Are Nuclear or mitochondrial viral infections trapped and need to be released by Th17 's il-26 to be seen by the immune system?

il-1 beta stimulates Th17 cells.  Th17 cells produce il-26 which is a membrane pore forming.  il-26 kills bacterias but what is it doing when a viral infection is involved?

TLR9 and TLR7 have been found to increase levels of il-1 beta. il-1beta stimulates Th17.

TLR3, TLR9, TLR7, and TLR8 are located intracellularly of cells catching viral infections/foreign bacterial nucleotides via net and  when the are triggered they tell the cells to wear the correct HLA and express a specific IFN

Hypothesis of location was based on viruses snagged

TLR3 cytosol RNA virus (like the flu )
TLR9 mitochondrial DNA virus (herpes zoster)
TLR7 nuclear DNA virus (hpv, HIV)
TLR8 endoplasmic reticulum RNA virus (polyomavirus)

Review of Tlrs 3, 9, 7 and 8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC406426/

the internal location of tlr 3, 9, 7 and 8
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4037363/

When the immune system breaks open virally infected cells if the viruses are inside the nucleus or inside the mitochondria they are still not visible. Hence the mitochondria or nucleus need to be popped.  il-26 could be the tool here.

(just like il-26 is used to create pores in mycobacterias in Crohn's disease)
https://www.researchgate.net/publication/5368756_The_role_of_the_novel_Th17_cytokine_IL-26_in_intestinal_inflammation
(mycobacteria and crohn's)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4894645/


il-26 and extracellular DNA transporter
http://www.jimmunol.org/content/early/2017/03/29/jimmunol.1600594

il-26 as a pore
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776746/

Nuclear viruses

HIV and tlr7
https://www.nature.com/ni/journal/v16/n1/full/ni.3036.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3700304/
http://www.bloodjournal.org/content/bloodjournal/113/2/377.full.pdf?sso-checked=true

HPV16 and tlr7
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952342/

note that Epstein barr and tlr7 are some how connected but it is not clear if tlr7 is a sensor for it
http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1249&context=virologypub

il-1beta and hiv
https://www.ncbi.nlm.nih.gov/pubmed/9218824

il-1beta and HPV
https://www.ncbi.nlm.nih.gov/pubmed/23935506 

il-1beta and epstein barr
http://www.sciencedirect.com/science/article/pii/S0042682298994417



Mitochondrial viruses

Herpes zoster and tlr9
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465860/
Herpes simplex 1 and tlr9
https://www.ncbi.nlm.nih.gov/pubmed/14563635/

il-1beta and herpes zoster
http://www.jbc.org/content/286/20/17921.full

il-1beta triggers the Th17

Note that Th17 cells make the il-26

il-26 and tlr9
https://www.researchgate.net/publication/294167676_Interleukin_IL-26_is_over_expressed_in_psoriasis_and_regulates_TLR9_activation_to_self-DNA

tlr7 and Th17 cells
http://www.jimmunol.org/content/jimmunol/184/3/1159.full.pdf

Tlr9 and Th17 cells
https://www.jci.org/articles/view/35647

Previous blog post linking up TAMS, TLRs, IFNs, and HLAs
http://angelabiggs.blogspot.com/2017/02/tam-receptors-and-ifns.html

il-1 beta induces TGF-beta
https://www.ncbi.nlm.nih.gov/pubmed/7980594
https://www.ncbi.nlm.nih.gov/pubmed/21779356

TGF-beta then stimulates Th17

Th17 and mold infections

People with mold infections have elevated TGF-beta elevated (CIRS chronic inflammatory response syndrome)

Th17 produces the il-26 pore protein which would aid in the destruction of mold infections


TGF is key in wound healing, it increases extracellular matrix proteins, decreases Red blood cells, and triggers neutrophils to release traps...the body is trying to contain the mold in a confined area.

Neutrophil traps
https://www.ncbi.nlm.nih.gov/pubmed/27486461