Attempting to match up the TLRs of bacterial infections with the TGF-betas: added TGF-beta5

So which TLRs trigger the the TGF-Bs?  The location and the behavior of the bacterias determine which TLR

Are TGF-betas triggered to repair a damaged organelle?

TLR 7/9 and TGF-B1 : mitochondria bacteria

TLR9 stimulant produced TGF-B1
https://www.ncbi.nlm.nih.gov/pubmed/22536167

TGF-B1 and mitochondria
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444292/ 
https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcp.20753

TLR9/7 and TGF-B1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372299/


TLR2/1  and TGF-B3 : Vacuole bacteria

TLR2 which senses modulins (staph example)
https://www.nature.com/articles/ncomms12304

These bacterias, like staph, if they move into cell do so through vacuoles
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3417557/

lysteria and TLR2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC375211/

TLR2 triggers  il-23 and TGF-B3 (assuming vacuole damage)


TLR2/6 with TLR4 and TGF-B2: cytosolic bacteria

TLR6 bind lipoproteins found on gram positive bacteria like strep or mycobacterias

cytosolic replication of strep in macrophages
http://mbio.asm.org/content/7/2/e00020-16.full

lipoproteins on mycobacterias
https://www.ncbi.nlm.nih.gov/pubmed/15539077

there is a cytosolic sharing between Tcells and cancer cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3813479/

TGF-B2 is high expressed by fibroblasts interacting with cancer cells
https://www.ncbi.nlm.nih.gov/pubmed/27880067/

Does TLR6 trigger il-22 and TGF-B2?

TLR
http://www.pnas.org/content/108/9/3683.full.pdf

mycobacteria triggers: tlr2 tlr6 tlr4

synergism of tlr2 tlr6 and tlr4....causes TNF alpha
https://www.ncbi.nlm.nih.gov/pubmed/19428561

TNF alpha means the immune system is infected

TLR3 and TGF-B4 : golgi bacteria

salmonella and il-24
https://www.ncbi.nlm.nih.gov/pubmed/19830736

salmonella infects the golgi

salmonella trigger tlr3 and tlr4

https://www.researchgate.net/publication/295503655_Salmonella_Suppresses_the_TRIF-Dependent_Type_I_Interferon_Response_in_Macrophages

Does tlr3 trigger il-24 and TGF-B4 ? as well as IFN beta and HLA-D?


note that the golgi and melanoma are linked
http://cancerres.aacrjournals.org/content/30/9/2326

melanoma cell death, il-24 and IFN-beta are linked
https://www.ncbi.nlm.nih.gov/pubmed/18511292


What about the ER? Mycoplasmas hide there....can this link to TGF-beta5 ?
TLR2/6

Mycoplasmas trigger TLR2 and TLR6
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613965/

tlr2 with tlr6 trigger IFNgamma then CXCL10 (in cancer cells)
https://www.ncbi.nlm.nih.gov/pubmed/25765738

CXCL10 is the IFNgamma inducing cytokine
https://en.wikipedia.org/wiki/CXCL10

When a virus infects the ER we have already linked il-8 with IFNgamma

Obviously your immune system has already learned that the combination of tlr2 and tlr6 means something that likes to hide in the Endoplasmic reticulum (ER)

Does ER stress trigger the TGF-beta5 pathway?

ER stress and TGF-beta pathways
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5247721/

The ER is intimately involved with the calcium fluxes in neurons
https://www.ncbi.nlm.nih.gov/pubmed/12543098

In amphibians TGF-beta5 has been linked to neurogenesis
http://www.jbc.org/content/265/2/1089

which makes sense if the ER's ability to flux calcium is so involved with neuron function

Can we link the TLR2 with TLR6 with TGF-beta5?

Brucella abortus also hides in the ER
https://www.ncbi.nlm.nih.gov/pubmed/9826346?dopt=Abstract

tlr6 with tlr2 detects Brucella infections
https://www.ncbi.nlm.nih.gov/pubmed/23460520

Validating the pattern

Looking at TGF beta when there are bacterial infections inside the cell

Looking at TGF beta for bacterial infections inside the cell: Is this growth factor for repairing the damaged organelle? Or fighting cancer?

il-17 TGF-B1 mito/nuclear infections (il-17a?)

il-23 TGF-B3 vacuoles infections

il-22 TGF-B2  cytosol infections or cancer (cytosolic exchange with T cells)

il-24 TGF- B4 golgi infection and neurulation?

