Im thinking the effect of autoantibodies might be indirect. For example a autoantibody might be targeting some protein somewhere in the body which causes a chain of events that eventually leads to cytokine release, and these being able to demand RBCs to change deformabilty parameters. I dont know if this route is possible though.
Good point, seems entirely possible. Oxidative stress and inflammation in general could simply be the answer, as RBCs soak a lot of oxidative stress from the body and don't have the capability to self repair much.
However im linking a study below here if you havent seen it. Seems to me like deformability, form and structure of immune cells might also be affected, not just RBC.
https://pubmed.ncbi.nlm.nih.gov/34087216/
Thank you, it looks familiar but I'll check it out again. I should say also that membrane phospholipid composition is important for all cells, and yes definitely immune cells, not just RBCs.
The reason I'm skeptical is because mature RBCs lack a nucleus, mitochondria, and other organelles, so this kind of narrows the possibilities down for direct interaction between the putative autoantibodies and RBCs from what I can tell. GPCRs work via several signaling mechanisms, one of which is via IP3 and calcium release in the cell, the latter of which absolutely can alter membrane phospholipid composition, the problem is that this signaling pathway utilizes the endoplasmic reticulum, which RBCs don't have. The other mechanism is cyclic AMP, which it does look like RBCs are responsive to, so my skepticism is probably not well founded.