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Printable Handouts
Navigable Slide Index
- Introduction
- We are surrounded by viruses
- Our Immune system is diverse
- How immunity diversity is achieved
- The challenge posed by immune system diversity
- Tolerance induction with monoclonal antibodies (1)
- Tolerance induction with monoclonal antibodies (2)
- Proving tolerance induction (1)
- Proving tolerance induction (2)
- The mechanism of tolerance induction (1)
- The mechanism of tolerance induction (2)
- Dominant tolerance displays linked suppression (1)
- Dominant tolerance displays linked suppression (2)
- Tolerance induction using allogenic bone marrow (1)
- Tolerance induction using allogenic bone marrow (2)
- Bone marrow tolerance induction is not dominant
- Tolerance induction to a protein (1)
- Tolerance induction to a protein (2)
- Adjuvant can facilitate tolerance induction
- Tolerance induction in haemophilic mice
- The tolerance state is antigen specific
- Transplantation tolerance is Foxp3-dependent
- Protein tolerance is Foxp3-independent
- Tolerance induction depletes antigen-specific cells
- IL-10 mediates suppression of proliferation in vitro
- Conclusions
- Acknowledgements
Topics Covered
- The immunogenicity of foreign tissues and proteins
- Induction of immune tolerance with monoclonal antibodies
- Properties of therapeutic immune tolerance
- The challenges to achieve tolerance to clotting factors in hemophilia
- The importance of appropriate antigen presentation for effective immune tolerance induction
- Cellular and molecular mechanisms underlying immune tolerance: IL-10, Foxp3, regulatory T cells, and T cell depletion
- Different routes of antigen presentation can recruit different tolerance mechanisms
Links
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Talk Citation
Graca, L. (2020, July 30). Tolerance induction to clotting factors with monoclonal antibodies [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 26, 2024, from https://doi.org/10.69645/NFEF1634.Export Citation (RIS)
Publication History
Financial Disclosures
- Luís Graça has no commercial/financial relationships to disclose
A selection of talks on Immunology
Transcript
Please wait while the transcript is being prepared...
0:00
Hello. I'm Luis Graca.
I'm a Professor of Immunology at the University of Lisbon Medical School,
and I direct a research group at Instituto de Medicina Molecular, also in Lisbon.
0:13
We live surrounded by viruses and other microorganisms.
One of the challenges that we face is how to protect ourselves
against organisms that can adapt very quickly.
The life-cycle of a virus or a bacterium is very short compared with our own life-cycle,
and as a consequence,
with a body that cannot change very fast,
we need to adapt to new infections that may
happen next year or in a few years with agents
that have a chance to evolve to overcome an immune response
that was effective to clear that same pathogen today.
We know from experience,
that if we get flu this year,
we will be protected from another flu infection in the same season,
but we cannot be protected against a flu infection from next year,
because the flu virus from next year,
will be different from this year's viruses.
One way the immune system developed to tackle this problem,
is to have receptors that can anticipate
any molecular change that can happen in a virus in
order to be ready to respond to an infection,
no matter what are the mutations that were acquired by that virus.
1:31
Many years ago it was discovered by Karl Landsteiner,
the same scientist that discovered the blood groups,
that in fact there are antibodies that can recognize many different antigens.
When he immunized animals with different antigens,
he found that no matter what was the antigen used for the immunization,
it was always possible to get an immune response against that antigen.
Even when antigens were not normally present in nature,
the immune system had the ability to create
antibodies specific to that particular antigen.
This means that the immune system is complete,
and can anticipate any mutation that the flu virus from next year may acquire.