Mitochondrial respiration and TGF-b1
http://www.jbc.org/content/early/2012/12/04/jbc.M112.431973.full.pdf

TGF-B1 and the appearance of the mitochondria
http://onlinelibrary.wiley.com/store/10.1002/aja.1002030304/asset/1002030304_ftp.pdf?v=1&t=jal68y40&s=122ea55960ca0b6d4b21a9aad0428cf0f75d6f47&systemMessage=Wiley+Online+Library+usage+report+download+page+will+be+unavailable+on+Friday+24th+November+2017+at+21%3A00+EST+%2F+02.00+GMT+%2F+10%3A00+SGT+%28Saturday+25th+Nov+for+SGT+

TGF-B1 and DNA repair
https://www.ncbi.nlm.nih.gov/pubmed/12384514

male infertility and TGF-b3
https://www.nature.com/articles/srep17151

spermhead vacuoles and fertility debate
https://www.hindawi.com/journals/bmri/2014/927841/

Chlamydia which infects in a vacuole triggers TGF-B3
http://iai.asm.org/content/81/12/4583.full.pdf

Tcells,  tumors, and the cytosol : there is an exchange of cytosol content
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0078558

cytosolic viruses increase TGF-B2
http://onlinelibrary.wiley.com/doi/10.1002/hep.29319/abstract
http://pubmedcentralcanada.ca/pmcc/articles/PMC4583434/

il-22 is produced by cancer associated fibroblasts
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134496/

Does mycobacteria which infects the cytosol increase TGF-B1 and  TGF-B2 ?

increased expression of the receptors in Tuberculous
https://www.ncbi.nlm.nih.gov/pubmed/12641657

Salmonella infects the golgi

Salmonella and TGF-B4
https://www.ncbi.nlm.nih.gov/pubmed/25935756

TGF-B4 higher in muscles and nerves
https://www.ncbi.nlm.nih.gov/pubmed/1304823

How much golgi exists in nerves and muscles? Is there a lot which is why the golgi was discovered in nerves?

So...T17 cells secrete cytokines: il-17a, il-23, il-22, il-24 which can stimulate repair in the areas infected through the linked TGF-beta?

20 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

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)

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 polymerase..so 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.  

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.

Cytokine families

The functionality of cytokines becomes obvious when they are organized into groups.

Type one cytokines work primarily at the Hematopoiesis and these can be divided into 3 groups:

Cytokines using beta chains, cytokines using gamma chains, and the GP130 cytokines.

The development from myeloid progenitor cells involves the beta chain cytokines;

the development from lymphoid progenitor cells involves the gamma chain cytokines;

 and the GP130 cytokines are powerful regulators.  GP130 cytokines control neutrophils,

macrophages, natural killer cells, the "on switches or launch codes" for B cell development il-4 and

il-12, and the  "on switch " for either Treg or TH17 cells.

cytokine receptor family review
http://www.sinobiological.com/Cytokine-Families-Cytokine-Family-a-5797.html

The GP130 Family: il-6, il-11, and TGF-beta

il-6 monocytes to macrophages
https://www.ncbi.nlm.nih.gov/pubmed/10848814

il-6 controls il-4
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2196041/

il-11 stops the macrophages from producing il-12
https://www.ncbi.nlm.nih.gov/pubmed/11940481

il-11 and Nk development
https://www.ncbi.nlm.nih.gov/pubmed/15499555

TGF beta and TH17
https://link.springer.com/chapter/10.1007/978-1-4419-9371-7_3

(TH17 can be started by il-6 or TGF-beta1 but it is my hypothesis that different cytokines result )

GP130
https://en.wikipedia.org/wiki/Glycoprotein_130

il-10 is the stop cytokine

il-10 stops pg130 cytokines (neutrophils macrophages and NKs)

il-10 stops T FH cells from secreting il-4 and il-21 which stops the GC from producing B cells

 il-10 and gp130
https://www.ncbi.nlm.nih.gov/pubmed/22140267


Cytokines using Beta chains: il-3, il-5, GM-CSF are all on the myeloid side

Cytokines using Gamma chains: il-2, il-7, il-15, il-21, il-4, il-9  are all on the lymphoid side


The il-1 family cytokines and Chemokines

When an infection occurs the first cytokine made by macrophages and monocytes is the  il-1 family cytokines.

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

il-1 induces fibroblasts to produce chemokines which are attractant proteins.

