The 2 antigen zones of the peritoneal cavity

The omentum protects the peritoneal cavity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5812451/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754314/

the peritoneal cavity contains the stomach, liver, large and small intestines, the kidneys, the gall bladder, pancreas, and the adrenal glands.

omentum stromal cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481843/

there are two types of omentum cells involved in tissue repair as stromal cells
myeloid derived suppressor cells and MSC cells
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0038368

pericytes and myeloid derived suppressor cells
https://www.ncbi.nlm.nih.gov/pubmed/26296362

subgroup of myeloid derived suppressor cells : fibrocytes
https://www.ncbi.nlm.nih.gov/pubmed/26405600/
https://www.ncbi.nlm.nih.gov/pubmed/23757729

fibrocytes are potent stimulators of T cytotoxic cells
https://www.ncbi.nlm.nih.gov/pubmed/15767291

Based on our patten of inside and outside antigens is seems that the outer antigens would be collected by the B1 cells and processed by the MSC cells while the inner antigens would be taken up by the pericytes and shown to the myeloid derived stromal cells.

Chorioid Plexus compared to the BBB blood brain barrier

Chorioid Plexus compared to the BBB blood brain barrier and the hypothesis that they deal with different antigens.


Each of the brain's ventricles has their own CP region

Capillary blood is filtered here at the CP to become cerebrospinal fluid.

Resident macrophages and dendritic cells are in the CP
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3496674/

Note that resident macrophages come from the yolk and focus on outer antigens while travel monocytes come from bone marrow and develop into dendritic cells or macrophages that deal with inner antigens based on the hormone that they see. High insulin favors macrophages while IGF-1 or GH exposed monocytes develop into dendritic cells.

IGF-1 made by CP epithelial
https://www.ncbi.nlm.nih.gov/pubmed/7513042

this would favor dendritic over macrophages (traveling)

myeloid dendritic cells of the cp
https://www.ncbi.nlm.nih.gov/pubmed/16817190

CP : fibroblasts, macrophages, dendritic cells
https://www.frontiersin.org/articles/10.3389/fncel.2015.00136/full

astrocytes (stromal cells) attract dendritic cells
https://www.ncbi.nlm.nih.gov/pubmed/16106219

astrocytes activate B cells
https://www.ncbi.nlm.nih.gov/pubmed/29673365
https://www.ncbi.nlm.nih.gov/pubmed/26223505

pericytes and and astrocytes communication
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042982/

FRC-like cells in CNS
https://www.cell.com/immunity/pdfExtended/S1074-7613(16)30001-2

At the intestine: inner antigens are processed at ILFs while outer antigens are processed in Peyer patches (hypothesis)

At the intestine: inner antigens are processed at ILFs while outer antigens are processed in Peyer patches.

ILF: inducible lymph follicle
https://www.ncbi.nlm.nih.gov/pubmed/12759424

"In contrast to the spleen, LNs and PPs, ILFs are inducible structures developed after birth due to the presence of external stimuli43"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5015111/

The MRC marginal reticular cells develop here at the inducible ILF of the intestine.

pericytes in the gut
https://www.ncbi.nlm.nih.gov/pubmed/30937864

Peyer patches have the FRC fibroblast reticular cells.

Brain macrophages : pericytes
https://www.ncbi.nlm.nih.gov/pubmed/10611494

MHC2 expression by pericytes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5844098/

pericytes and the BBB
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4292164/

peyer patch lacking mice had no IgA only IgG from ILFs
https://www.jimmunol.org/content/jimmunol/173/2/762.full.pdf

Remember the lymph structure and the separate zones for inner and outer antigens:

Then the spleen's separate zones:

Now looking for the MRC and the FRC we find very separate zones in the intestine:

Bee allergy, t.gondii, and the cells cytosol : I am not sure what I am looking at.

cd16 is on Basophils of patients with insect venom allergy
https://www.ncbi.nlm.nih.gov/pubmed/30288810

IgG2 and insect venom allergy
https://link.springer.com/article/10.1007%2FBF00441707

malaria and IgG2
https://iai.asm.org/content/68/3/1252

t.cruzi and IgG2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1577053/

malaria also infects the cytosol
https://science.sciencemag.org/content/328/5980/862/F2

old post about Bee allergy and T.gondii
https://angelabiggs.blogspot.com/2015/04/tgondii-and-bee-venom.html

T.gondii infects the cytosol. Previous hypothesis was that IgG2 is the antibody made against cytosol infections.  I was sorting the Fc receptors with the IgGsubsets...when this occurred to me.

