of host cells . While mycoplasmas which hide in organelles trigger il-17A

Tc17 (the hiding virus)

Tcells interacting with Bcells through the HLA and Tcellreceptor produce il-4 and il-21

TLR 7/9  (butterfly nets triggered by DNA) produce TGF-beta1 
these TLRs identify mitochondrial or nuclear viruses

il-21 with TGF-beta1 triggers Tc17

Tc17 cells produce il-17A/A ad il-17A/F

Tc17 expresses il-17A/A and Th expresses more il-17F/F


il-33 stimulates Th2 (inflammation pathway)

il-33 during fungal infections suppresses some T17 pathways

Does a fungal infection increase il-26  at times? il-26 is the pore cytokine which would help break a fungal infection down

Sunday, December 10, 2017

Cytosolic Viruses bind HLA-dr and HLA-dp bind Large infections so do HLA-dq bind membrane crossers?

HLA class one stimulate T cd8 cells (cytotoxic)  involving viral infections
HLA class two stimulate T cd4 cells (helper) involving large visible infections...or cytosolic viruses?

What is the difference between HLA-DR, HLA-DQ, and HLA-DP?

After the inane response, the T cells are informed through the HLA mailboxes.  Either large infections have be broken down by APC or infected host cells have started leaking viruses. When the viruses are in the cytosol only one "popping" of the host cell is needed for things to be visible to the immune system.

HLA-DR are viruses that exist in the cytosol enough so that when the infected cells are popped the viruses are immediately seen.


Flu of the cytosol HLA-DR

E.coli outside the cell: HLA-DP

Reoviruses damages the golgi

Flu damages the golgi

However they replicate their viral RNA in different places. The flu moves into the nucleus while the reoviruses stay in the cytosol.

Reoviruses and the cytotol

Flu uses the RNA polymerase II

Flu viruses move into the cytosol before moving into the nucleus

RNA Polymerase I makes Ribosomal RNA  (rRNA)
RNA Polymerase II makes mRNA
RNA Polymerase II makes tRNA

Which means that the flu as an RNA virus does make it into the nucleus but it is not binding DNA polymerases. Is this the difference between cancer causing viruses?

Herpes viruses on the other hand involve the DNA polymerase...replacing it with their own


HLA-DP and large infections

HLA-DP and HLA-DQ are connected to the Hepatitis B virus

Like the flu, hepatitis B enters the cytosol first and then the virus enters the nucleus but it is HLA-DQ?

Maybe because retroviruses like HBV have a special DNA polymerase called a  reverse transcriptase which takes mRNA in the cytosol and converts it to DNA.

T.gondii and HLA-DQ3

celiac HLA-DQ2 and HLA-DQ8

Strep HLA-DQ4

21 Medical Hypotheses

1. Allergy hypothesis: Allergies reveal the infections we have.  Severe allergies and infections can be matched up: peanut and Staph, bee and T.gondii, daisy and Clostridium, poison ivy and spirochetes. If an infection can be killed by a compound or inhibited by the compound our immune system sees the interaction and we associate all the compounds present with the infection.  If an infection makes a pigment from a compound we will react to that too.  For example aflatoxin with peanuts could cause staph to counter respond.  Our immune system would identify everything there at the scene of the crime as part of the infection.

2. Quorum hypothesis: Infections talk using quorums and these quorums interfere with our body's pathways. ( for example mycobacteria's cGMP causes such things as type 2  diabetes, high cholesterol, and synuclein bodies)

3.. Autoimmune cross-targeting hypothesis:  The Cross-targeting of simultaneous infections on one tissue, one infection inside and one infections outside, triggers autoimmunity.  Antibodies or chemicals/drugs can replace one of the infections.  By antibodies I mean even those triggered by vaccines.  For example a flu virus inside of the pancreas and e.coli latching on to the outside could trigger type one diabetes.

4. Co-carcinogenesis: a virus and a carcinogen together cause cancer. Taking Francis Peyton Rous’ hypothesis further, the carcinogen is a polymerase inhibitor which binds the viral polymerase with higher affinity. Thus the DNA methylation state has been changed but the virus is no longer viable.  DNA damage does not cause most cancers, the interaction of carcinogens and viruses do.  Further these cancers wear the receptors that the virus that triggered it used to enter and the characteristics of the cancer will be from the receptor's pathways.

5. Barrier crossing infections are ones that can cross the intestine or the blood brain barrier causing gluten sensitivity with the hole they leave behind. This explains the gluten sensitivity of Schizophernia from T.gondii, Celiac disease from e.coli, Tourettes from staph, and crohn’s from mycobacteria.

6. Viral families use receptor families. Influenzas use dopamine receptors. HPVs use Cannabinoid receptors. Herpes viruses use estrogen and estrogen-like receptors. Flaviviruses use melanocortin receptors. Polyomaviruses use serotonin receptors.

7. Aflatoxin like compounds cause tau bodies.  ALS and picks disease are caused by different infections but both have tau.  Both infections secrete an aflatoxin like compound.  Vitamin D is protective against it because aflatoxin uses the vit D receptor.

