Il-13, Fas, and phagocytes

Neutrophils secrete fasL
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278510/

Monocytes, eosinophils, and neutrophils express fas and this is a way to stop quickly inflammation

il-13 suppresses apoptosis
http://www.jimmunol.org/content/jimmunol/161/6/2863.full.pdf

Monocytes, eosinophils, and neutrophils all have il-13 receptors which means they do not go through apoptosis if il-13 is around.

During cytosolic infections by bacteria or parasites the myeloid Dendritic cells instead of intereacting with TH1 hands the MHC2 with a protein in it off to a basophil who then as the liaison shows the TH2 cells instead. TH2 cells then make il-13 not just il-4.

This means that when a cytosolic infection occurs and the CTL-fas ligand pathway is triggered the phagocytes are not going to apoptosis only the parasite infected cells. At least until the il-13 wears off.


Like viruses of the cytosol there is more than one way to kill bacterial infections of the cytosol.

cytosolic receptor for bacteria
https://www.nature.com/articles/s41586-018-0433-3

Do TH17 cells pop the infected organelles?

Hypothesis: TH17 are cells secrete il-20 cytokines which pop the organelles because they appear with infections that are further inside like vacuoles or the mitochondria.  A second popping is needed for the immune system to see the infection.  The question is how?

il-17a does call neutrophils which helps fight fungal infections

virus activates il-1beta
https://www.ncbi.nlm.nih.gov/pubmed/10358182

il-1beta and il-23 activate the differentiation of TH17
https://www.cell.com/cell-reports/pdf/S2211-1247(18)30225-0.pdf

il-23 is triggered by intracellular bacteria
http://www.jimmunol.org/content/183/12/8026

Hypothesis
The cytokines of  TH17 cells pop the organelles of the cell.

Reposted from before:

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  with DNA (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

Mitochondria il-19

il-19 and acute kidney failure due to mitochondrial induced apoptosis
https://books.google.com/books?id=n9ocHWITPnoC&pg=PA51&lpg=PA51&dq=il-19+mitochondria&source=bl&ots=1sfmQISyik&sig=bgu8tG8Vy7EB0Q5SueB8jaFX8fE&hl=en&sa=X&ved=2ahUKEwi1nJrxk6PfAhVF4IMKHddSD_0Q6AEwBnoECAgQAQ#v=onepage&q=il-19%20mitochondria&f=false

th17 and herpes zoster
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5597651/

Golgi: il-24

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

il-24 protects against salmonella infection
https://www.ncbi.nlm.nih.gov/pubmed/1983073

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/

chlamydia and il-22
http://europepmc.org/abstract/MED/24531835

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