Lecture 19 - Memory T Cells Flashcards
2 things that happen when infection gets resolved
- contraction
- memory
what happens during contraction of immune response?
apoptosis kills most effector T cells but some cells remain as memory cells
what is AICD?
Activation-Induced Cell Death in activated T cells
why does AICD occur?
ensures homeostasis so we don’t have accumulation of lymphocytes from each response
what 2 things can trigger AICD
- Fas-L binding Fas
- TNFalpha/beta binding TNFR-1
role of IL2 in AICD
how does this relate to its normal role?
promote Fas-FasL dependent AICD on activated T cells
normally IL2 promotes T cell growth
what cells express FasL?
effector T cells
wha cells express Fas? what is the form of Fas?
activated T cells
Fas is in a trimer
what is the domain on Fas and TNFR-1 that mediate apoptosis
cytoplasmic death domains –> caspases 8/3
role of caspases
to chop up DNA inducing apoptosis
what happens with mutated Fas and FasL?
Leads to lymphoproliferative and autoimmune disorders
what occurs in a successful primary immune response?
pathogen is eliminated and there is long-lasting immune memory
besides T cells, what other component of the immune system protects against a re-infection?
Abs
how do Abs protect against re-infection?
neutralization and opsonization
4 effector functions of memory T cells
- cytokines
- cytotoxicity
- help
- regulation
how does Ab response change in primary vs secondary response? (2)
amount and affinity of Ab increases
lifespan of human memory T cell vs lifespan of human T cell memory
memory T cell: 30-160 days
T cell memory: 10-15 years
if T cell memory lasts much longer than a memory T cell, what does this indicate about memory T cells?
longevity is not an intrinsic characteristic of circulating memory T cells –> there is self-renewal of specific and highly differentiated/rapid effector functions
in CMV-carrying patient who underwent immunosuppressive treatment, what happens to CD8+ T cells when there is an increase in viral load and then when virus is cleared?
increase in viral load = increase in virus-specific effector CD8+ T cells
virus is cleared = 5% of activated T cells become memory T cells
describe relative number of Ag-specific T cells throughout immune response
Infection: increase up to 10,000x more Ag-specific T cells than naive
Memory: decrease to 100x more Ag-specific T cells than naive
describe how the relationship btwn number of memory cells and control of infection changes with age
young: more memory cells = more control of infection
old: more memory cells does not correlate to control of infection
why does the amount of memory cells not correlate to control of infection?
IMMUNOSENESCENCE
what is immunosenescence?
function/efficiency of the memory T cells decreases with age
what are 3 things that can cause immunosenescence?
- genetics
- epigenetics
- host factors
is it possible for a “new” infection to be mediated mainly by memory T cells? example
yes –> for example, influenza has different antigenic proteins that can make up the virus and individual can be infected with virus that has similar components as one they had previously been infected with
what happens if someone is infected with influenza with epitopes A,B,C and then later in life is infected with epitopes B,C,D?
Will have HIGH response to B and C because already previously exposed to them
describe competition of memory vs naive T cells
memory T cells compete with naive T cell response to the same antigen –> if memory has been developed, memory will predominate
is memory dependent on repeated exposure to infection?
no, the memory for an epitope from 1 infection can be long-lasting
how does a memory response change with each infection?
strength declines/weakens
if a memory response weakens with each infection, when can a new + strong primary response take over?
at the 5th infection there is no memory response so disease occurs and a new primary response occurs
where do T cells migrate? (2)
lymphoid tissues or peripheral tissues
