TH17 Called for a "second popping of membranes" then the cytokines that signify where

TH17 are called with the infections is too huge for macrophages to consume or if the infections are hiding inside cells where a second popping of membranes is required.

TH17 and mycobacteria
https://www.hindawi.com/journals/mi/2015/854507/

TH17 and mycoplasmas
https://www.ncbi.nlm.nih.gov/pubmed/27240139

TH17 and chlamydia

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0162445

TH17 and candida / salmonella
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652671/

TH17 and herpes zoster (mitochondria)
http://www.globethesis.com/?t=2284330488484866

TH17 and HIV (nucleus)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886291/

TH17 and EBV (nucleus)
http://www.bloodadvances.org/content/1/17/1324

Now lets look at the cytokines to help identify where in the cell the infections are

il-18 mycoplasmas nesting in the ER and is NOT an in the il-20 Family

Endoplasmic Reticulum:

ER and il-18
http://www.jimmunol.org/content/196/1_Supplement/207.1

mycoplasmas and the ER (electron microscope images)
https://www.ncbi.nlm.nih.gov/pubmed/25651334
http://www.tandfonline.com/doi/pdf/10.1080/00087114.1970.10796399
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4325531/

polyomavirus and il-18
https://www.ncbi.nlm.nih.gov/pubmed/26863474

polyomaviruses infect the ER

il-18 acts on TH1 cells to make IFN gamma

Note that when the ER is infected self proteins do not make it to the surface which means there will be no self proteins to be recognized.  An ER infected cell will look like a foreign cell which explains why IFNgamma is the default.  Kill anything that doesn't have self proteins on the outside.


The il-20 Family is secreted by Th17

il-20 Family includes: il-26, il-19, il-22, and il-24

il-26 nucleus

il-19 disruption of mitochondria

il-22 chlamydia/ gonorrhoeae/ h.pylori in vacuoles

il-24 salmonella in the golgi

Nucleus: il-26

il-26 PORE (used for a second popping of membranes like the mitochondria and nucleus or internalized infections)
https://www.nature.com/articles/ni.3211

( TLR-9 I had linked to being the net of the mitochondria )
http://angelabiggs.blogspot.com/2017/01/tlrs-toll-like-receptors-summary.html

il-26 and herpes viruses
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070281


Golgi: il-24

salmonella nests inside of cells in vacole near golgi
https://www.ncbi.nlm.nih.gov/pubmed/18778407

Golgi and il-24 with melanoma (supporting connection)
https://www.ncbi.nlm.nih.gov/pubmed/15126330

golgi and ER relationship....IFNgamma
https://www.ncbi.nlm.nih.gov/pubmed/10712678

ifn gamma and tnf with salmonella
https://www.karger.com/Article/Pdf/163643


Vacuoles: il-22

Chlamydia moves inside of cells to replicate
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4886739/

il-23 triggers Th17 to release il-22 and il-17
https://www.ncbi.nlm.nih.gov/pubmed/24238108


H.pylori and il-23
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342083/

H.pylori and il-22
https://www.ncbi.nlm.nih.gov/pubmed/26867135

H.pylori replicates in vacuoles
http://iai.asm.org/content/78/10/4157.full




Immunology Review paper
https://manugowdagn.files.wordpress.com/2016/01/kuby-immunology-7th-edition-2013.pdf

Think of the surface of infections:

Staph has a fairly flat surface and the antibodies of complement work well.

Strep has sugars sticking up making it harder for antibodies to touch but the lectin-mannose pathway works.

E.coli has a furry mess of a surface making it next to impossible for things to collect on the surface so the alternative pathway is followed.

Then you have the TH17 infections.  These are the infections that are too large or moving inside of the host cells.  Which means a second wave of membrane breaking must occur.

I believe that some cytokines help coordinate where the infections are.

The trick is when infections like Staph decide to move inside of the host to escape the immune system.

Th17 cells and then Th22 cells would then become involved.