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Body's Immune System can be Redirected
Ridgelift writes "BBC News have this story of a key chemical signalling system, called Notch, which governs how our body develops immune cells. By pre-treating patients who are about to undergo an organ transplant, it's possible to 'redirect' the immune system so it does not launch an attack on the donor organ. This may soon eliminate the need for transplant patients having to take a lifetime of powerful immunosuppressive drugs that have many unwanted side-effects."
immunesystem > /dev/null
By pre-treating patients who are about to undergo an organ transplant, it's possible to 'redirect' the immune system so that it does not launch an attack on the donor organ.
A couple of quick points:
1. The experiments were done in mice, not humans.
2. All the mice undergoing the treatment underwent graft rejection.
During the early 80s scientists at the Fred Hutchinson Cancer Research Center experimented with T-cell depleted stem cell transplants in an effort to prevent graft-versus-host disease (GvHD), a principal cause of death following bone marrow transplantation. The principle behind GvHD is similar to that of an organ rejection, except that the immune system recognizes the whole body as foreign and attacks it. When mice were given T-cell depleted transplants from MHC mismatched donors (something that promotes GvHD and is why you have to find a bone marrow donor match), their survival rates were identical to that of mice who receaved autologous transplants (they donated bone marrow to themselves - no GvHD). To say that the transplant community was excited would be an understatement. One prominent scientist even wrote that "we've (the transplant community) solved the problem of GvHD".
However, when clinical trials involving humans begain, it was quick discovered that while GvHD was reduced (not eliminated), there was a huge increase in graft failure (in otherwords, the patients didn't develop an immune system - very bad).
The immune system is a tricky thing. While mice are the experimental model, the experimental results don't always match those from humans. We can do a whole lot of things in vitro to mice cells that we can't even begin to duplicate in human lymphocytes. Additionally, mice and humans don't always share the same functional receptors (mice Ly-108 vs the human KIRs).
I applaud the BBC news report - at least they identified that the study was simply a step, used animals, and didn't cure the mice. The Slashdot summary is simply flat out incorrect.
You're confusing "too strong" and "too weak" with specificity. Autoimmune diseases result from the immune system attacking the wrong target (self). Having a given autoimmune disorder does not provide a boost in defending against cancer or an attack by a pathogen.
Immune suppressive drugs work by non-specifically decreasing the immune system as a whole. Immune suppressive drugs work by a method totally foreign to the immune system and parallels to how the immune system is regulated in a healthy individual can not be made.
I'm not that familiar with CD8+ suppressor T cells, however the jury is still out regarding if CD4+CD25+ suppressor cells are target specific or non-specific (data to support both).
The immune system is far more complicated that you're making it out to be.