* upbeat music *
Hello, I'm Ann-Charlott and I'm currently
in the final phase of my doctoral thesis at the University of Cologne,
My research is about corneal transplants and why and these are rejected.
Cornea, not to be confused with calluses,
is the outermost layer of our eye.
The cornea is incredibly important for our vision.
Why is easy to explain:
Now you can see me well, and that's because
the lens of the camera that films me is functional and transparent.
But when I now do this...
* Crash noise *
then you cannot see clearly anymore.
What I now did with this tool,
illnesses or injuries do to your cornea.
Now you need a transplant that replaces the broken cornea.
Tataaaa, your vision works once again.
But unfortunately that is not always so easy, because often the cornea is not only broken, but..
blood vessels grow into the cornea, these do not exist in a healthy one.
And that's a problem, because if those vessels are there,
the transplant will be rejected by the patient's immune system.
The vessels are thus responsible for the poor prognosis of
corneal transplantations. If researchers prevent
the ingrowth of the vessels with a drug, then
the acceptance of the transplant is improved.
Problem solved?
Unfortunately, no...
Because even if there are already vessels present, treatment with the drug
improves acceptance of the graft. How can this be?
And this is what I look at with my doctoral thesis, I try to see
whether this drug does not just affect the vessels
but also affects the immune system and so
leads to the improvement of corneal transplantations
To discern this I look at treated versus
untreated mice and compare their immune system.
I use the mouse model for corneal transplantation, because unfortunately
you can not do these experiments completely in the Petri dish yet
because I need a functioning organism
so that I can look at the immune system as a whole.
Even tests on people are more problematic
because to guarantee an acceptance of the transplants
we would have to treat for a long time,
and that carries the risk of side effects.
The mouse experiment is limited in time and so the side effects do not occur.
the long-term goal is to understand the mechanism of action
of the drug so that we can improve it
to the point that the drug acts specific,
works efficiently and does not cause side effects in humans.
When a transplant is detected by cells of the immune system,
These cells raise an "attack signal"
This signal must now be brought to the command center
to start an attack mission.
The vessels work as a means of transport.
And that is prevented by the drug
with two complementary mechanisms:
1. It blocks the vessels, so disrupts the means of transport.
If there are no vessels,
the cells have to "walk"
That takes a long time and is really exhausting for them,
which is why they lose their "attack signal" by exhaustion.
2. At the same time, the drug works as a
thief and steals the "attack signal".
This leads to the final result:
attack signals do not arrive in the command center,
the graft will not be attacked!
These results are an important step, because it helps us
to understand the mechanism behind the drug better.
And by this my doctoral thesis paves the way for the development of
better drugs that prevent rejection of corneal transplants!
*upbeat music plays again *
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