Tissue effector memory T cells Lymphoid central memory T cells

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Transcript Tissue effector memory T cells Lymphoid central memory T cells

T-CELL MEMORY
Central
Effector
Immunological memory
Inhabitants: 46 000
Area: 1400 km2
1781:
Measles epidemic in the Faroe Islands
No measles for 65 years
1846:
Measles epidemic
Those individuals, who were older than 65 years and were infected
in 1781 did not became sick, but some elderly people got the
infection
1. Life-long protection can be induced against some viruses
2. Presence of the virus is not needed for the maintenance of
immunological memeory
DEVELOPMENT OF CELLULAR MEMORY
Negative regulation of the immune system
AICD
DIFFERENTIATION
Naive
lymphocytes
Az antigen-specific cell
number
Activation Induced Cell Death
Memory
Secunder
effector cells
Primary effector
cells
EXPANSION
AICD
MEMORY
5
10
15
20
25
30
Days
Days
Presence of specific antibodies during primary and secondary immune
responses protects against repeated infections
• A successful primary immune response eliminates the pathogen and results in
long-lasting immunological memory
• Antibodies produced during the primary immune response protect against reinfection by neutralization and opsonization.
Both effector B and T cells and memory B and T cells
are produced during a primary immune response
Comparison of the B-cell populations that participate
in the primary and secondary adaptive immune responses
The amount and affinity of
antibody increase after
successive immunizations
with the same antigen
IgG antibody suppresses the activation of naive B cells
by cross-linking the B-cell receptor and FcγRIIB1
on the B-cell surface
Passive immunization with anti-Rhesus antigen IgG prevents
hemolytic anemia of the newborn
Highly mutable viruses such as influenza gradually
escape from immunological memory without stimulating
a compensatory immune response
Memory CD4 T cells express an altered CD45 isoform
that works more effectively with the T-cell receptor
and co-receptors
Naive T
Effector T
AICD
Cytokines/cytotoxicity
Central memory T
Effector memory T
PERIPHERAL TISSUES
Skin dermis, gut lamina propria,
alveolar space
PERIPHERAL
LYMPHOID ORGANS
Tissue-specific migration
Effector T
Effector T
Cytokines/cytotoxicity
ANTIGEN/ SITE OF INFLAMMATION
Cytokines/cytotoxicity
T-cells differentiate into central and effector memory cells
AGE
THYMUS
PERIPHERY
M
E
N
M
A
O
I
R
V
Y
E
IMMUNOLOGICAL EXPERIENCE
CYTOTOXIC MEMORY T LYMPHOCYTES
PRODUCTION OF
EFFECTOR
MOLECULES
Tissue effector memory T cells
Resting
Activated
Lymphoid central memory T cells
Resting
Activated
Proliferation
Cytotoxicity
DEPENDENCE OF ANTIGEN IN THE MAINTENANCE OF MEMORY T
LYMPHOCYTES IN AIRWAYS
MONTHS AFTER INFECTION
1
3
6
After successful elimination of viral infections the number of antigen presenting DC and the
newly activated memory T cells is decreased
Secondary antigen-specific effector T cells developing from effector memory (TEM ) cells
Memory T cells
LYMPH NODE
24 – 72 hrs
Non antigen-specific
Secondary antigen-specific
effector T cells developing from
central memory (TCM ) cells
Antigen-specific
Woodland DL & Kohlmeier JR 2009 Nat Rev 9:153