il-25 aka il-17E is a parastic endoplasmic reticulum cytokine

Hypothesis: the il-25 cytokine appears to be linked to parasites, large infections, that infect/stress the endoplasmic reticulum and stimulates ER growth/repair.

il-17 types (il-17a  is similar to il-25)
https://www.nature.com/articles/emi201358

il-25 and mammary tumors
https://www.nature.com/articles/ncomms11311

increased ER in mammary glands
https://www.ncbi.nlm.nih.gov/pubmed/21920588

is il-25 the growth cytokine for the ER?

Do other infections that move into the ER trigger il-25?

il-17E aka il-25 has been linked to parasite infections ?

il-17E and parasites (il-17 review)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3811766/
https://www.ncbi.nlm.nih.gov/pubmed/22476048
https://www.sciencedirect.com/topics/immunology-and-microbiology/interleukin-17-receptor

trichinella spiralis and ER stress/apoptosis
https://www.ncbi.nlm.nih.gov/pubmed/24996067

trichinella spiralis and il-25
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3811766/

ER and round worms
https://www.ncbi.nlm.nih.gov/pubmed/24996067

Trichinella spiralis uses the host cells a nursery. Specifically the SR of muscles grow the larva
https://link.springer.com/article/10.1007/s004360050494 (electron microscope pictures)

note that il-25 triggers apoptosis in breast cancer cells expressing the il-25R receptor
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199022/

ER stress and cancer
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204165/

Note that this infection is different from viral or mycoplasma infection of the ER which would trigger IFNgamma. In those cases it would be very hard for the immune system to identify an infection was in the cell because of the ER malfunction causing a lack of surface proteins....in the case of worms...a large worm is sitting outside of the host cell.