TGF-B1 burst part of the CTL pathway (nuclear or mitochondrial viral infections)

TGF-B1 burst part of the CTL pathway (nuclear or mitochondrial viral infections)

cmv (a herpes virus) and epithelial cells secreted TGF-b1
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001170

TGF-b1 release by platelets when exposed to herpes
https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2567.1997.00202.x

Platelets cause a TGF-b1 burst

il-4 and tgf-b1 induced Th9 differentiation from Th0
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3090036/

IFNalpha from tlr9 of pDendritic cells in response to herpes simplex
http://www.pnas.org/content/101/31/11416

IFN alpha causes the correct MHC one to be expressed on the dendritic cells

IFN alpha raised il-21 levels from th9
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3090036/

IFN alpha and il-21 receptor on T cells
https://www.ncbi.nlm.nih.gov/pubmed/15178704

TH9 and cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5222918/

il-25 triggers il-9 release from th9
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982928/

platelets and CTL
https://www.ncbi.nlm.nih.gov/m/pubmed/18184798/

note that the Co-carcinogenesis hypotheses claims that most, not all but most cancers are a carcinogen with a nuclear virus.

TH9 secretes il-9 which inhibits tumor growth and il-21 which is involved with nuclear or mitochondrial viruses.

il-21 helps differentiate CTL and triggers TH17 ( TGF-B1 and il-21 together trigger TH17 to secrete il-26 (nuclear membrane popping) il-19 mitochondria popping and il-17F which calls CTL to the area.

CTL and platelets
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908083/

platelets and TGF-B1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271718/

TGF-B1 and CD8 differentiation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3062738/

plasmacytoid dendritic secretes ifnalpha
https://www.ncbi.nlm.nih.gov/pubmed/11713464?dopt=Abstract

ifn alpha triggers proliferation of cd8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212878/

ifn alpha induces B7
https://www.ncbi.nlm.nih.gov/pubmed/8752897

il-21 CD8 differentiates into CTL
https://www.ncbi.nlm.nih.gov/pubmed/23479229

follicular cd8
http://www.jimmunol.org/content/194/1_Supplement/71.9

th9 and CTL
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484462/

TH9 makes il-9 and il-21 (anti-tumor too)

https://www.ncbi.nlm.nih.gov/pubmed/28918288

CTL active in both cytosol or organelle viral infections

B7 activation or il-2 can trigger CTL
http://www.jimmunol.org/content/jimmunol/165/6/3088.full.pdf

il-2 induces fas ligand in CTL
https://www.ncbi.nlm.nih.gov/pubmed/9190908

note that B7 would be used with MHC1 which are mito or nuclear viruses while il-2 would be with TH1 infections of the cytosol...thus the CTL kills with FAS apoptosis

Specialized antibody clean-up : If the hormones influence the type of antibody produced by Bcells are there specialized cells in those areas to clean up the antibodies?

If the hormones influence the type of antibody produced by Bcells are there specialized cells in those areas to clean up the antibodies?

Insulin IgG at the liver

Growth Hormone IgA at the peyer's patches

IGF-1 IgE at the lymphs near the skin

kupffer cells uptake IgG in  the liver
https://www.ncbi.nlm.nih.gov/pubmed/8707258

Mesangial cells uptake IgA in the kidney
https://www.ncbi.nlm.nih.gov/pubmed/9555658

High levels of IgE and eosinophils? the main uptake of IgE at the skin
https://jamanetwork.com/journals/jamaotolaryngology/fullarticle/484777

previous post: Antibodies Explained
http://angelabiggs.blogspot.com/2018/03/antibodies-explained.html

Elucidating the function of natural Treg and inducible Treg

Natural Treg aka Thymus Treg are the T regulatory cells responsible for focusing the immune system on one zone.

3 Zones are involved in infections:

1.Outside of host cells which involves a burst of il-4 from basophils trigger TH2 reaction pathways

2. Just inside the cytosol of host cells which involves TH1 and a burst of il-2 and CTLs kill using FAS.

3. Then inside of the organelles of cells (the mitochondria or the nucleus)  where TGF-B1 levels are high  from platelets and CTLs kill infected cells with mhc1.

Natural Treg have receptors for each of these: il-2r (cd25),  il-4r, and a TGF-B1 receptor so that when Treg are circulating in the bloodstream they can immediately help focus the reactions.

When natural Treg see one pathway started they secrete cytokines to shut down the other 2 pathways.

il-4 bound and it secretes il-10 which stops TH1 and il-35 which stops CTL or cd8 reactions

il-2 bound and it secretes TGF-B1 which stops TH2 pathways and il-35 which stops CD8 reactions

TGF-B1 bound and it secretes TGF-B1 which stops TH2 pathways and il-10 which stops TH1 pathways.

Inducible Treg aka Adaptive Treg stop the immune reactions when the infection is killed off and gone.

They are specialized and secrete to stop the ongoing pathway used to kill the infection.

Tr1 secretes il-10 stopping TH1
TH3 secretes TGF-B1 stopping TH2
iTr35 secretes il-35 which inhibits and stops CTL

RANTES which is also involved in producing memory cells at the end of an infection may recruit and differentiate the iTregs.

Rantes and iTreg
https://onlinelibrary.wiley.com/doi/pdf/10.1111/aji.12013

nTreg get a TGF-B1 burst from platelets?

