03 Adaptive Immune System (1)

8/9/2019 03 Adaptive Immune System (1)

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ADAPTIVE IMMUNE SYSTEM

Selectively attack by limiting or neutralizing particular target

Two classes of adaptive immune response:

o Antibody-mediated (humoral ) immunity production of antibodies by plasma

cellso

!ell-mediated immunity production of activated T lymphocytes " cells recognize free-e#isting foreign invaders ie$ bacteria and their to#ins and a

few viruses where they secrete antibodies speci%c for invaders

T cells recognize and destroy body cells gone awry& including virus-infected cells

and cancer cells

T'*S+,: hormone that maintains lineage of T cell

o nhances proliferation of new T cells within peripheral

lymphoid tissueo +ncreases immune capabilities of e#isting T cells

Antibody-Mediated Immunity; B cells

.$ "inding of "!/ to antigens :

" cells have receptors ( " cell receptors 0 "!/s1 ) for antigens

They bind to two main antigens:

o T-independent antigens(polysaccharide antigens) 2 stimulate production of

antibody without T cell involvemento T-dependent antigens(typically protein antigens) 2 re3uires help of helper T

cells for production of antibody

4$ !onversion of " cells to plasma cells 5 production of antibodies

6pon binding to antigens& " cells di7erentiate into active plasma cells while others

become dormant memory cellso 8uring " cell di7erentiation& " cell swells as the rough / e#pands

o 9lasma cells formed become proli%c protein factories producing up to 4

antibodies;so 9lasma cells die after


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tearso +g8 present on surface of " cells

" cells di7erentiate into two cell types plasma cells and memory cells

o 9lasma cells then switch to produce +g? antibodies which are secreted rather

remaining membrane boundo emory !ells

Small portion of " lymphocytes becine memory cells& which do not

participate in current immune attack against antigen but remains

dormant and e#pand speci%c clones

emory cells are primed and ready for immediate action when personis ree#posed to same antigen

@$ /ole of antibodies

Antibodies cannot directly destroy foreign organisms but e#ert protective inuence

by physically hindering antigens ( amplifying innate immune response)

Antibodies physically hinder antigens through neut!ali"ation and

a##lutination$

.$ ,eutralizationo Antibodies combine with bacterial to#in& preventing harmful chemicals from

interacting with susceptible cellso Antibody neutralize some viruses by binding with their surface antigens&

preventing these viruses from entering cells4$ Agglutination

o ultiple antibodies cross-link numerous antigen molecules into chains; lattice of

anti#en-antibody com%le&eso Boreign cells( bacteria& mismatched transfused rbc) will then bind together in a

clumpo Sometimes& antigen-antibody comple# which involve soluble antigens(tetanus

to#in) forms lattice that is so large that it precipitates out of solution

Antibodies amplify innate immune responseso ark foreign materials as targets for actual destruction by complement

system& phagocytes or natural killer cells while enhancing the activity of

these other defense systems Activation of complement system

Antigen bind with antibody& receptors on tail portion of antibody

bind with and activate !.$


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Activation of !. activated other proteins and forms memb!ane

attac' com%le&( A!) which is directed at membrane of

invading cell nhancing phagocytosis

Antibodies especially +g? acts as opsonins$

The tail portion of antigen-bound +g? antibody binds with

receptor on surface of phagocyte and thus promotesphagocytosis of antigen-containing victim

Stimulating ,C cells

,C cells have receptor for tail portion of antibodies

Dhen target cell is coated with antibodies& tail portion of

antibodies link target cells to ,C cells which then destroy the

cells by lysing the plasma membrane

This process is called antibody-de%endent cellula!

cytoto&icity (AD))*


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E$ A!T+F A,8 9ASS+F +6,+T


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P!ima!y !es%onse: 6pon contact with microbial antigen& antibody response is

delayed for several days until plasma cells are formed and then reaches its peak

for a couple of weeks$o After reaching peak& antibody levels gradually decline over period of time

although some are still circulating in the blood

Seconda!y !es%onselonger-lasting& rapid and more potent response by long-lived memory cells in contact with same antigen

o +mportant in preventing and minimizing overt infection on subse3uent

e#posure to same microbes& forming long term immunity against speci%c

disease

Bormation of memory cells occur through the person either actually having the

disease; being vaccinized already

Active Immunity

A production of antibodies as a results of e#posure to an antigen

Faccination:

o #poses person to pathogen that has been stripped of its disease-inducing

capability but still can induce antibody formation against itself

Passive Immunity


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Second way in ac3uiring active immunity

o 8irect transfer of antibodies actively formed by another person; animal$

o 6sually occurs from transfer of antibodies of +g? class from mother to fetus

across placenta during intrauterine developmento otherGs colostrums(%rst milk) contains +gA antibodies that provide further

protection for breast-fed babies

9assively transferred antibodies are usually broken down in less than a month 9rovides immediate protection; bolster resistance against e#tremely virulent infectious

agent ; potentially lethal to#in to which a person has been e#posed( rabies& tetanus

to#in)

