T-CELL MEMORY Central Effector. 1781:Measles epidemic in the Faroe Islands No measles for 65 years 1846: Measles epidemic Those individuals, who were.

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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: Area: 1400 km 2

DEVELOPMENT OF CELLULAR MEMORY Negative regulation of the immune system 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 ag ains t 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 TEffector T C y tokines/cytotoxicity AICD Central memory T Effector T C y tokines/cytotoxicity PERIPHERAL LYMPHOID ORGANS PERIPHERAL TISSUES Skin 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 THYMUSPERIPHERY NAIVENAIVE IMMUNOLOGICAL EXPERIENCE MEMORYMEMORY

Resting Activated Resting Activated Tissue effector memory T cellsLymphoid central memory T cells PRODUCTION OF EFFECTOR MOLECULES CYTOTOXIC MEMORY T LYMPHOCYTES Proliferation Cytotoxicity

DEPENDENCE OF ANTIGEN IN THE MAINTENANCE OF MEMORY T LYMPHOCYTES IN AIRWAYS MONTHS AFTER INFECTION 136 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 (T EM ) cells LYMPH NODE Memory T cells Antigen-specific Non antigen-specific 24 – 72 hrs Secondary antigen-specific effector T cells developing from central memory (T CM ) cells Woodland DL & Kohlmeier JR 2009 Nat Rev 9:153