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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
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6. Leukocyte recruitment in vivo
- Prof. Paul Kubes
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8. Eosinophils
- Prof. Tim Williams
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9. Dendritic cells: linking innate to different forms of adaptive immunity
- Prof. Ralph Steinman
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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
- Prof. Sir John Savill
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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
- Short introductory video
- Conservation of homeostatic mechanisms
- Why study host-pathogen interactions?
- Natural habitat of C. elegans
- Worldwide distribution of C. elegans
- Characteristics of natural isolates
- Relationship between nematodes and pathogens
- Infectious diseases of lower animals and plants
- Describing diseases of nematodes by fungi
- Interaction between nematodes and fungi
- Fungal pathogens of nematodes
- Infection of C. elegans by the fungus D. coniospora
- New tools on the fungal side
- Phylogeny of nematophagous fungi
- No common mechanism among fungi
- Countering host defenses: saposins
- SapA is expressed on spores and at hyphal tips
- Genes differentially regulated after fungal infection
- C. elegans-specific genes induced by Drechmeria
- NLPs, CNCs, FIPs and FIPRs in Caenorhabditis
- nlp clusters in 3 Caenorhabditis species
- Expression of nlp cluster in C. elegans
- nlp-29p::GFP as a reporter of immune response
- Induction of nlp-29p::GFP
- D. coniospora penetrates the cuticle
- Physical injury of C. elegans (1)
- Physical injury of C. elegans (2)
- Wounding causes rapid calcium transients
- The peni, hipi and nipi mutants
- Multiple snf-12 alleles
- A STAT protein as a SNF-12 interactor
- SNF-12 moves towards wound sites
- Controlling the response of C. elegans to infection
- RNAi by feeding (1)
- RNAi by feeding (2)
- Automated RNAi screen - process
- Automated RNAi screen
- A genome-wide RNAi screen results
- Clone selection
- Glycan changes sensitivity to pathogen
- Glycan balance
- Decreased infectional genes expression clones
- Pathways controlling C. elegans fungi response
- dcar-1 required for response to injury and infection
- Potential DCAR-1 ligands (1)
- Potential DCAR-1 ligands (2)
- HPLA increases upon infection
- HPLA is a derivative of tyrosine
- HPLA acts as a DAMP via DCAR-1
- VHP-1 is a negative-regulator of p38
- Ectopic expression of nlp-29p::GFP
- Ospf: a phosphthreonine lyase
- Ospf: a phosphthreonine lyase pathway
- Akirin in Drosophila
- Akirin and the NuRD complex
- nlp genes pathway
- Global functional analysis
- Functional analysis of nlp-29
- Mitochondrial unfolded protein response
- Conservation of foundling genes
- An orphan foundling gene
- Conclusions
- Thanks to our collaborators
- Acknowledgments
Topics Covered
- Ecology of C. elegans
- Historical background to host-parasite studies with nematodes
- D. coniospora, a natural pathogen of C. elegans
- Fungal infection and injury induce antimicrobial peptide genes
- Genetics to understand the control of antimicrobial peptide gene expression
- The importance of the nematode surface coat
- Signal transduction pathways that control antimicrobial peptide gene expression
Talk Citation
Ewbank, J. (2018, February 28). Antifungal innate immunity in C. elegans [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/IQSV8004.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Jonathan Ewbank 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. I'm Jonathan Ewbank.
Researcher. Ciml in Marseille, France.
0:06
Today, I'm going to be talking in some detail about the interaction
between C. elegans and a specific fungal pathogen.
Before you watch this lecture,
you may want to see the one that I recorded in 2011,
which gives some background information about C.
elegans and about its interaction with various pathogens.
0:26
Organisms throughout evolution have needed active homeostatic mechanisms that
maintain stable internal environment in the face of external variations.
Many of these environmental changes concern abiotic parameters like
ph or temperature that are the same now as they were when life first evolved.
Perhaps, not surprisingly, the molecular mechanisms,
that are deployed, for example,
to counter heat shock, are highly conserved.
Pathogens represent another challenge to organismal homeostasis.
But in this case, the challenge is not static.
Pathogens can evolve rapidly.
As a consequence, post defense mechanisms need to adapt to a constantly evolving threat.
Along each branch of the phylogenetic tree,
species have evolved their own specialized forms of defense.
For example, adaptive immunity is only found in jawed vertebrates.
We have chosen to look at host defenses in the nematode Caenorhabditis elegans,
a widely used model in biology.
1:26
C. elegans diverged from mammals hundreds of millions of years ago.
Studying its interactions with pathogens promises to
give insights into origins and evolution of host defenses.
C. elegans is well suited to investigations at the molecular,
cellular, and organismal level.
So it can help us, not only understand how an immune system works,
but also how it functions in the context of the physiology of a whole organism.
We chose C. elegans for many reasons,
but principally because it is a very powerful genetic model.
There's a strong research community that collectively
has generated a broad set of experimental tools and resources.
Further, it represents a branch of the evolutionary tree that had not been
explored and so is complementary to other models used to investigate innate immunity.