Antiserums:

o Antibodies that are harvested from another nonhuman source that has been

e#posed to attenuated form of antigen ( usually horse;sheeps)

Sometimes recipient may be allergic to serum serum sickness

)ell-mediated immunity ;T lym%+ocytes


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T cells do not secrete antibodies but directly contact their targets$

!ontains receptor proteins called T-cell receptors ( T!/s)

Are only activated by foreign antigen when it is on the surface of a cell that also

carries marker of individualGs identityo #ample: both foreign antigens and self antigens ( '! molecules) must be

on a cellGs surface before a T cell can bind with it

echanism:o A delay of few days generally follows e#posure to the appropriate antigen

before activated T cells are prepared to launch cell-mediated immune attack$o Dhen e#posed to speci%c antigen combination& cells of complementary T cell

clone proliferate and di7erentiate & yielding large numbero T cells will also form memory pool and displays primary and secondary

responseso 9rimary response >

+nitiated in lymphoid tissue

HI of T cells in primary response die by apoptosis after infection is

cleared

o *nce pathogen is gone& maJority of lymphocytes commit suicide becauseantigens and stimulatory signals are withdrawn

This prevents congestion in lymphoid tissue

o /emaining surviving T cells become memory T cells that migrate to all area of

bodies& ready for a secondary response

.$ Types of T cells:

!lassi%ed by function : !ytoto#ic T cells & helper T cells& regulatory T cells

!lassi%ed by speci%c membrane protein type: !8K5 T cells& !8E5 T cells& !8E5!84


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Activated by +M-E

o T'.=(new subclass)

9roduces +M-.=$

+M-L from macrophages guide their production

9romote inammation> e7ector molecules in development of

inammatory autoimmune disease

iii$ e#ulato!y T cells. su%%!esso! T cells

'ave same !8E coreceptors as helper T cells& in addition !84< ( component of

receptor for +M-4 which promotes Treg activities)

/epresent


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?ranzymes enter target cell

through perforin channels$ *nce inside& these chemicals

trigger virus-infected cell to self

destruct through apoptosis

6pon released of virus in !B& it is destroyed

by phagocytic cells& neutralizing antibodiesand complement system

Surrounding healthy cells replace lost cells by

cell division

To stop virus infection& some of the host cells

must be destroyed ( sometimes T killer cells

sacri%ce loads of host cells when virus

replicated )


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@$ T helper cells in immune response

Secrete cytokines that aid in nearly all aspect of immune system

!hemicals secreted by T helper cells:

a$ IL-4,IL-5,IL-6 that serve as " cell growth factor contributing in " cell

function in concert with +M-. secreted by macrophages

IL-4promotes development of +g antibodies for defense against

parasitic worms

IL-5activates eosinophils


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b$ IL-2T-cell growth factor which increases activity of T killer cells and other

helper T cells

+M-. secreted by macrophage not only enhances activity of " and T cellsbut alsmo stimulate secretion of +M-4 by activated helper T cells

c$ !hemicals act as chemotaxinluring more neutrophils and macrophage-to-bed$ Macrophage-migration inhibition actorreleased once macrophages attracted

to area$

Ceeps large phagocytic cells by inhibiting outward migration

/esulting more attraction of macrophages in inJured area

This factor also makes macrophagesG phagocytic power 0 angry

macrophage important in defending against bacteria that causes T"


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because the microbes can survive simple phagocytosis by nonactivated

macrophages1

+n order to perform tasks& T cells must be introduced to antigens %rst$

Antigen presenting cells(A9!s) process and process antigen& comple#ed with '!

molecule on their surface to T cells$

A9!s include : macrophages and dendritic cells

8endritic cells abundant in the skin and mucosal lining of lungs and

digestive tracts After e#posure to appropriate antigens& dendritic cells migrate

through lymphatic system to lymph nodes and activate T cells

echanism:

.$ 8endritic cells

phagocytize

invading bacteria :4$ ndocytic vesicle

containing engulfed

bacteria fuses with

lysosome& which

break down

bacteriumGs protein

into antigenic

peptides

@$ ach antigenic

peptide then binds

to newly

synthesized '!

molecule within the endoplasmic reticulum;?olgi comple#E$ 9eptides load onto '! through organelle within A9! ( compartment for

peptide loading )


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M,)

ach person has two main classes of '! encoded

o '! !lass + recognized by cytoto#ic T cells

o '! class ++ recognized by T helper cells

!lass + and ++ markers serve to guide both T cells to precise cellular location

!oreceptors on T cells bind with '! molecule on target molecules& linking both cells

together


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!lass + '! glycoproteins:

o !ytoto#ic T cells can only respond to foreign antigens associated with class +

'! glycoprotein which are only found on body cells /it+ nucleus

o !ytoto#ic T cells can only bind to invaded cells& and cancer cells ( because class +'! molecule also display mutate cellular proteins characteristics of these

abnormal cells)

!lass ++ '! glycoproteins

o /ecognized by helper T cells

o /estricted to surface of few special types of immune cells ( macrophages&

dendritic cells) & " cells

03 Adaptive Immune System (1)

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