These are not proven just appears to be a pattern
cd16 (fcgammaRIII) binds IgG3 which is high on platelets? mito/nucl viruses
cd16 (fcgammaRIV) binds IgG2b which is high on eosinophils? cytosol infection?
cd64 (fcgammaRI) binds IgG2a cytosol virus?
cd32 (fcgammaRII) binds IgG1 and is high on Langerhans?  outer antigens

Is this why the patients with insect allergy would have cd16?

T.gondii and Bee venom

Do people with bee sting allergies have t.gondii infections?

I have connected T.gondii with a variety of things: Seizures, Epilepsy, schizophrenia....but they are all  autoimmune which means cross-targeting autoimmunity must be occurring. A virus has to trigger the attack at the target tissue from the inside.  Are these autoimmune diseases all bee sensitive because of their connection to T.gondii?


Schizophrenia: t.gondii and the cytomegavirus
http://www.sciencedaily.com/releases/2013/03/130308111315.htm

Bee sting reactions have been found in schizophrenia patients
http://www.ncbi.nlm.nih.gov/pubmed/5239954

I have connected in the past seizures/epilepsy with t.gondii and enteroviruses 
http://angelabiggs.blogspot.com/2015/01/nodding-disease-epilepsy-seizuresare.html

Seizures and bee stings 
http://epilepsyfoundation.ning.com/group/support-for-cps/forum/topics/bee-stings-and-seizures?commentId=2217546%3AComment%3A908079&xg_source=activity&groupId=2217546%3AGroup%3A819391
http://www.ncbi.nlm.nih.gov/pubmed/22100477
http://www.japi.org/february_2012/11_cr_stroke_after_multiple.pdf

epilepsy and wasp stings
http://www.ncbi.nlm.nih.gov/pubmed/8844507
http://jnnp.bmj.com/content/74/1/134.2.full

Does Apis mellifera venom (honey bee venom) effect T.gondii?

I can't see this paper to find out: 

• Effect of Bee Venom on Toxoplasma gondii Tachyzoites in vitro - Ahmad G. Hegazi, Hassan A. El-Fadaly and Ashraf M. BARAKAT (Egypt)

T.gondii is carried by mice and cats
T.cruzi is carried by kissing bugs and the dogs that eat them

T.cruzi which causes changas is killed by honey bee venom
http://www.ncbi.nlm.nih.gov/pubmed/23562368

The Kissing bug carries the T.cruzi the way mice carry T.gondii
http://blog.mysanantonio.com/animals/2013/09/san-antonio-humane-society-says-chagas-disease-possible-in-local-dogs/
note that kissing bugs are nocturnal so keep your pet in at night

Hymenoptera are the venom group of  Apoidea (bees), Vespoidea (wasps, hornets, and yellow jackets), and Formicidae (ants). 

What is it in the bee sting that Toxoplasmas dislike? perhaps the compound apamin which can cross the blood brain barrier. (our nerves don't like it either)
http://pubs.acs.org/doi/abs/10.1021/bi00682a035

Interestingly HoneyBee venom has been a remedy for malaria too.

Panafrican News Agency (PANA). 17 September 1997. Yahya el Hassan. "Curing Malaria with Bee Stings in Sudan." [Internet]. [Accessed 24 Dec. 1998].

https://books.google.com/books?id=JlSJDj5Lt98C&pg=PA153&lpg=PA153&dq=bee+stings+and+malaria&source=bl&ots=kXRWjUnlba&sig=Q7s5Av9JLOys_nMEi8I5pfzmRUg&hl=en&sa=X&ei=oeQlVZaHA8K1oQTxpoHACQ&ved=0CCkQ6AEwAg#v=onepage&q=bee%20stings%20and%20malaria&f=false

il-27, 25HC, and IgG2a against cytosol viral infections ?

