Download - The Body's Defence
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Chapter 43 Caesar Tin-U, Danh Vu
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Contents.
! 1stdefence: Nonspecific Defences
! 2nddefence: Inflammation
! 3rddefence: Specific Immunity
! Immune Response
! Immunity in Health and Disease
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Foreign Invaders
! Called Pathogens" Viruses, bacteria or
other living thing thatcausesdisease/immune
response.
! Antigens" Toxins that pathogens
produce that cause
harm to an organism.
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#$ They dont distinguish between foreign organisms
%$ Can be viewed in relation to a besieged city:
#$ 1stline of defence Skin = City walls
2ndline of defence Phagocytes = Foot soldiers
3rdand last defence Immune system = Secret Agents
Nonspecific Defences
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Nonspecific Defenses
Against Infection! Organisms must find a means of defence against
antigens such a viruses described on the previouspage.
! If this was not the case, bacteria, fungi and viruseswould replicate out of control inside other organismswhich would most likely already be extinct.
! Therefore organisms employ many types of defence tostop this happening.
! Means of defence can be categorized into first andsecond lines of defence, with the first line usuallyhaving direct contact with the external environment.
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The First Line of Defence
Got own3d?
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The First Line of Defence
! First Lines of Defence
! Skinis an excellent line of defence because it provides an almost
impenetrable biologicalbarrierprotecting the internal environment.
ALactobacillusspecies, possiblyDoderlein's bacillus, in association
with a vaginal epithelial cell.
(Squamous epithelial)
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!
Lysozymeis an enzyme found in tears and saliva that haspowerful digestive capabilities, and can break down foreign
agents to a harmless status before they enter the body.
! It damages bacterial cell walls by catalyzing
hydrolysis of 1,4-beta-linkages between
N-acetylmuramic acid andN-acetyl-D-glucosamine residues in a
peptidoglycan and between
N-acetyl-D-glucosamine residues in
chitodextrins.
! (In Plain English: It just disassembles their cell walls)
(They can also be found largely in your favorite product: eggwhites)
Lysozyme
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The primary structureof egg white
lysozyme - shown here - is a single
polypeptide chain of 129 amino acids.
There are four pairs of cysteinesthat
form disulfide bridges between positions
6 and 127
30 and 115
64 and 80
76 and 94
(counting from the N-terminallysine).
These cross-bridges force us to realize
that this polypeptide is not a straight
chain (like cellulose, for example).
Rather the chain must fold to allow these
cysteines to be close to each other.
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And the rest of the stuff!
Mucusand ciliafound in the nose and throat can catchforeign agents enteringthese open cavities then sweepthem outside via coughing, sneezing and
vomiting.
! The cell wallof plants consists of fibrousproteins which provide a barrierto
potential parasites (antigens).
! If these first lines of defence fail, then there are further defenses found within
the body to ensure that the foreign agent is eliminated.
Figure 1. Gram stain of a species of Micrococcus,commonly isolated from the skin and nasal membranes of humans.
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Contents.
! 1stdefence: Nonspecific Defences
! 2nddefence: Inflammation
! 3rddefence: Specific Immunity
! Immune Response
! Immunity in Health and Disease
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The 2ndline of defence.
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These series of slides will take you though thebasic response to outside stimuli and bodily
responses of tissue injury.
The Inflammatory Response
Summary
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InjuryTissue injury occurs
Sequence 1: Tissue injury
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#$ Tissue injury
#$ Causes release of pain
mediators
%$ Release of ATP,
acetycholine and serotonin.
#$ Forms prostaglandin E2= bradykinin release
&$ Bradykinin +
Prostaglandins=
#$ Vasodilatation & flag for
leucocytes to follow.
Pain inflammatory mediators
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Which leads to the actions of the 2ndline of defence.
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Pha -> Go -> Cytosis!
Second lines of defence dealwith antigens that have
bypassed the first lines of
defence and still remain a
threat to the infected
organism.
-WBC home on to
Interferons, chemical signals
released by cells under attack.
(Click for video)
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These phagocytes contain digestive enzymes in
their lissome (an organelle in phagocytes) such
as lysozyme.
White blood cells such as a neutrophilor a
monocyte are capable of undergoingphagocytosis, which is illustrated below.
Monocyte:
(Video)
Neutrophil: (Video)
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Copyright 2006 American Society of Hematology. Copyright restrictions may apply.
Fukumoto, J. et al. ASH Image Bank 2006;2006:6-00023
Pathology:Hemophagocytosis
Associated with:
EpsteinBarr virus-T-
cell lymphoma.
EpsteinBarr virus
(EBV) can infect T
lymphocytes and
manifests as
hemophagocyticlymphohistiocytosis
(HLH), a distinct entity
of hemophagocytic
syndrome (HPS)
characterized by fever,
hepatosplenomegaly,
cytopenia,hypercytokinemia, and
systemic macrophage
activation with
hemophagocytosis.