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


The IFN family cytokines 
These cytokines identify where inside the host cell the virus is hiding and coordinates the immune response attack. Which HLA to express and which TAM hands to wear.

cytosol            TLR4     IFNbeta      HLA-D               Tyro3

Nucleus/ Mito    TLR7/9   IFNalpha    HLA-A HLA-B   Mer

Endoplasmic R   TLR 8     IFNgamma HLA-C                 Axl
Golgi               TLR3 IFN lambda


The il-20 Family Cytokines: the H+ pore cytokines il-20, il-19, il-24, and il-26 ? this hypothesis is still being tested

il-26 and pore structure...and TLR9
https://www.ncbi.nlm.nih.gov/pubmed/?term=il-26+pore

The TH17 cells are involved with the second popping.

il-23 and il-6 trigger Th17 secreting cytokines against hiding bacteria: il-24 the golgi and il-22 the vacuoles.

(dendritic cells secrete il-23 after TLR4 stimulation and B cells secrete il-6 after TLR4 stimulation which is two sources of verification. )

When the virus is hiding in the nucleus or the mitochondria these organelles must be opened in order for the virus to be seen.

il-21 is made by Tcd8+ cells exposed to il-6  and TGF-B1 ( secreted when the mitochondria and nuclear TLR 9/7  of cells are triggered) cause Th17 to secrete il-19 the mitochondria and il-26 the nuclear pore.

Summary:
 il-24 golgi
il-22 vacuoles
il-19 mitochondria ?
il-26 nuclear membrane  (or extra cellular bacteria)

is il-20  the plasma membrane?

il-24 salmonella in the golgi
https://www.ncbi.nlm.nih.gov/pubmed/19830736    il-24 salmonella
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC204495/  Salmonella and golgi

il-22 inhibited autophagy
http://www.ijbs.com/v08p0249.htm

autophagy is required for hyper mucus production
https://www.ncbi.nlm.nih.gov/pubmed/26671423
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5044763/

Is il-19 the mitochondria and il-26  the nucleus?
http://angelabiggs.blogspot.com/2018/02/il-19-is-mitochondrial-pore-il-26-is.html

 il-18 is the ER which means the cells have lost their self proteins and can be attacked like an infection but still need the TH17 because the infection is hiding in the ER.



il-35 is the complete stop cytokine, one level up from il-10, this cytokine stops inflammation as well as the immune reaction.  The key cytokine of Treg and Breg suppressing reactions. 

il-35 is secreted by T regulatory and is required for their function
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008395/

il-35 and B regulatory cells
https://f1000.com/prime/718289707
http://www.sciencedirect.com/science/article/pii/S0091674917314343

il-35 stops th17
https://www.ncbi.nlm.nih.gov/pubmed/17874423 

This Th17 section with the hiding infections is a hypothesis and needs to be proven.

4 possible types of asthma from fungal, mycobacteria, staph, and H.pylori infections?

Mycobacteria Asthma

SERT and cGMP
http://www.ncbi.nlm.nih.gov/pubmed/19656393
http://www.jneurosci.org/content/27/40/10878.full

bipolar and type 2 diabetes
http://www.ncbi.nlm.nih.gov/pubmed/22621171

bipolar, metabolic disorder, and autoimmune disorder
http://www.ncbi.nlm.nih.gov/pubmed/25237732

older post with 2 types of bipolar:
http://angelabiggs.blogspot.com/2015/07/is-bipolar-disorder-autoimmune-disorder.html

CMV with schizophrenia and bipolar..is this bipolar 1 which is autoimmune while the mycob. is not?
http://www.ncbi.nlm.nih.gov/pubmed/24083998

Mycobacteria's cGMP : asthma, type 2 diabetes, and metabolic syndrome

cGMP and asthma
http://www.ncbi.nlm.nih.gov/pubmed/6258958

 asthma and metabolic syndrome
http://www.ncbi.nlm.nih.gov/pubmed/25789301

high cholesterol and asthma
http://www.ncbi.nlm.nih.gov/pubmed/16754527

cGMP is inhibited at night
http://www.jneurosci.org/content/23/20/7543.full.pdf

Is this the nighttime asthma?