il-27 induces IgG2a from Bcells
https://www.ncbi.nlm.nih.gov/pubmed/15294962

il-27 induces 25hc
https://www.researchgate.net/figure/IL-27-specifically-induces-cholesterol-25-hydroxylase-Ch25h-expression-and-25-OHC_fig1_320017159

https://www.researchgate.net/publication/320017159_IL-27-Induced_Type_1_Regulatory_T-Cells_Produce_Oxysterols_that_Constrain_IL-10_Production

25HC blocks viral entry
https://www.ncbi.nlm.nih.gov/pubmed/25501851

https://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=27086126

Does 25hc help create exosomes which then binds with dendritic cells and SCS lymph cells?

cd169 binds 25HC to capture exosomes
https://www.ncbi.nlm.nih.gov/pubmed/24255917
https://www.ncbi.nlm.nih.gov/pubmed/29425504

Complement and  IgG2a
https://www.jimmunol.org/content/178/1_Supplement/S159.5
https://www.ncbi.nlm.nih.gov/pubmed/6610105

IgG2a and influenza
https://cvi.asm.org/content/13/9/981

IgG2a with viruses and parasites?
https://academic.oup.com/intimm/article/12/2/223/652665

Does 25hc hold viruses on the surface? how would complement work?

Hypothesis: il-27 cytokine is secreted by B cells when there is a viral infection or cancer damage involving the cytosol of cells.

Hypothesis: il-27 cytokine is secreted by B cells when there is a viral infection or cancer damage involving the cytosol of cells.

p53 and il-27
http://clincancerres.aacrjournals.org/content/clincanres/early/2016/05/27/1078-0432.CCR-15-2052.full.pdf

Is il-27 involved with DNA damage?

melanoma and il-27
https://www.ncbi.nlm.nih.gov/pubmed/18453571

melanoma is a cancer caused by DNA damage (from sun exposure)

DNA damage and the cytosolic sensors
http://jem.rupress.org/content/215/5/1287

B cells major source of il-27
https://www.jimmunol.org/content/200/1_Supplement/107.5

B cells produce IgG2a (class switch) after il-27
https://www.jimmunol.org/content/173/4/2479.long?utm_source=TrendMD&utm_medium=cpc&utm_campaign=J_Immunol_TrendMD_0

IgG2a against reoviruses and parasites
https://academic.oup.com/intimm/article/12/2/223/652665

il-27 attracts myeloid dendritic cells to the lymph
https://www.jimmunol.org/content/192/6/2634

previous hypothesis:
myeloid dendritic cells are involved with infections of the cytosol
plasmacytoid dendritic cells are involved with infection of the mitochondria/ nucleus

il-27 not il-35 suppresses gm-csf
https://www.nature.com/articles/s41598-017-16702-w


GM-csf is involved with vacuole bacteria and TH17 triggering

GM-csf exposed Basophil's produce il-6 and trigger th17
https://www.nature.com/articles/srep41744

GM-csf exposed mDendritic make il-23
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297527/

As a cytosol infection TH1 is involved
https://www.nature.com/articles/7310017?error=server_error

il-27 is saying it is in the cytosol..what ever it is...not a bacteria hiding in the cytosol or in a virus in the nucleus or mitochondria.

Furthermore

il-27 suppressed il-5 and il-13 from TH2 cells which is used against parasites in the cytosol. Which means il-27 could be strictly a cytokine for viruses or for DNA from cancer in the cytosol?

https://www.jimmunol.org/content/179/7/4415

When does the B cell decide to make il-27? Does the T follicular cell recognize it as DNA and signal back to the B cell?

IgG2, cytosol infections, and the lectin pathway.

Complement activation and Antibodies
https://www.ncbi.nlm.nih.gov/pubmed/20151159

Classical pathway: IgG1 and IgG3

Alternative and lectin: IgG2 and IgG4

LPS triggers the TLR4 or the lectin-mannose complement activation.  These tend to be the type of infections that can move inside of cells.  Some infections move into the vacuoles and organelles others the cytosol.

Strep has even been shown to move inside of cells allowing the bacteria to survive antibiotics. https://www.ncbi.nlm.nih.gov/books/NBK333420/

basophils as APC to TH2 inducing il-13
https://onlinelibrary.wiley.com/doi/pdf/10.1002/eji.201040588