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- Models of Investigation
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1. Antifungal innate immunity in C. elegans
- Dr. Jonathan Ewbank
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2. The anti-microbial defense of Drosophila: a paradigm for innate immunity
- Prof. Jules Hoffmann
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3. Phagocytosis in the fruit fly, Drosophila melanogaster
- Dr. Lynda Stuart
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4. Innate immune sensing and response
- Prof. Bruce Beutler
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5. Macrophages and systems biology
- Prof. David Hume
- Cell Types and Recruitment
-
6. Leukocyte recruitment in vivo
- Prof. Paul Kubes
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8. Eosinophils
- Prof. Tim Williams
-
9. Dendritic cells: linking innate to different forms of adaptive immunity
- Prof. Ralph Steinman
-
11. Innate-like lymphocytes 1
- Prof. Adrian Hayday
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12. Innate-like lymphocytes 2
- Prof. Adrian Hayday
- Recognition and Signaling
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13. Colony stimulating factor-1 regulation of macrophages in development and disease
- Prof. E. Richard Stanley
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14. Fc receptors: linking innate and acquired immunity
- Prof. Ken G C Smith
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15. Phagocytosis
- Prof. Joel Swanson
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16. Clearance of apoptotic cells and the control of inflammation
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17. Signaling by innate immune receptors
- Prof. Michael Karin
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18. Nuclear receptors at the crossroads of inflammation and atherosclerosis
- Prof. Christopher Glass
- Modulation of Effector Responses
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19. Humoral innate immunity and the acute phase response 1
- Prof. Alberto Mantovani
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20. Humoral innate immunity and the acute phase response 2
- Prof. Alberto Mantovani
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21. Cytokines regulating the innate response
- Prof. Anne O’Garra
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22. Arginase and nitric oxide
- Dr. Peter Murray
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23. Novel lipid mediators in resolution of inflammation
- Prof. Charles Serhan
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25. Cationic peptides in innate immunity
- Dr. Dawn Bowdish
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26. Iron metabolism and innate immunity
- Prof. Tomas Ganz
- Pathogen-Host Interactions
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27. Innate recognition of viruses
- Prof. Caetano Reis e Sousa
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28. Type I interferons in innate immunity to viral infections
- Prof. Christine Biron
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29. HIV-1 and immunopathogenesis: innate immunity
- Prof. Luis Montaner
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30. Understanding and combating tuberculosis
- Prof. David Russell
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32. Innate immunity and malaria
- Prof. Douglas Golenbock
- Health and Disease
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33. Innate immunity in children
- Prof. David Speert
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34. From bench to bedside: evolution of anti-TNFalpha therapy in rheumatoid arthritis
- Prof. Sir Ravinder Maini
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35. NOD-like receptors in innate immunity and inflammatory disease
- Prof. Gabriel Nunez
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36. Paneth cells in innate immunity and inflammatory bowel disease
- Prof. Satish Keshav
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37. Innate immunity in the brain in health and disease
- Prof. V. Hugh Perry
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38. The fate of monocytes in atherosclerosis
- Prof. Gwendolyn Randolph
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39. Macrophages, a cellular toolbox used by tumors to promote progression and metastasis
- Prof. Jeffrey Pollard
- Archived Lectures *These may not cover the latest advances in the field
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40. Monocyte/macrophages in innate immunity
- Prof. Emeritus Siamon Gordon
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41. Innate immunity in C. elegans
- Dr. Jonathan Ewbank
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43. NLR genes: infection, inflammation and vaccines
- Prof. Jenny Ting
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44. Manipulation of innate immune response: lessons from shigella
- Prof. Philippe Sansonetti
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45. Innate immunity of the lung and adaptation to air breathing at birth
- Prof. Jeffrey Whitsett
Printable Handouts
Navigable Slide Index
- Introduction
- T cells recognise class I and II MHC molecules
- Dendritic cells activate naive T cells
- Key features of dendritic cells (DC)
- Talk outline
- Class II MHC pathway
- Ii / MHC class assembly and processing
- Class I MHC pathway
- Non-canonical antigen presentation pathways
- Function of non-canonical pathways
- Antigen capture
- DC maturation and antigen capture/presentation
- Endocytosis is initially stimulated by LPS
- Rsk mediates TLR-signalled antigen capture
- Microbial stimuli transiently arrest migration
- Invariant chain processing and DC migration
- Distinct antigen capture pathways
- Antigen processing
- Constructive vs. destructive processing
- How do T cell epitopes survive?
