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1. Mononuclear phagocytes - origins, fates and functions
- Prof. Steffen Jung
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2. Transcription factors in macrophage differentiation
- Dr. Michael Sieweke
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3. Fetal macrophages
- Prof. Paul Martin
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4. The alveolar macrophage
- Dr. Ronald G. Crystal
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5. Airway macrophages in health and disease
- Prof. Tracy Hussell
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6. Intestinal macrophages - heterogeneity, origins and functions
- Prof. Allan Mowat
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7. Osteoclasts: what do they do and how do they do it?
- Prof. Steven L. Teitelbaum
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8. The biology of Fc receptors and complement receptors
- Prof. Steven Greenberg
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10. Tumour-associated macrophages
- Prof. Michele De Palma
- Dr. Mario Squadrito
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11. The recognition of pathogens by C-type lectins
- Prof. Gordon D. Brown
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12. Macrophage phagocytosis
- Prof. Joel Swanson
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13. Macrophage CD36 and atherosclerosis
- Dr. Maria Febbraio
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14. Toll-Like receptor signaling and the innate immune response
- Dr. Kate Fitzgerald
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15. Innate immune receptors as mediators of systemic inflammation and pathogenesis of malaria
- Prof. Ricardo Gazzinelli
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17. Triggering receptors expressed on myeloid cells (TREM)
- Dr. Daniel W. McVicar
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18. Influence of eicosanoid lipid mediators on macrophage innate immune functions
- Prof. Marc Peters-Golden
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19. Macrophage paired receptor interactions
- Prof. Neil Barclay
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20. Macrophage heterogeneity in atherosclerosis regression
- Prof. Edward Fisher
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21. Gaucher disease: from lysosomal storage to immunopathology
- Prof. Johannes M.F.G. Aerts
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22. Macrophage in asthma
- Prof. Douglas Robinson
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23. The macrophage mannose receptor
- Dr. Luisa Martinez-Pomares
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24. Myeloid-derived suppressor cells in cancer
- Prof. Dmitry Gabrilovich
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25. EGF-TM7 receptors
- Dr. Jörg Hamann
- Dr. Hsi-Hsien Lin
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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
- Regression: from bad to better?
- Mouse model of regression (1)
- Absence of macrophages after regression
- Mouse model of regression (2)
- Rapid exit of monocyte-derived cells
- First hint of macrophage heterogeneity
- Heterogeneity of cell types in arterial lesions
- Example of LCM of macrophage foam cells
- Blocking the CCR7 pathway blocks regression
- Summary of part 1
- Lipoprotein changes from apoE-/- to WT mice
- HDL and vascular protection
- Model to test selective normalization of HDL-C
- Normalization of HDL-C promotes regression
- Regression is impaired
- HDL modulates CCR7 levels
- Molecular mechanism for CCR7 regulation
- Evidence for SRE-activation in vivo
- Summary of part 2
- Part 3: changes in macrophage polarization
- Classification of macrophages in tissues
- HDL regulates the inflammatory state (1)
- HDL regulates the inflammatory state (2)
- HDL enriches CD68+ cells in M2 markers (1)
- HDL enriches CD68+ cells in M2 markers (2)
- Are the changes model dependent?
- MiR-33 negatively regulates ABCA1 expression
- Predicted effects of blocking miR-33
- miR-33 in LDLr-/- mice regulates HDL Levels
- Less inflammation in plaque macrophages
- Some models of macrophage "plasticity"
- Summary of part 3
- Overall summary (1)
- Overall summary (2)
- Acknowledgements
Topics Covered
- Novel research tools
- Developing mouse models to study atherosclerosis regression
- Developing the tools to analyze macrophage trafficking and molecular phenotypes in vivo
- The regression of atherosclerosis by HDL due to its effects on the quantity and phenotype of macrophages in plaques
- Macrophage polarization
- Plasticity during atherosclerosis regression
- Models for the enrichment in cells in the M2 state
Links
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Talk Citation
Fisher, E. (2012, June 11). Macrophage heterogeneity in atherosclerosis regression [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/IODW9558.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Edward Fisher, Consultant: Merck; Speaker’s Bureau: Merck; Grant/Research Support (Principal Investigator): Merck