8. Pituitary tumors are caused by an infection releasing butyrolactones which interfere with normal GABA signals and cause the immune system to confuse nerves with the infection. (or someone taking too many GHB sleeping pills)

9.  The receptors used by a virus when triggering autoimmunity cause pathways to be activated which makes the various types of one autoimmune disease.  There are 3 types of schizophrenia which match up with the 3 receptors use by the 3 herpes viruses. (sort of a continuation of 6)

The receptor pathway triggered by a virus involved in an autoimmune disease can cause symptoms of the disease that will be distinct. Example:  The 3 types of schizophrenia has all 3 herpes virus families and each receptor activated can be matched to symptoms.  Estrogen-related receptor and disorganized symptoms for example.  3 receptors used equals 3 types of schizophrenia

10. Alzheimer's disease is caused by damage to the mitochondria: alpha-herpes family, diacetyl, inherited and linked to down syndrome, or radiation damaged mitochondria.

11. Postural orthostatic tachycardia could be caused by reoviruses and the adrenergic receptors they bind.

12.  The HLAs are mailboxes for T cells from different areas of the cell. HLA-A is the nuclear mailbox. HLA-B is the mitochondria's mailbox. HLA-C is the endoplasmic reticulum's mailbox. HLA-DR is the cytosol's mailbox for RNA viruses. 

HLA-DQ is the cytosol's mailbox for non-encapsulated viruses there. HLA-DP is the plasama membrane mailbox.

13. Carcinogens use certain receptors to get into cells which matches them up with specific cancers.

14. TLRs, toll like receptors, are the innane immune system of nets catching conserved molecules in a non specific way but identifying the region as well as general type of infection. Like HLAs they exist in the different areas of the cell.  When the internal viral seeking TLRs are activated the IFN matches the region they are in thus the appropriate HLA is produced helping to find the exact culprit.

15. TLRs send IFNs which tells infected cells to express the corresponding HLAs and macrophages to wear the corresponding TAMs (hands to grab infected cells) TAMS: tyro T , axl A , mer M

Gogli  (cytosol)            TLR3      IFNbeta      HLA-D               Tyro3
Nucleus/ Mito    TLR7/9   IFNalpha    HLA-A HLA-B   Mer
Endoplasmic R   TLR 8     IFNgamma HLA-C                 Axl

  Because an ER infected means little gets to the surface of a cell Natural killer cells step in here and secrete IFNgamma.

Cytosolic viruses go through the golgi before exiting which is why they are trigger TLR3.

16. Nuclear viruses awaken embryonic Hervs.  They do so by methylating or demethylating DNA.  If the virus family demethylates the cancer will be aggressive while the methylating viruses are slow growing.  (Cancer occurs when a carcinogen inhibits the viral the virus opens the DNA up but can't use it)

17. Bacterial infections will hide inside of host cells like viruses. Hypothesis:  Like the IFN cytokines there should be cytokines that signify where in the host cell they are hiding.  Mycoplasmas nest inside the ER, chlamydia hide in vacuoles, salmonella hide in the golgi, and mycobacteria sit in the cytosol.   The cytokines seem to match up the features of an infection family with where they hide inside.  

For example infections that use modulins tend to move into vacuoles when infecting the host so TLR2 triggers il-23 which then (in hypothesis 20) triggers TGF3 which repairs vacuoles.

18. Could there be 4 different types of asthma caused by different infections which could be diagnosed using cytokine patterns and the allergies present in the host.

19.  The problem concerning autism and vaccines could be solved if autism is viewed as an autoimmune disease.  The autoimmune cross-targeting hypothesis when applied to autism reveals there could be 3 different types of autism:

Group Flu and RA : frontal lobe autism
Group DTP (tetanus) and HHV6 : temporal lobe autism
Group MMR and sutterella/ campylobacteria: cerebellum autism

Two of these have been linked to vaccines the MMR and the DTP.

Combining the notion that viruses use receptors to enter cells with the notion that "parts" of a virus can set off autoimmunity on the tissue one can only conclude that what is contaminating vaccines setting off autoimmunity are the tiny pieces the virus uses to bind the receptors.  Running vaccine solutions through binding columns of the receptors could "clean " the vaccine of the one piece that triggers the autoimmunity.

20. TGF-Beta has been linked to both embryogenesis and cancer as well as the immune system.  The area an infection could be damaging causes a specific TGF-B to repair the area. First the TLR butterfly net is triggered by the infection.

TLR7 or TLR4  trigger TGF-B1 which stimulates the mitochondria, TLR2 triggers TGF-3 because the infections that use vacuoles tend to be the same ones that use modulins, TLR-6 which binds lipoproteins found on gram positive bacteria and mycobacterias which divide in the cytosol triggers TGF-b2 which encourages Tcells to check the cytosol of cells, finally TL3 of the golgi triggers TGf-B4.  TGF-B4 stimulates growth of the golgi.

21. T helper17 and Tc17 cells are involved in second pops.  When does this happen? When large infections move inside of host cells or viral infections are hiding inside of the mitochondria or nucleus. When the viruses are not visible in the cytosol or ER which would be visible when the host cell is popped. Thus a "second popping" must occur.