Fungal Asthma

Baker's asthma and rhinitis
http://www.ncbi.nlm.nih.gov/pubmed/0009847440

female athletes were found to have worse asthma when the cycle had high progesterone which effects smooth muscles

https://books.google.com/books?id=HY9PiQL3kQMC&pg=PA394&lpg=PA394&dq=exercise+induced+asthma+thyroid&source=bl&ots=ahNvkskYXH&sig=BBdmHlRXtcEbwh7UTKaFdsgaBcE&hl=en&sa=X&ved=0ahUKEwiFsOSal4fKAhUB6WMKHRPDBDsQ6AEIQzAF#v=onepage&q=exercise%20induced%20asthma%20thyroid&f=false

vitamin D and p450
http://www.ncbi.nlm.nih.gov/pubmed/23564710

p450 causes vasodilation issues

exercise in cold air normally induces vasodilation

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4580801/

vit D and exercise asthma
https://www.researchgate.net/publication/47755411_Serum_vitamin_D_levels_and_exercise-induced_bronchoconstriction_in_children_with_asthma

asthma, hypothyroid, and noncardiogenic pulmonary edema
http://www.ncbi.nlm.nih.gov/pubmed/25866647

Second generation anti-histamines are substrates or modulators of p450

Are fungal infections the cause of exercise induced asthmas?


Staph asthma

eczema was connected to indoor allergies

is this the aspirin sensitive asthma?
http://www.ncbi.nlm.nih.gov/pubmed/23564710

note that staph does not like aspirin
http://dartmed.dartmouth.edu/winter03/html/vs_aspirin.shtml

the quorum of MARSA is phenol-soluble modulin (not in normal staph)
https://en.wikipedia.org/wiki/Phenol-soluble_modulin

high phenols where found in the urine of asthma patients but were assumed to be that of pesticides
http://www.medpagetoday.com/MeetingCoverage/AAAAI/37516

phenols induce vasodilation...red wine
http://www.ncbi.nlm.nih.gov/pubmed/15967426

 chronic urticaria can also be triggered by aspirin and has good response to second generation antihistamines

Aspirin induced asthma
https://en.wikipedia.org/wiki/Aspirin-induced_asthma

Samters triad: asthma, polyps, aspirin allergy


H. pylori/ Campylobacteria with asthma or it really COPD ?

COPD increases the risk of infection
https://www.ncbi.nlm.nih.gov/pubmed/15534156
https://www.ncbi.nlm.nih.gov/pubmed/21175903

gerd (gastric reflux ) and asthma
http://www.mayoclinic.org/diseases-conditions/asthma/expert-answers/asthma-and-acid-reflux/faq-20057993

asthma and COPD overlap
https://www.ncbi.nlm.nih.gov/pubmed/25712010
https://www.ncbi.nlm.nih.gov/pubmed/28283854

GERD and COPD
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4574848/

COPD and h.pylori? questionable
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261373/
https://www.ncbi.nlm.nih.gov/pubmed/15733502

h.pylori and adult onset asthma (it is protective in children)
https://link.springer.com/article/10.1007%2Fs10096-017-2972-1

COPD and peptic ulcers
https://www.ncbi.nlm.nih.gov/pubmed/22348540
https://www.jwatch.org/jg201203090000003/2012/03/09/copd-associated-with-increased-risk-peptic-ulcer

smoking and peptic ulcers
https://www.ncbi.nlm.nih.gov/pubmed/3053883

smoking, peptic ulcers, and H.pylori
https://www.ncbi.nlm.nih.gov/pubmed/10958211

H.pylori and bronchitis
https://www.ncbi.nlm.nih.gov/pubmed/16565595

Fish allergy
Tree nut allergy not involving peanuts : walnuts, pecans
Cat hair allergy

almond milk and GERD
http://www.aaaai.org/ask-the-expert/food-reaction-gerd

Pine nut oil as a cure for peptic ulcers
https://www.linkedin.com/pulse/get-rid-peptic-ulcers-good-pine-nut-oil-janice-rosenthal/

http://www.sacredearthnetwork.net/group/medicinewheelnaturesremediesandrecipeslotionsandpo/forum/topics/siberian-pine-nut-oil-how-a-folk-remedy-found-its-way-into-scient

Does h.pylori and campylobacteria not like something in tree nuts?

Bacteria ulcers are a common fish problem.  Could this cause the fish allergy somehow?


ataxia and GERD
https://www.ehealthme.com/cs/gerd/ataxia/

ataxia, h.pylori and Stomach problems
https://healthunlocked.com/ataxia-uk/posts/134618233/ataxia-stomach-problems-and-lycopene

could this cause the fish allergy?

histamine fish poisoning ???
https://emedicine.medscape.com/article/1009464-overview

h.pylori and histamine ????
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC496809/

Follicular dendritic lymphoma and Co-carcinogenesis

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.

follicular lymphoma
http://www.cancerresearchuk.org/about-cancer/follicular-dendritic-cell-fdc-sarcoma/about

Castleman's disease and HHV8
https://en.wikipedia.org/wiki/Castleman%27s_disease

HHV8 is the Kaposi's sarcoma virus
https://en.wikipedia.org/wiki/Kaposi%27s_sarcoma-associated_herpesvirus

vaccine against follicular lymphoma
https://www.news-medical.net/news/2005/11/09/14390.aspx

Tattoo ink as the carcinogen of the lymph nodes
https://www.researchgate.net/publication/230570212_Tattoo_Pigment_Lymphadenopathy_Mimicking_Metastasis_in_Vulvar_Cancer

With the current popularity of Tattoos will this form of cancer increase?

