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