The immune system

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Transcript The immune system

Honors Anatomy & Physiology
Chapter 21
 nonspecific
defense that is active immediately
upon infection
 found in all animals & plants
 includes:

outer covering


skin or shell
chemical secretions

@ openings to interior of body
 skin,
mucous membranes & their secretions
highly effective barriers…unless not intact
 epidermis with thick keratinized layers of
cells blocks most microorganisms
keratin resistant to most bacterial enzymes &
toxins
 intact mucosae just as protective

1. Acid
 acidic pH inhibits bacterial growth
(bacteriostatic)
2. Enzymes


Lysozyme in saliva, tears, sputum bacteriocidal
gastric enzymes also bacteriocidal
3. Mucin
 + water  sticky lining of digestive &
respiratory passages: traps pathogens
4. Defensins:
broad-spectrum antimicrobial peptides secreted
by mucous membranes & skin
5. Other: lipids in sebum & dermicidin in eccrine
sweat toxic to bacteria
1. Phagocytes:
 Neutrophils

become phagocytic when find infectious
material
Fixed & Wandering Macrophages

from monocytes
2. Natural Killer Cells

in lymph

 phagocyte
must adhere to pathogen in order
to ingest it
 bacteria with external capsules elude capture
 Opsonins: proteins released by immune cells
that coats the capsules (opsonization) 
phagocytes can capture them
 nonspecific
killers of any cell w/out “self” cell
surface markers
 travel through body patrolling for:


virus-infected cell
cancer cells
 Not
phagocytic
 induce target cell  apoptosis
 secrete potent chemicals that enhance
inflammatory response
 triggered
when tissues injured by:
physical trauma
2. intense heat irritating
3. chemicals
4. infection by viruses, fungi,
or bacteria
1.
 beneficial
1.
2.
3.
4.

effects:
prevents spread of damaging agents to
nearby tissues
diposes of cell debris & pathogens
alerts adaptive immune response
sets stage for repair
*ultimate goal: clear injured area of
pathogens, dead tissue cells, other debris so
tissue can be repaired
1.
2.
3.
4.
Redness
Heat
Swelling
Pain
 1st
step: “chemical alarm”
 chemicals released by:



injured or stressed cells immune cells
mast cells  histamine
macrophages recognize type of invader using
surface receptors called TLRs and release specific
chemical in response  triggers release of
cytokines
 other



chemicals released:
kinins
prostaglandeins
complement
1.
2.

vasodilation  hyperemia (congestion with
blood)  2 of cardinal signs: redness & heat
increased permeability = exudate  other 2
cardinal signs: swelling (edema), pain
capillaries allow fluid containing clotting
factors & antibodies  swelling  pain
 macrophages
predominant cell cleaning up
cell debris @ sites of prolonged or chronic
inflammation
 pus: mixture of dead or dying neutrophils,
damaged or dead tissue cells, living & dead
pathogens
 if inflammatory response has failed to clear
area collagen fibers may be laid down 
walling off area  abscess: may require
surgical drainage to heal
1. Interferons
 secreted by cells in response to viral
invasion
 not viral specific
 help nearby cells make proteins that
interfere with viral replication
2. Complement provides major mechanism for
destroying foreign substances in body
 releases inflammatory chemicals
 lyses & kills certain bacteria
 abnormally
high body temperature
 pyrogens: chemicals released by neutrophils &
macrophages  alters thermostat in
hypothalamus
 adaptive response that benefits body:
1. liver & spleen sequester iron & zinc making
them less available to support bacterial
growth
2. increases metabolic rate of tissue cells in
general
 https://www.khanacademy.org/science/hea
lth-and-medicine/human-anatomy-andphysiology/introduction-toimmunology/v/inflammatory-response
 body‘s
built -in specific defense system
 3 features:
1. Specific
2. Systemic
3. Memory
 2 parts
1. Humoral or antibody-mediated immunity
 B Cells
2.Cellular or cell-mediated immunity
 T Cells
 1.
complete antigens
 2. incomplete antigens
 Functions:
1.
2.
Immunogenicity: ability to elicit certain
lymphocytes to proliferate (multiply)
Reactivity: ability to react with activated
lymphocytes & the antibodies released
B
lymphocytes  T lymphocytes
 make antibodies  cellular immunity
humoral
 mature in thymus
immunity
1. Immunocompetence
 mature in bone
 ability of immune cells
marrow
to recognize (by binding)
to specific agns;
recognition implies
presence of plasma
membrane receptors
2. Self-tolerance
 APCs
 engulf
agns  present fragments of them
onto their cell-surface markers
 major types:
1. Dendritic cells
2. Macrophages
3. B cells
 most
important APC (only job they have)
 internalize agn  migrate to nearest lymph
node  present agn to T cells
 present
agns to T cells in order to be activated
by effector T cells  release chemicals that in
turn activate the macrophage  increases
their phagocytic activity
 do
not activate naïve T cells like dendritic
cells or macrophages
 only present to T helper cells in order to get
help for their own activation
 once
activated, most of the clone members
become effector cells = plasma cells

plasma cells secrete antibodies
 rest
become memory cells
 http://web.biosci.utexas.edu/psaxena/Micro
biologyAnimations/Animations/HumoralIm
munity/micro_humoral.swf
 Memory
cells capable of mounting a rapid
attack against the same antigen in any later
encounters (secondary immune response)
 Memory B cells provide humoral
immunological memory
 http://web.biosci.utexas.edu/psaxena/Micro
biologyAnimations/Animations/HumoralIm
munity/micro_humoral.swf
 acquired
during
1st exposure to
agn:
 Infection
 Vaccination
provides memory
 acquired




