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Printable Handouts
Navigable Slide Index
- Introduction
- Learning objectives
- Complement evolution
- The 'classic' view of complement
- Complement activation pathways
- Complement deficiencies lead to infections
- Revised view of complement
- Complement deficiencies & autoimmune disease
- Complement's impact on adaptive immunity
- Complement recognizes and removes 'threats'
- Complement receptors act as sensors & effectors
- Complement receptors activate immune cells
- Complement-mediated indirect activation of T cells
- Complement and human Th1 biology
- CD46: structure and function
- The lack of an in-vivo model for CD46 research
- CD46-signaling requirements
- Th1 induction/contraction is CD46/IL-2 dependent
- CD46 and IL-2 regulate the 'Th1 life cycle'
- CD46-deficient T cells & Th1 responses
- CD46 deficient patients
- CD46/C3 dysregulation contributes to disease
- Th1 induction: mice vs. humans
- C5aR1 & C3aR1 role in T cell responses
- Impact of anaphylatoxin receptors on CD4+ T cells
- Impact of complement receptors on CD4+ T cells
- Complement and CD8+ T cells
- Evidence for intracellular complement activation
- Signaling pathways driven by CD46/IL-2R
- Inside-in versus outside-in signaling
- The implications of intracellular C3 activation
- CD46 co-stimulation during CD4+ T cell activation
- Cell metabolism in immune biology
- What about C5?
- C5-NLRP3 inflammasome & normal Th1 induction
- ‘Normal’ Th1 cells have a NLRP3 signature
- NLRP3 inflammasome activation
- Th1 immunity requires inflammasome activity
- The ‘Complosome’ regulates Th1 responses
- Intracellular/autocrine systems in cell metabolism
- Intracellular complosome-driven pathways
- Summary
- Acknowledgements
Topics Covered
- Complement in the regulation of general immune cell activity
- Indirect (APC-mediated) effects of complement on T cell activation
- Direct effects of complement on T cell responses
- Role of autocrine and intracellular complement (the Complosome) in Th1 responses
- Crosstalk between the NLRP3 inflammasome and the Complosome
- Regulation of cell metabolism by intracellular/autocrine complement
Links
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Talk Citation
Kemper, C. (2017, August 31). Complement and T cells [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 6, 2024, from https://doi.org/10.69645/WMOI8573.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Claudia Kemper has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: The Complement System
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, everybody. My name is Claudia Kemper.
I'm a Senior Investigator and the Chief of
the Complement and Inflammation Research section at the National Heart,
Lung and Blood Institute at the National Institutes of Health in Bethesda,
Maryland, the United States.
Today, I will tell you a little bit about Complement and T cells.
After my lecture, you should know now the direct and indirect impact of complement on
T cell responses and the importance of circulating versus immune cell-derived complement.
0:33
So, the learning objectives for my lecture today
are that you understand the direct and indirect impact that
complement can have on T cell responses and also
the importance of circulating versus immune cell-derived complement.
0:50
So, complement has evolved from
a serum effector system to an autocrine functioning system.
And, surprisingly, recent data indicate that this system
also works intracellularly and has been coined, 'the complosome'.
1:07
When people hear the word complement,
usually certain ideas pop into their mind.
One is that they remember that the key effector molecules of complement are C3 and C5,
and that complement is an ingrained part of innate immunity.
Also, complement is strongly pro-inflammatory.
It is the key mediator of the inflammatory reaction.
People remember that complement is liver-derived and serum-effective,
and people believe that complement is explored
and probably most think it's actually slightly boring.