HHV8 and the alpha estrogen receptor
http://d-scholarship.pitt.edu/13517/

alpha estrogen receptor is a marker for follicular dendritic cells
https://www.ncbi.nlm.nih.gov/pubmed/14507640

In order for Cancer to occur the virus must trigger the cell division cycle.  Knudson's Retinoblastoma protein genes are the target of nuclear viral proteins.
http://www.nature.com/onc/journal/v25/n38/full/1209621a.html

Knudson's 2 hit RB cancer gene is the lynch pin to the cell division cycle start
http://angelabiggs.blogspot.com/2017/10/knudsons-heredity-2-hit-cancer-compared.html
(this form does not involve a viral start but most cancers will need a virus to pull this lynch pin)

TNF family, Follicular Dendritic Cells, Macrophages, and MAST cells

TNF beta (lymphotoxin-alpha)  Is secreted and worn by Bcells to stimulate Follicular Dendritic Cells.  This TNF-beta is required for the Peyer Patch and secondary lymph nodes development but how is it involved in infection?

FDC are not really dendritic cells; they are non migratory cells at the lymph nodes involved in the development of Bcells

TNF C (lymphotoxin-beta) Is worn by macrophages and dendritic cells (APC) when they are infected by bacterias.  The lymphotoxin receptor is on Mast cells.   While TNF-alpha is secreted by macrophages infected themselves by viruses or bacteria.

lymphotoxin-beta and macrophage intracellular infection
https://www.ncbi.nlm.nih.gov/pubmed/12734369

lymphotoxin-beta receptor of mast cell triggers TLR4 and impairs TLR9
http://www.jimmunol.org/content/188/7/3426

Mast cells normally produce TGF-B1 which triggers a viral response acting on T9 cells .
When the TNF-c receptor of the mast cell is activated the TLR9 (mitochondrial virus butterfly net) is impaired and the TLR4 which is a bacterial vacuole butterfly net is focused on by the Mast cell.  The Mast cells which were focused on viruses are refocused on bacterias that can infect the host's cells.

lymphotoxoin-beta also leads to il-8 release (receptor is on most cells but not B and T cells).

il-8 calls the neutrophils to poison and trap bacteria coming out of host cells

So the question is does the Bcell TNF-beta (lymphotoxin-alpha) expression match up with the possible infections of B cells?

Flu virus and Bcells with TNF
http://www.jimmunol.org/content/169/11/6193
https://onlinelibrary.wiley.com/doi/full/10.1002/eji.200626255

Follicular dendritic cells, the Fc receptor, and albumin antigen binding

Follicular dendritic cells

Review paper of FDC
https://www.ncbi.nlm.nih.gov/pubmed/12163300

Albumin and IgG: the Fc receptor binds both
https://www.frontiersin.org/articles/10.3389/fimmu.2014.00682/full

Fc receptors on Follicular dendritic cells
https://www.ncbi.nlm.nih.gov/pubmed/10843680
https://www.ncbi.nlm.nih.gov/pubmed/14634109

HIV infects FDC cells
https://www.ncbi.nlm.nih.gov/pubmed/12163303

HIV is a retrovirus. Retroviruses infect using LH/albumin binding receptors (my hypothesis). Could HIV infect using the Fc receptors?
http://angelabiggs.blogspot.com/2017/03/albumin-binding-receptors-and.html

human serum albumin alone binds bacterial products
http://www.sciencedirect.com/science/article/pii/S0168827814002657

albumin and the immune system
http://www.scopemed.org/?mno=10124


FDC have high levels of C3 complement receptors and they display the antigen carried by them or from antibodies taken in by Fc receptors.

Could FDC also be taking in albumin with antigens bound to them using the Fc receptor?

TNF alpha increased plasma albumin
https://www.ncbi.nlm.nih.gov/pubmed/9513905

peyer's patches removed caused higher albumin
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1554968/

the lymph fluid contains albumin as well...think of albumin as an protein sponge collecting things

How do follicular dendritic cells collect antigens for display? Can FDC collect antigens from albumin?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3023135/