11–20 of 112 posts
I so do not want to click on this link in case there are pictures. I really do not want to see what this looks like. Are there pictures?
This is to be expected. Any time we do any transplant immunosupressants are given to the recipient for the rest of their life, but this only slows the inevitable. Heart transplants recipients all get accelerated atherosclerosis. Lung transplant recipients all get long term fibrosis. We buy time with these procedures and do everything we can to keep them going, but if you have a transplant, you're in a really bad spot…
I so do not want to click on this link in case there are pictures. I really do not want to see what this looks like. Are there pictures?
This is to be expected. Any time we do any transplant immunosupressants are given to the recipient for the rest of their life, but this only slows the inevitable. Heart transplants recipients all get accelerated atherosclerosis. Lung transplant recipients all get long term fibrosis. We buy time with these procedures and do everything we can to keep them going, but if you have a transplant, you're in a really bad spot…
I just finished up an introductory biology lecture series, and this suddenly makes less sense to me than it did before. What is it about the foreign cells that is identified as foreign by the host cells? The cells ought to be remarkably similar. They're human, with the same function/pluripotency using the same protein interactions. So why attack it?
See, for example, blood types, where giving an A type person B type blood will cause serious issues.
Each human has a largely unique signature of HLAs (https://en.wikipedia.org/wiki/Human_leukocyte_antigen).
This is to be expected. Any time we do any transplant immunosupressants are given to the recipient for the rest of their life, but this only slows the inevitable. Heart transplants recipients all get accelerated atherosclerosis. Lung transplant recipients all get long term fibrosis. We buy time with these procedures and do everything we can to keep them going, but if you have a transplant, you're in a really bad spot…
I just finished up an introductory biology lecture series, and this suddenly makes less sense to me than it did before. What is it about the foreign cells that is identified as foreign by the host cells? The cells ought to be remarkably similar. They're human, with the same function/pluripotency using the same protein interactions. So why attack it?
This is to be expected. Any time we do any transplant immunosupressants are given to the recipient for the rest of their life, but this only slows the inevitable. Heart transplants recipients all get accelerated atherosclerosis. Lung transplant recipients all get long term fibrosis. We buy time with these procedures and do everything we can to keep them going, but if you have a transplant, you're in a really bad spot…
I just finished up an introductory biology lecture series, and this suddenly makes less sense to me than it did before. What is it about the foreign cells that is identified as foreign by the host cells? The cells ought to be remarkably similar. They're human, with the same function/pluripotency using the same protein interactions. So why attack it?
Dendritic cells 'teach' lymphocytes what a foreign invader is, right most of us know that from high school, but here's where it goes beyond me:
>They found that differences between the mice donor's and recipient's SIRPα gene correlated with the recipient's immune responses.
SIRPα isn't an unknown protein, already understood to bind to another protein called CD47 that triggers a range of immune responses in different white blood cells.
>Joining the dots, the researchers believe CD47 on monocytes – the white blood cells that grow into dendritic cells – interact with SIRPα receptors on foreign tissues, setting off the entire ID check process.
>"Once these cells are activated, then they turn around and activate the rest of the immune system, and that leads to the full-blown rejection of the organ," lead researcher Fadi Lakkis from the University of Pittsburgh told Liz Reid at 90.5 WESA.
Here's the paper https://immunology.sciencemag.org/content/2/12/eaam6202
This seems to be the relevant bit
>Using an elegant positional cloning approach, Dai et al. have identified polymorphisms in the mouse gene encoding signal regulatory protein α (SIRPα) to be key in this innate self-nonself recognition. They show that SIRPα receptor CD47 binds SIRPα variants with distinct affinities and propose this affinity sensing to be the mechanism that triggers dendritic cell maturation, the first step in the initiation of the alloimmune response. Given that the SIRPα gene is also polymorphic in humans, it remains to be seen whether human SIRPα variations influence transplantation success.
Earlier quoted context omitted.
I just finished up an introductory biology lecture series, and this suddenly makes less sense to me than it did before. What is it about the foreign cells that is identified as foreign by the host cells? The cells ought to be remarkably similar. They're human, with the same function/pluripotency using the same protein interactions. So why attack it?
There's a lot more to immune response than "does this look like a human cell?" See, for example, blood types, where giving an A type person B type blood will cause serious issues. Each human has a largely unique signature of HLAs ( https://en.wikipedia.org/wiki/Human_leukocyte_antigen ).
This is also why many species reproduce by sex.
If anyone hasn't been through some tragic medical shit in their life, pay attention to that. You'll understand it later.
Earlier quoted context omitted.
I just finished up an introductory biology lecture series, and this suddenly makes less sense to me than it did before. What is it about the foreign cells that is identified as foreign by the host cells? The cells ought to be remarkably similar. They're human, with the same function/pluripotency using the same protein interactions. So why attack it?
Because it's part of the arms race with pathogens that has been going on for a billion years since multi-cellular life first appeared. Pathogens do lots of very clever things to hide from the immune system, so the immune system is tuned to detect very subtle changes. The body largely operates on zero-trust network models, except for a few locations where the benefit of a too-active immune system has serious consequen…
This is to be expected. Any time we do any transplant immunosupressants are given to the recipient for the rest of their life, but this only slows the inevitable. Heart transplants recipients all get accelerated atherosclerosis. Lung transplant recipients all get long term fibrosis. We buy time with these procedures and do everything we can to keep them going, but if you have a transplant, you're in a really bad spot…
Is this true that it is inevitable? My understanding, from my girlfriend attending medical school (only M1), is that for many types of transplants, when immunosupressants are taken properly, it is unlikely that the organ will ever be rejected.
For example, only 10-20% of patients who receive a kidney transplant will experience rejection[1].
[1] https://columbiasurgery.org/kidney-transplant/organ-rejectio...