Active
through
injection of abys into
body
passage of abys
from mother 
fetus in utero
passage of abys to
newborn in
breastmilk
*NO MEMORY
Passive
 Immune
system exposed
to harmless version of pathogen



triggers active immunity
stimulates immune system to produce
antibodies to invader
rapid response if
future exposure
 Most
successful
against viral diseases
1914 – 1995
April 12, 1955
 Developed

first vaccine
against polio

attacks motor neurons
Albert Sabin
1962
oral vaccine
4



polypeptide chains
2 heavy chains
2 light chains
held together by disulfide bonds
 constant
areas determine function & aby class
 variable area enable recognition of specific
agn
1.
2.
3.
4.
5.
Ig M: 1st aby secreted from plasma cell
during 1◦ response, potent agglutinator
Ig A: found in body secretions: saliva,
sweat, milk, blocks attachment of agns to
mucous membranes
Ig D: functions as B cell membrane agn
receptor
Ig G: most #’s in plasma, main aby of 1◦
& 2◦ responses, only 1 to cross placenta
Ig E: binds to mast cells & basophils 
release histamine, levels rise during
allergic rx or chronic parasitic infections
of GI tract
http://highered.mheducation.com/sites/0072507470/stude
nt_view0/chapter22/animation__the_immune_response.ht
ml
 pure
preparations (a clone) of a single aby
type
 useful in diagnostic tests
1.
2.
3.

pregnancy
STDs
Hepatitis
treating some types of cancer


Leukemia
Lymphomas
You need trained assassins to kill off these
infected cells!
T
Attack
of the
Killer T cells!
2007-2008
 agn
presentation to T cells  provokes
cellular immune response
 2 major populations of T cells (based on
which of 2 surface proteins a mature T cell
displays:; both  memory cells:
1. CD4 = helper T cells: TH


activate B cells, macrophages
direct adaptive immunity (does not happen
w/out TH
CD8= cytotoxic T cells: TC
2.

destroy any cell in body that has anything
foreign in it
infected cell
killer
T cell
or
activated
macrophage
helper
T cell
helper
T cell
stimulate
B cells &
antibodies
helper
T cell
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
helper
T cell
Y
Y
Y
interleukin 1
activate
killer T cells
Y
helper
T cell
 Destroys


infected body cells
binds to target cell
secretes perforin protein

punctures cell membrane of infected cell
Killer T cell
binds to
infected
cell
infected cell
destroyed
Killer T cell
vesicle
cell
membrane
perforin
punctures
cell membrane
target cell
cell
membrane
http://highered.mheducation.com/sites/0072507470/st
udent_view0/chapter22/animation__tcell_dependent_antigens__quiz_2_.html
skin
free antigens in blood
humoral response
Y
Y antibodies
Y
Y
Y
Y
memory
B cells
Y
Y
Y
Y
Y
macrophages
(APC)
helper
T cells
B cells
plasma
B cells
pathogen invasion
antigen
exposure
skin
antigens on infected cells
cellular response
T cells
memory
T cells
cytotoxic
T cells
 cell-mediated
responses reject grafts & foreign
transplants unless the recipient is
immunosuppressed
 infections are major complications
SCID
1.




Severe Combined Immunodeficiency
group of genetic disorders deficit of
functioning T and B cells
untreated:fatal
tx:bone marrow transplant
acquired immunodeficiencies
1.Hodkins lymphoma
2. AIDS
 Human


Immunodeficiency Virus
virus infects helper T cells
helper T cells don’t activate rest of immune system: T
cells & B cells

also destroy T cells
 Acquired


ImmunoDeficiency Syndrome
infections by opportunistic
diseases
death usually from other
infections

pneumonia, cancer
 occurs
when the body regards its own tissues
as foreign & mounts an immune attack
against it
 Rheumatoid arthritis
 Graves disease
 Hashimoto’s thyroiditis
 Multiple sclerosis
 Celiac disease
 Lupus (SLE)
 abnormal
reaction to otherwise harmless agn
immediate hypersensitivity
1.
allergies/ Ig E aby
2. subacute hypersensitivity:
 abys & complement

3. delayed hypersentsitivity:

cell-mediated
4
attributes that characterize the immune system
as a whole

specificity


diversity


react to millions of antigens
memory


antigen-antibody specificity
rapid 2° response
ability to distinguish self vs. non-self

maturation & training process to reduce auto-immune
disease
