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Printable Handouts
Navigable Slide Index
- Introduction
- Content of the talk
- The role of the immune system: criteria for immune ageing
- Older individuals are more susceptible to infection and have higher morbidity and mortality
- SARS-CoV-2 infection: age and sex differences amongst hospitalised patients
- COVID-19 severity: age and sex differences amongst hospitalised patients
- COVID-19 mortality: age and sex differences amongst hospitalised patients
- Reduced vaccination efficacy with age
- Existing immune memory fades
- Cancer incidence increases with age
- Autoimmunity increases with age
- The age-related increase in systemic inflammation: inflammageing
- Causes of inflammaging
- Cells of the immune system
- Impact of Advancing Age on Innate Immunity
- NK cell subtypes
- CD56DIM NK cell cytotoxicity
- NK cytotoxicity decreases with age
- Mechanism of functional decline
- NK cell number and function in COVID-19
- Senescent cells upregulate NKG2D ligands
- Senescent cells also express HLA-E evading killing by CD8 and NK cells
- Ageing and neutrophils
- Typical migratory pathway – young subjects
- Typical migratory pathway – older subjects
- The decline is age-related
- Increased serum NE activity in healthy elders
- Compromised chemotaxis is a leukocyte-wide phenomenon
- Effect of age on phagocytosis
- Reduced NET generation with age
- Age, superoxide and NET generation
- Bacterial infections and age
- Key functions of monocytes and dendritic cells
- Effect of age on monocyte and DC phenotype
- Monocytes/macrophages are basally active but compromised when challenged
- Impact of Advancing Age on Adaptive Immunity
- Cells of the adaptive immune system
- Memory:naïve T cell ratio increases with age
- Thymic output reduces with age due to fat infiltration
- Telomere erosion in CD8+ T cells with age
- T cell senescent-like phenotype in older adults
- IMM-AGE: an integrated score for immune ageing
- Hallmarks of T cell ageing
- Inducing senescence in CD4 T cells accelerates ageing in other body systems
- Effect of age on B cells
- Correcting immunesenescence
- Boosting T cell autophagy improves T cell responses
- Improving T cell function and vaccination responses: Rapamycin
- Old mice are more susceptible to coronavirus infection but senolytics improve survival
- Statins improve neutrophil migration in vitro
- Simvastatin to modify Neutrophil functiOn in Older patients with PneumonIa (SNOOPI)
- Summary
Topics Covered
- Immunesenescence
- Immune ageing
- Inflamaging
- Age-related inflammation
- SARS-CoV-2 and COVID-19
- Age and innate immunity
- Age and adaptive immunity
- Bacterial infections and age
- Telomere erosion
- T cell ageing
- B cell ageing
- Rapamycin
Talk Citation
Lord, J. (2024, September 30). Immune system ageing: immunesenescence [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 10, 2024, from https://doi.org/10.69645/BSAU5922.Export Citation (RIS)
Publication History
Financial Disclosures
- There are no commercial/financial matters to disclose.
Other Talks in the Series: Aging
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, my name is
Professor Janet Lord
from the Institute of
Inflammation and Ageing
at the University of Birmingham.
In today's talk,
I'm going to be talking
about the impact of
advancing age on
the immune system
which has been termed
Immunesenescence.
0:17
What I'm going to cover is
the evidence that
age does compromise
your immune function and
then going to work through
the age-related changes to
the two arms of
the immune system,
the innate immune system and
the adaptive immune system.
Moving on then to how this
influences health generally
and may have an impact beyond
the immune system itself
and finally finishing on ways
that are coming to light
to overcome immune
system ageing.
0:48
We're going to be thinking about
what it is that your
immune system does
and the criteria we might have
for saying that your
immune system ages.
The primary job of
your immune system
is to detect and kill pathogens.
These are viruses,
bacteria, parasites.
It also has to be able
to develop memory
so that when it experiences
that pathogen again,
it responds more quickly
and more precisely.
It has a third function
which is to detect and
kill transformed cells in
the early stages of cancer.
It also, we now know,
removes senescent cells
and it can also remove cells
that have got any damage.
Finally, it has to be
able to detect non-self,
pathogens and cancers, and
delineate them from self
so that we don't have
auto-immune reactions.
This is immune tolerance.
I'll now work through some
of the evidence that shows
these functions are compromised
with advancing age.