Just my general training in biology. I work mostly in non-animal organisms, but recall enough of my education and what I read during the COVID pandemic. This is a complex topic, and I was simplifying above.
Basically getting infected by some things can help provide protection against some other things, can make infection by some other things worse, or can have no effect on protection against other things. All in all it's generally better to not get infected by a particular thing, but if you're going to be exposed to worse things that infection by the particular thing provides protection against this is an exception.
> Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena.
Just my general training in biology. I work mostly in non-animal organisms, but recall enough of my education and what I read during the COVID pandemic. This is a complex topic, and I was simplifying above.
https://en.wikipedia.org/wiki/Cross-reactivity#In_immunology
This seems to be a good article on the benefits and limits of cross-reactivity: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352416/
And here seems to be a decent review looking at Antibody-Dependent Enhancement, a key limitation of antibody cross-reactivity for viruses: https://www.sciencedirect.com/science/article/pii/S016158902...
Basically getting infected by some things can help provide protection against some other things, can make infection by some other things worse, or can have no effect on protection against other things. All in all it's generally better to not get infected by a particular thing, but if you're going to be exposed to worse things that infection by the particular thing provides protection against this is an exception.
A book chapter on infections causing, or curing autoimmune diseases: https://www.ncbi.nlm.nih.gov/books/NBK459437/
And a review article on the same: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723519/
> Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena.