Hypothesis: When a second popping is needed when fighting an infection Th17 and Tc17 are created

Bacterial infections can move inside of host cells and hide. Viral infections can further hide inside of organelles. When these states occur a second popping must occur in order to expose the infections.

Two types of 17 cells exist.

Th17 (the hiding bacteria)

dendritic cells produce il-23 when calling macrophages

Bcells produce il-12 to stimulate Th1, il-6 to stimulate Th17, and il-15 to stimulate Tc

il-23 together with il-6 activate Th17 cells

Th17 cells produce il-17F/F and il-17A/F

Hypothesis: mycobacteria triggers il-17F by hiding in the cytosol of host cells . While mycoplasmas which hide in organelles trigger il-17A


Tc17 (the hiding virus)

Tcells interacting with Bcells through the HLA and Tcellreceptor produce il-4 and il-21

TLR 7/9  (butterfly nets triggered by DNA) produce TGF-beta1 
these TLRs identify mitochondrial or nuclear viruses

il-21 with TGF-beta1 triggers Tc17

Tc17 cells produce il-17A/A ad il-17A/F


Tc17 expresses il-17A/A and Th expresses more il-17F/F
http://www.jimmunol.org/content/182/3/1237


note:

il-33 stimulates Th2 (inflammation pathway)

il-33 during fungal infections suppresses some T17 pathways
https://www.ncbi.nlm.nih.gov/pubmed/28784844

Does a fungal infection increase il-26  at times? il-26 is the pore cytokine which would help break a fungal infection down