Some viral infections trigger platelet activation. Platelets have tlr7 and tlr9 which I previously linked to nuclear and mitochondrial antigens. Do Platelets release most of the TGF-B1?

platelets and TGF-B1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271718/

Herpes and Platelets
https://www.ncbi.nlm.nih.gov/pubmed/6307229
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4270245/
https://www.ncbi.nlm.nih.gov/pubmed/566472

https://www.researchgate.net/publication/228341940_Acyclovir-Induced_Immune_Thrombocytopenia_in_a_Patient_with_Herpes_Zoster_of_the_Trigeminal_Nerve

platelets and tlr7/ tlr9
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4118487/
http://jcb.rupress.org/content/198/4/561
https://www.researchgate.net/publication/261800204_Platelet-TLR7_mediates_host_survival_and_platelet_count_during_viral_infection_in_the_absence_of_platelet-dependent_thrombosis

two types of ulcerative colitis ?

ulcerative colitis misdiagnosed campylobacteria cases
https://www.ncbi.nlm.nih.gov/pubmed/1541961
https://www.ncbi.nlm.nih.gov/pubmed/16723859
https://www.ncbi.nlm.nih.gov/pubmed/16027651

review of Campylobacteria
https://www.ncbi.nlm.nih.gov/pubmed/7941533

The H. pylori use to be a type of Campylobacter.  (campylo means  curved rod, comma shape)

like H.pylori,  Campylobacter fetus can cause ulcers
https://www.ncbi.nlm.nih.gov/pubmed/6967840

H.pylori and peptic ulcers
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1539101/

Cranberries inhibits h.pylori
https://www.ncbi.nlm.nih.gov/pubmed/19120894

Broccoli sprouts kill h.pyloir
https://www.ncbi.nlm.nih.gov/pubmed/19349290

broccoli sprouts can be found at whole food and other organic food stores?

The dairy sensitive ulcerative colitis


Ulcerative colitis and c. diff
http://www.ncbi.nlm.nih.gov/pubmed/22508484
http://www.ncbi.nlm.nih.gov/pubmed/18484669
http://www.ncbi.nlm.nih.gov/pubmed/19913210
http://www.ncbi.nlm.nih.gov/pubmed/19944802
http://www.ncbi.nlm.nih.gov/pubmed/21915178
http://www.ncbi.nlm.nih.gov/pubmed/22405170

allergy and ulcerative colitis
http://www.ncbi.nlm.nih.gov/pubmed/10912663

Leukocytes and c. diff
http://www.ncbi.nlm.nih.gov/pubmed/22421720

C.diff appearing in low risk populations outside the hospital
http://www.ncbi.nlm.nih.gov/pubmed/17482995 

My thoughts....c.diff may not really be the culprit. C. sordellii which is closely related makes urease like H. Pylori.  H. pylori we know causes ulcers.

I wish I could tell if c.sordellii is one of the few that can use Casein.
 http://www.bd.com/ds/productCenter/221858.asp

Other thoughts:
Daisy/chamomile allergy
The natural treatment of ulcerative colitis is chamomile and people I know with ulcerative colitis have Daisy/mum/chamomile allergies. I wonder what is going on.  There are more thoughts on the earlier ulcerative colitis page

Alzheimer's and the dysfunctional mitochondria: antivirals found to work in some cases

New evidence of viruses damaging the mitochondria causing the dysfunction we see in some Alzheimer's cases

alzheimer's medicine protects against alzheimer's
https://www.medicalnewstoday.com/articles/322463.php
https://www.ncbi.nlm.nih.gov/pubmed/29889070

HSV and the mitochondria
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1796774/

herpes and alzheimer's
https://www.ncbi.nlm.nih.gov/pubmed/11867022
https://www.ncbi.nlm.nih.gov/pubmed/15319093
https://www.ncbi.nlm.nih.gov/pubmed/10604442

amyloid and herpes virus
http://www.ncbi.nlm.nih.gov/pubmed/21085580
http://www.ncbi.nlm.nih.gov/pubmed/26836158

previously I when over the other types of mitochondrial damage that causes amyloid and thus alzheimer's

Alzheimer's and the dysfunctional mitochondria

http://angelabiggs.blogspot.com/2015/08/alzheimers-and-dysfunctional.html

Somatic hypermutation: prediction that IgG2 like IgG3 has very little

CD8 cells not found in GC
http://clincancerres.aacrjournals.org/content/23/1/250

IgG3 has very little somatic hypermutation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5413556/

FDC follicular dendritic cell
mD myeloid dendritic cell
pD plasmacytoid dendritic cell

Dendritic cells are " pacmans " of the immune system picking up antigens  (related to macrophages)

MHC are mailboxes for showing antigens to T cells

The CD4  and CD8 are clips that hold the mailbox while the TCR t cell receptor looks at the antigen.

Note that T cells are educated in the thymus to know inside self antigens. While the B cells and the BCR b cell receptor is educated to know outside self antigens.  The BCR is the reason for somatic hypermutation. BCRs are literally worn antibodies.  The somatic hypermutation improves the binding and creates a strong binding antibody.

Comparing T and B memory cells: is this possible?

T cells

Central memory cells : lymph : TCR weak high number of interactions: medium life

Effector cells: circulating: TCR strong: short life

Tissue resident memory cells: tissue: il-7 : long life

memory t cells and il-7
https://www.ncbi.nlm.nih.gov/pubmed/28912605

TCR and il-7
http://www.jimmunol.org/content/169/7/3752

Does il-7 replace the activation of the TCR in the B zone and over time creates the T memory cells with long life?

B cells

Central memory : lymph : BCR weak high number of interactions : medium life

Effector: circulating: BCR strong (plasma to bone marrow): short life

Spleen resident memory in red pulp  : spleen : il-6? : long life

Megakaryocytes produce il-6

we already know that b cells will produce the IgM antibody with just il-6 and no BCR activation

so is this how high affinity B memory cells are made? il-6 exposure in the red pulp ?


Note that T cells' TCR memory is involved with inner antigens: TH the cytosol and Tc the mitochondria/nucleus while Bcells' BCR and memory are involved with outer antigens.