- Reducing proteolysis can improve presentation
- Antigen presentation
- Models for display in immature and mature DC
- MHC II ubiquitination and cell surface expression
- TLR signalling effects on DC antigen presentation
- TLR ligand enhances presentation
- How does cross-presentation actually work?
- Different pathways for cross-presentation
- 'ER-phagosome' and class I loading
- Elements of the ER required for cross-presentation
- TAP and Sec61 effect on cross presentation
- Endosomal TAP is needed for cross-presentation
- Distinct parallel compartments for MHC l and II
- Two other pathways of cross-presentation
- Antigen presentation by DC in vivo
- DC sub-types in lymphoid organs
- CD8+ and CD8- DC and MHC class I or II
- Why are some DC better at cross-presentation?
- Antigen transfer from migratory to resident DC
- Migratory and resident DC involved in T cell priming
- Plasmacytoid DC can present antigens to T cells
- Summary
- Acknowledgements
Topics Covered
- Conventional and non-conventional antigen processing pathways
- Innate stimuli boost antigen capture, processing and presentation
- Destructive antigen processing is minimised in dendritic cells (DC)
- Class II MHC display is regulated by ubiquitination
- Linking antigens and TLR ligands can enhance presentation
- Distinct endocytic compartments and/or distinct dendritic cell sub-sets may host antigen presentation on class I MHC molecules (cross-presentation) and on class II MHC molecules
- Antigen bearing migratory DC and lymph node resident DC can collaborate to induce T cell responses
Talk Citation
Watts, C. (2009, June 30). Antigen processing and presentation: modulation by innate immune signals [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/FQLZ6313.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Colin Watts has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Antigen processing and presentation: modulation by innate immune signals
A selection of talks on Immunology
Transcript
Please wait while the transcript is being prepared...
0:00
This is a
talk on antigen processing
and presentation, and
in particular how it's
regulated by innate immune signals.
And it's given by Colin Watts
from the University of Dundee.
0:13
Antigen presentation refers to
the display of short process
peptides on so-called MHC,
or major histocompatibility
complex molecules.
Seen here is a class I MHC molecule
with the short 8-residue peptide
found in a peptide binding groove.
Class I MHC molecules generally
have peptides between 8
and 10 amino acid residues.
Whereas class II MHC molecules
display considerably longer
peptides due to a more open
ended peptide-binding groove.
It's the recognition
of these peptide MHC
complexes by the T
cell antigen receptors
that initiates most
immune responses.
We can distinguish the two
classes of MHC molecule
by the types of
peptide they present.
As simply diagrammed here, class
I MHC molecules display peptides
which are derived
from intracellular,
i.e. cytosolic or nuclear proteins,
which as we'll see in a moment,
become loaded in the
endoplasmic reticulum
and transported to
the cell surface where
they're recognized by CD8 T cells.
Usually the outcome
of recognition is
killing, for example, of the
virally infected or a tumor cells.
In contrast, class II MHC molecules
capture and display peptides
derived from exogenous
proteins, i.e. proteins taken up
into the cell by one or
more forms of endocytosis,
for example, bacterial
toxins like tetanus toxin.
Here the endocytic pathway acts
as the site for peptide loading.
And then following transport
to the cell's surface,
the CD4 T cell can perform various
functions, for example can help
a B lymphocyte to differentiate and become
an antibody producing cell.
The two T cells seen in this slide
are so-called effector T cells.
They have previously
been activated and are
primed to perform an effector
function, which was just described.
But these T cells must have already
been activated by a different type
of antigen presenting cell.
And it's clear, and as well
discussed elsewhere in the series,
that dendritic cells are uniquely
able to prime naive T cells.
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