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1. Mononuclear phagocytes - origins, fates and functions
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4. The alveolar macrophage
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5. Airway macrophages in health and disease
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6. Intestinal macrophages - heterogeneity, origins and functions
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8. The biology of Fc receptors and complement receptors
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10. Tumour-associated macrophages
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11. The recognition of pathogens by C-type lectins
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12. Macrophage phagocytosis
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13. Macrophage CD36 and atherosclerosis
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14. Toll-Like receptor signaling and the innate immune response
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15. Innate immune receptors as mediators of systemic inflammation and pathogenesis of malaria
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17. Triggering receptors expressed on myeloid cells (TREM)
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18. Influence of eicosanoid lipid mediators on macrophage innate immune functions
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19. Macrophage paired receptor interactions
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20. Macrophage heterogeneity in atherosclerosis regression
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21. Gaucher disease: from lysosomal storage to immunopathology
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22. Macrophage in asthma
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23. The macrophage mannose receptor
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24. Myeloid-derived suppressor cells in cancer
- Prof. Dmitry Gabrilovich
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25. EGF-TM7 receptors
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26. Macrophages in helminth infection
- Prof. Judith Allen
- Archived Lectures *These may not cover the latest advances in the field
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27. Immunosuppressive mechanisms in myeloid cells
- Prof. Dmitry Gabrilovich
Printable Handouts
Navigable Slide Index
- Introduction
- Elie Metchnikoff, Nobel prize winner
- Metchnikoff's experiment
- T-helper 1 immunity
- T-helper 2 immunity
- Th1 vs. Th2 response
- Lymphatic filariasis
- Larval killing is IL-4 dependent
- Brugia malayi implant model
- The role of macrophages
- Macrophage activation (1)
- Are NeeMacs "alternatively activated"?
- Evidence for alternative activation of NeeMacs
- Arginine metabolism pathway
- Arginase 1
- What genes are expressed by NeeMacs?
- YM1 and RELM-alpha: Th2 markers
- IL-4 and IL-13 both utilize the IL-4alpha receptor
- Alternatively-activated macrophages & worms
- Do NeeMacs kill worms?
- Depletion of macrophages and worm survival
- Interfering with macrophages and worm survival
- Latex beads found within macrophages
- Latex bead treatment enhances worm survival
- Alternative activation is normal
- Are AA Macrophages regulatory cells?
- Are AA Macrophages wound healers?
- Ym1/RELMalpha elevated by surgery alone
- Th2 activated macrophages and tissue repair
- Is response to injury dependent on Th2 cytokines?
- Wound response independent of T cells
- Wound response dependent on IL-4/IL-13
- Sustained response requires Th2 cells
- Macrophage activation (2)
- Wound healing model
- Wound healing model after worm infection
- Two important questions
- A hookworm parasite
- Importance of alternatively activated macrophages
- Helminth migratory phase through the lung
- Nippostrongylus brasiliensis
- Hypothesis
- Repair is slower without IL-4 receptor signaling
- Treg cells are necessary for wound healing
- The anti-inflammatory cell
- Mouse model of filariasis
- Litomosoides sigmodontis
- A mouse model of filarial nematode infection
- Gradual recruitment of inflammatory cells
- Monocyte depletion and macrophage recruitment
- L. Sigmodontis infection vs. Thioglycollate
- Type 2 vs. classical inflammation
- Nematode infection
- Macrophage proliferation during nematode infection
- Tissue macrophages proliferate in situ
- Inflammatory macrophages proliferation: the cavity
- Accumulation of macrophages dependant on IL-4
- IL-4 alone drives macrophage proliferation
- The macrophages aren't bone marrow derived
- Proliferation is a generalized feature of IL-4
- IL-4 impact is independent of macrophage origin
- Summary (1)
- Summary (2)
- Summary (3)
- Acknowledgements
Topics Covered
- Discovery & functions of macrophages
- Th1 and Th2 immunity
- Macrophage activation states
- Macrophage function in helminth infection
- Evolution of Th2 immunity
- Macrophages in inflammation
- Macrophage proliferation in the tissues during Th2 immunity
- New modes of inflammation
Links
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Categories:
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Talk Citation
Allen, J. (2017, March 8). Macrophages in helminth infection [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 6, 2024, from https://doi.org/10.69645/GYOS6986.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Judith Allen has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Immunology & Inflammation
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, my name is Judy Allen and I'm
a professor at the University of Edinburgh in Scotland.
I'm interested in the immune response to parasitic worms,
also known as helminths.
And I've become particularly interested in the role of macrophages,
both in practical terms of host defense but also in terms of their evolutionary origins.
0:18
I'd like to start with a historical perspective since it's been
a little over 100 years since Elie Metchnikoff
won the Nobel Prize for the discovery of macrophages.
And as I have been,
he was strongly influenced by evolutionary biologists and in 1893 made the statement,
"I have indeed dared to put forward a new theory of inflammation,
only because I felt that I had
Darwin's great conception as a solid foundation to build upon."
His most famous experiment which led
to his theory of inflammation was the one in which he put
a rose thorn into a transparent starfish larvae that he had found on the beach.
0:51
This is his description of the experiment and I quote,
"I fetched a few rose thorns and introduced them at once under
the skin of some beautiful starfish larvae as transparent as water.
I was too excited to sleep that night in the expectation of the result of my experiment,
and very early the next morning,
I ascertained that it had fully succeeded.
That experiment formed the basis that the phagocyte theory to
the development of which I devoted the next twenty five years of my life."
What Metchnikoff saw when he looked down
the microscope was that there was a collection of cells around the thorn.
His enormous insight was to understand that
this inflammatory response was a host defense response.
Now, people have witnessed inflammation before,
in mammals and in other systems,
but it assumed it was just damage.
They'd even even seen cells containing bacteria or yeast but thought that was accidental.
This is where Darwin's influence was so strong.
Metchnikoff thought if this very ancient primitive organism is responding
the way mammals are in terms of the influx of cells to the site of injury or infection,
this must have an important function.
Then he was really quite visionary in how he described these cells,
how macrophages could tell self from non-self,
their role in clearing bacteria and fungi,
that they were important for injury repair,
and that overall, that they had critical functions in
returning the organism to homeostasis.