il-17F has a TGF-b like motif.
Hypothesis: Is it the transforming growth factor for the endoplasmic reticulum?
over expression of il-17F causes Airway Neutrophilia
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4009148/
Vit E reduces Airway neutrophilia and is a vitamin that relieves ER stress
https://www.ncbi.nlm.nih.gov/pubmed/23402870
Mature neutrophils have no endoplasmic reticulum.
Erlotinib a lung cancer drug promotes ER stress and induces il-17f
https://www.ncbi.nlm.nih.gov/pubmed/24768708
Review:
TGF-b1 mitochondria growth
http://onlinelibrary.wiley.com/doi/10.1002/aja.1002030304/full
TGF-b2 plasma membrane
http://onlinelibrary.wiley.com/store/10.1002/iub.1112/asset/1112_ftp.pdf?v=1&t=jeoxq1dl&s=8431847e65fff2bfe12c939d1d4117466ad73072
TGF-b3 vacuoles
https://www.nature.com/articles/srep17151 (sperm and vacuoles)
https://www.omicsonline.org/open-access/sperm-vacuoles-and-reproductive-outcome-2375-4508-1000e118.php?aid=63872
TGF-b4 golgi
https://www.ncbi.nlm.nih.gov/pubmed/25935756
This could be important because when they show up during infections the organelle they grow is often involved as if the body is trying to repair as well as inform.
TGF-b1 shows up for viral infections of the nucleus and the mitochondria.
TGF-b4 appears during salmonella infections.
Another interesting way to look at it is:
If you split the Th17 into bacterial and viral:
Bacterial Th17
il-6 and il-23 triggering the bacterial Th17 releasing: il-22 (vacuole) il-24(golgi) and il-17F (ER)
il-17F also produced il-8 calling neutrophils to trap the bacteria coming out of host cells
https://www.sciencedirect.com/science/article/pii/S0022202X15342408
Viral Th17
TGF-b1 and il-21 trigger the viral Th17 let's call it Th17v releasing: il-26 (nucleus) il-19 (mitochondria) and il-17a which binds the receptors on Tc.
Hypothesis: Is it the transforming growth factor for the endoplasmic reticulum?
over expression of il-17F causes Airway Neutrophilia
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4009148/
Vit E reduces Airway neutrophilia and is a vitamin that relieves ER stress
https://www.ncbi.nlm.nih.gov/pubmed/23402870
Mature neutrophils have no endoplasmic reticulum.
Erlotinib a lung cancer drug promotes ER stress and induces il-17f
https://www.ncbi.nlm.nih.gov/pubmed/24768708
Review:
TGF-b1 mitochondria growth
http://onlinelibrary.wiley.com/doi/10.1002/aja.1002030304/full
TGF-b2 plasma membrane
http://onlinelibrary.wiley.com/store/10.1002/iub.1112/asset/1112_ftp.pdf?v=1&t=jeoxq1dl&s=8431847e65fff2bfe12c939d1d4117466ad73072
TGF-b3 vacuoles
https://www.nature.com/articles/srep17151 (sperm and vacuoles)
https://www.omicsonline.org/open-access/sperm-vacuoles-and-reproductive-outcome-2375-4508-1000e118.php?aid=63872
TGF-b4 golgi
https://www.ncbi.nlm.nih.gov/pubmed/25935756
This could be important because when they show up during infections the organelle they grow is often involved as if the body is trying to repair as well as inform.
TGF-b1 shows up for viral infections of the nucleus and the mitochondria.
TGF-b4 appears during salmonella infections.
Another interesting way to look at it is:
If you split the Th17 into bacterial and viral:
Bacterial Th17
il-6 and il-23 triggering the bacterial Th17 releasing: il-22 (vacuole) il-24(golgi) and il-17F (ER)
il-17F also produced il-8 calling neutrophils to trap the bacteria coming out of host cells
https://www.sciencedirect.com/science/article/pii/S0022202X15342408
Viral Th17
TGF-b1 and il-21 trigger the viral Th17 let's call it Th17v releasing: il-26 (nucleus) il-19 (mitochondria) and il-17a which binds the receptors on Tc.
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