Hypothesis: TGF-beta1 is associated with viral infections

Hypothesis: TGF-beta1 is associated with viral infections either through the mast cells of the mucosal membrane or the tlr7/9 of the M2 macrophages causing antibody switching to the secreted IgA2 dimer or the IgG3.  Both have a disulfide bond core that would attract DNA/RNA to the antibody.

TGF-beta induces Foxp3 in CD4 Th (Thelper cells converted to Tregs)
https://www.ncbi.nlm.nih.gov/pubmed/15367216

Tc cells CD8 are involved with viral infections

IgG3 has 11 disulfide bonds
https://ednieuw.home.xs4all.nl/IgGsubclasses/subkl23.htm

IgG3 and IgA2
https://www.researchgate.net/publication/295610598_Hyper_IgG3IgA2_syndrome_Gene_deletion_or_IgG_subclass_regulatory_defect

secretory component and the disulfide bonds
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2265853/
http://www.jimmunol.org/content/118/5/1816

does the dimer IgA2 have enough disulfide bonds on the SC that it compares to the 11 disulfide bonds of the IgG3?


Mast cells and influenza
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4435071/

M2 macrophages il-10 tgf-beta1 glucocorticoids
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900959/

(glucocorticoids are produced during viral infections)

M2 macrophages are also the tyrosine kinase wearing macrophages: tyro3, axl, mer which are the hands that allow macrophages to grab on and ingest virally infected host cells

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5332501/

Further il-21 and TGF-b1 stimulate TH17 cells to secrete il-26 (nuclear) and il-19 (mitochondria) suggesting that the viral infections hiding in the mitochondria or nucleus need to be popped out. 

il-21 is the cytokine expressed by Tc - B cells matching up the TLR with the MHC1.