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Printable Handouts
Navigable Slide Index
- Introduction
- The existing dogma
- Our working paradigm
- Protective autoimmunity
- The CNS immune enigma
- CNS response to injury
- A matter of interpretation
- Recruitment of macrophages is insufficient
- Site, dose, timing for macrophage implantation
- Emerging questions
- Local and systemic immune response
- Circulating T cells are needed for recovery
- Protective autoimmunity vs. autoimmune disease
- Key questions
- The two faces of macrophages
- Creation of chimeric mice with head protection
- Macrophages play anti-inflammatory role
- Transferred monocytes promote repair
- The infiltrated macrophages are beneficial
- T-cells boost monocyte recruitment
- Macrophages resolve microglia response
- Is the location of the macrophages important?
- The glial scar regulates microglia / macrophages
- CSPG production and degradation
- CSPG and the IL-10 expressing monocytes
- Loss of IL-10 in the absence of CSPG
- Macrophages are 'educated' by the scar
- Co-localization of macrophages with the glial scar
- Location determines macrophage phenotype
- Functional distinction between cells
- Are macrophages involved in neuroprotection?
- Macrophages and neuroprotection in the retina
- Macrophages support cell survival in retina
- Macrophages support progenitor cell renewal
- Interim conclusions
- Why monocyte recruitment is limited?
- Type, phenotype, location, timing
- Tissue repair is very demanding
- Neurogenesis: highest manifestation of plasticity
- CNS specific autoreactive T cells
- Spatial memory
- What is the immunological malfunction?
- Immunity to self and self-maintenance
- Local and systemic inflammation
- Circulating cells fight local inflammation
- Recruitment of monocytes in Alzheimer
- Take home message (1)
- Take home message (2)
- From immune deficiency to brain malfunction
- Immune cells are the nectar...
- Acknowledgements
- Financial support
- Conclusions
Topics Covered
- The CNS immune enigma
- CNS response to injury
- Recruitment of macrophages is insufficient
- Site, dose, timing for macrophage implantation
- Local and systemic immune response
- Circulating T cells are needed for recovery
- Protective autoimmunity vs. autoimmune disease
- Two faces of macrophages
- Creation of chimeric mice with head protection
- Macrophages play anti-inflammatory role
- Transferred monocytes promote repair
- T-cells boost monocyte recruitment
- Macrophages resolve microglia response
- The glial scar regulates microglia / macrophages
- CSPG production and degradation
- CSPG and the IL-10 expressing monocytes
- Co-localization of macrophages with the glial scar
- Location determines macrophage phenotype
- Macrophages and neuroprotection in the retina
- Macrophages support progenitor cell renewal
- Monocyte recruitment is limited
- Type, phenotype, location, timing
- Neurogenesis: highest manifestation of plasticity
- CNS specific autoreactive T cells
- Spatial memory
- The immunological malfunction
- Immunity to self and self-maintenance
- Local and systemic inflammation
- Circulating cells fight local inflammation
- Recruitment of monocytes in Alzheimer
- From immune deficiency to brain malfunction
Links
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Talk Citation
Schwartz, M. (2013, January 30). A paradigm shift in the brain-immune relationships: infiltrating macrophages in central nervous system repair [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 5, 2024, from https://doi.org/10.69645/UVOG1702.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Michal Schwartz has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A paradigm shift in the brain-immune relationships: infiltrating macrophages in central nervous system repair
Published on January 30, 2013
71 min
A selection of talks on Neuroscience
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