t-cell memory central effector. 1781:measles epidemic in the faroe islands no measles for 65 years...

T-CELL MEMORY

Central

Effector

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

Immunological memory

Inhabitants: 46 000Area: 1400 km2

DEVELOPMENT OF CELLULAR MEMORYNegative regulation of the immune system

Days5 10 15 20 25 30

Naive lymphocytes

Az antigen-specific cell number

Primary effector cells

Secunder effector cells

Memory

DIFFERENTIATION

AICD

EXPANSION

AICD

MEMORY

Days

Activation Induced Cell Death

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 re-infection 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

Cytokines/cytotoxicity

AICD

Central memory T

Effector T

Cytokines/cytotoxicity

PERIPHERAL LYMPHOID ORGANS

PERIPHERAL TISSUESSkin dermis, gut lamina propria,

alveolar space

Tissue-specific migration

Effector memory T

Effector T

Cytokines/cytotoxicity

ANTIGEN/ SITE OF INFLAMMATION

T-cells differentiate into central and effector memory cells

AGE

THYMUS PERIPHERY

N

A

I

V

E

IMMUNOLOGICAL EXPERIENCEIMMUNOLOGICAL EXPERIENCE

M

E

M

O

R

Y

Resting Activated Resting Activated

Tissue effector memory T cells Lymphoid central memory T cells

PRODUCTION OF EFFECTOR

MOLECULES

CYTOTOXIC MEMORY T LYMPHOCYTESCYTOTOXIC MEMORY T LYMPHOCYTES

Proliferation

Cytotoxicity

DEPENDENCE OF ANTIGEN IN THE MAINTENANCE OF MEMORY T LYMPHOCYTES IN AIRWAYS

MONTHS AFTER INFECTIONMONTHS AFTER INFECTION

11 33 66

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

LYMPH NODE

Memory T cells

Antigen-specific

Non antigen-specific24 – 72 hrs

Secondary antigen-specific effector T cells developing from

central memory (TCM ) cells

Woodland DL & Kohlmeier JR 2009 Nat Rev 9:153