6 members of the cytokine 17 family
IL-17A (commonly referred to as IL-17), IL-17B, IL-17C, IL-17D, IL-17E (also known as IL-25) and IL-17F.
https://www.nature.com/articles/emi201358
il-17A has homology to il-17F
il-17F strong associations to mycobacteria (infection that moves into the cytosol)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663007/
TLR3 and mycobacteria
https://www.sciencedirect.com/science/article/pii/S0898656814000345
TLR3 (cytosol) and il-17F
http://www.fasebj.org/doi/10.1096/fasebj.30.1_supplement.966.7
il-17A with mycoplasmas/viruses (infections that move inside of the organelles..vacuoles etc)
https://www.nature.com/articles/s41598-017-13292-5
TLR9 (mitochondria) and il-17A
https://www.hindawi.com/journals/mi/2016/3296307/
TLR7/8 (nuclear or ER) trigger il-17A
https://www.ncbi.nlm.nih.gov/pubmed/19265114
il-17A and the starvation of fungal cells ?
https://www.nature.com/articles/ncomms1685
il-17C fungal infections
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0122807
il-17C is very high in the colon when does this appear? is this made to stick to the outside of infections like fungus? not involved with second popping? made to help kill infections that are large but not as large as worms?
TLR3 and il-17C ?
https://www.ncbi.nlm.nih.gov/pubmed/23944933
does this try to stick to mycobacteria before they move into the cell's cytosol?
note that psoriasis and IBS which are both connected to mycobacteria also both have high il-17
TLR3 cytosol RNA virus (like the flu )
TLR9 mitochondrial DNA virus (herpes zoster)
TLR7 nuclear DNA virus (hpv, epstein barr)
TLR8 endoplasmic reticulum RNA virus (polyomavirus)
the switching to il-17F indicates mycobacteria
il-17 inhibition made IBS and psoriasis worse
https://www.ncbi.nlm.nih.gov/pubmed/28521565
TB mycobacteria is TLR2 dependent triggering il-17 ?
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004099
TLR2 and TLR5 triggers il-17C in the mucosa
TLR1 peptidoglycan (found on almost all bacterias and yeasts)
TLR2 modulins (compounds bacterias use to alter or modulate our cells cytokine messages)
TLR4 lipopolysaccharides (found on gram negative bacteria like e.coli and mycobacteria)
TLR5 flagellins (bacteria tails)/ fungus
TLR6 diacyl lipoproteins (found on gram positive bacteria..like strep)
il-17C and bacteria tails and fungus?
TLR5 and fungus
https://www.ncbi.nlm.nih.gov/pubmed/21067314
il-17D is the ancient cytokine also found in sea lamprey
https://www.ncbi.nlm.nih.gov/pubmed/26491201
il-17D triggers the cytokines il-6 (increases activation of neutrophils/macrophages) il-8 (neutrophil chemotactic factor) and gm-csf (beta side chain that favors myeloid side of development creating macrophages)
asks the immune system to come eat the infection without popping?
il-17E is il-25 which is used against parasitic infections
https://www.ncbi.nlm.nih.gov/pubmed/22476048
IL-17A (commonly referred to as IL-17), IL-17B, IL-17C, IL-17D, IL-17E (also known as IL-25) and IL-17F.
https://www.nature.com/articles/emi201358
il-17A has homology to il-17F
il-17F strong associations to mycobacteria (infection that moves into the cytosol)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663007/
TLR3 and mycobacteria
https://www.sciencedirect.com/science/article/pii/S0898656814000345
TLR3 (cytosol) and il-17F
http://www.fasebj.org/doi/10.1096/fasebj.30.1_supplement.966.7
il-17A with mycoplasmas/viruses (infections that move inside of the organelles..vacuoles etc)
https://www.nature.com/articles/s41598-017-13292-5
TLR9 (mitochondria) and il-17A
https://www.hindawi.com/journals/mi/2016/3296307/
TLR7/8 (nuclear or ER) trigger il-17A
https://www.ncbi.nlm.nih.gov/pubmed/19265114
il-17A and the starvation of fungal cells ?
https://www.nature.com/articles/ncomms1685
il-17C fungal infections
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0122807
il-17C is very high in the colon when does this appear? is this made to stick to the outside of infections like fungus? not involved with second popping? made to help kill infections that are large but not as large as worms?
TLR3 and il-17C ?
https://www.ncbi.nlm.nih.gov/pubmed/23944933
does this try to stick to mycobacteria before they move into the cell's cytosol?
note that psoriasis and IBS which are both connected to mycobacteria also both have high il-17
TLR3 cytosol RNA virus (like the flu )
TLR9 mitochondrial DNA virus (herpes zoster)
TLR7 nuclear DNA virus (hpv, epstein barr)
TLR8 endoplasmic reticulum RNA virus (polyomavirus)
the switching to il-17F indicates mycobacteria
il-17 inhibition made IBS and psoriasis worse
https://www.ncbi.nlm.nih.gov/pubmed/28521565
TB mycobacteria is TLR2 dependent triggering il-17 ?
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004099
TLR2 and TLR5 triggers il-17C in the mucosa
TLR1 peptidoglycan (found on almost all bacterias and yeasts)
TLR2 modulins (compounds bacterias use to alter or modulate our cells cytokine messages)
TLR4 lipopolysaccharides (found on gram negative bacteria like e.coli and mycobacteria)
TLR5 flagellins (bacteria tails)/ fungus
TLR6 diacyl lipoproteins (found on gram positive bacteria..like strep)
TLR5 and fungus
https://www.ncbi.nlm.nih.gov/pubmed/21067314
il-17D is the ancient cytokine also found in sea lamprey
https://www.ncbi.nlm.nih.gov/pubmed/26491201
il-17D triggers the cytokines il-6 (increases activation of neutrophils/macrophages) il-8 (neutrophil chemotactic factor) and gm-csf (beta side chain that favors myeloid side of development creating macrophages)
asks the immune system to come eat the infection without popping?
https://www.ncbi.nlm.nih.gov/pubmed/22476048
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