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Copyright 2002 American Society of Hematology. Copyright restrictions may apply.
Maslak, P. et al. ASH Image Bank 2002;2002:100540
Figure 1. Histiocytes ingesting red cell precursors may be seen in response to certaininfections
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Pyrogens- High-molecular-weight substances of
polymerous nature, like lipopolysacharids.
They increase the temperature of the body contributing todefence.
Inhibits growth of some microorganisms.
Facilitates phagocytosis
Catalyses bodily reactions (tissue synthesis)
Sometimes responsible for septic shock
Body temperature exceeds normal fever.
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The phagocytes:
Eosinophils
Natural killer (NK) (T
cells)
Monocytes
Neutrophils
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Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Maslak, P. ASH Image Bank 2005;2005:101382
Natural Killer (T-Cell)
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Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Maslak, P. ASH Image Bank 2005;2005:101369
Monocytes may be increased in chronic infections, chronic inflammatory disorders and
some forms of MDS and myeloid leukemia
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Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Maslak, P. ASH Image Bank 2005;2005:101375
Plasmacytoid lymphocytehas an oval nucleus with condensed
chromatin
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Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Lazarchick, J. et al. ASH Image Bank 2005;2005:101296
Figure 1. Peripheral smear from a 17 year old female with Chediak-Higashi syndrome is
shown
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Copyright 2004 American Society of Hematology. Copyright restrictions may apply.
Maslak, P. ASH Image Bank 2004;2004:100992
Figure 1. Lymphoblastsin the peripheral blood
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Contents.
! 1stdefence: Nonspecific Defences
! 2nddefence: Inflammation
! 3rddefence: Specific Immunity
! Immune Response
! Immunity in Health and Disease
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Cytokines (chemokines)Structure of interleukin 2
Schematic overview of the highaffinity
interleukin2 receptor complex, including
the receptor chains, downstream signaling
components and target genes
Fig. 1
Fig. 2
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exposed surface
hidden surface
hinge region
carbohydrate
Previously
hidden surface
Lambda
Kappa
Intact Immunoglobulin Free Light Chain
Bradwell, Serum free light chain assay
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Chemokines:
-50 different proteins-Induces inflammation
-Induces toxin production in lymphocytes
Called
chemo-taxis.
(like taxiing)
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Contents.
! 1stdefence: Nonspecific Defences
! 2nddefence: Inflammation
! 3rddefence: Specific Immunity
! Immune Response
! Immunity in Health and Disease
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The last line of defence.
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Antibodies
Interferons
How Specific Immunity Arises
Lymphocytes are the key cells to immunity
and bodily defence.
They generate the key responses thateliminate infections.
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This is a specific response to a specific
pathogen/antigen.
! The response involves the creation ofAntibodies.
Third Line of Defense Specific Immune Response
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Antibodies
! Y-shapedproteinmolecule.
! Made up of variableandconstantregions.
! Made up of Heavyand
Light chains.! Produced by B-
Lymphocytes
! Function:Recognizeantigens, bind to anddeactivate them.
" Note: Variable regionrecognizes the anitgens.
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How an antibody operates/works?
Deactivation of a bacterium by an antibody.
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Lymphocytes
1. 2 types:
1. B Lymphocyte (B-Cells)
2. T Lymphocyte (T-Cells)
2. Along with their variations:
1. Helper T Cells
2. Cytotoxic T cells
They display specificityonly targeting foreign cells
Lymphocytes detect foreign molecule marker
Antigen
Countered withAntibodies. (Antigen = Short for Antigen-
generator)
Created by B Cells
Video
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Origin of lymph
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How to Identify Friend or Foe?
While B cells and T cells are maturing in the
bone marrow and thymus, their antigen receptors
are tested for potential self-reactivity.
Lymphocytes bearing receptors for molecules
already present in the body are destroyed byapoptosis
Normally has lymphocytes that react against its
self
Failures of selftolerance leads to
autoimmune diseases.
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Autoimmune Disease
! Autoimmune diseases are diseases where theimmune system begins to attack itself.
" Ex:
! Rheumatoid Arthritis crippling disease of the
joints.! Lupus disease of blood and organs.
! Multiple Sclerosis disease of nervous system
! Cause(s): unknown
! Cures/Treatments: No known cures. Usually treatedwith drugs.
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Autoimmune diseasesAcute disseminated encephalomyelitis(ADEM) yes G04.0 is a form of encephalitiscaused by an autoimmune reaction and
typically occurring a few days or weeks after a viral infection or a vaccination.Addison's diseaseyes E27 is often caused by
autoimmune destruction of the adrenal cortex.Ankylosing spondylitisyes M08.1, M45. is a chronic, painful, progressive
inflammatory arthritis primarily affecting spine and sacroiliac joints, causing eventual fusion of the spine.Antiphospholipid
antibody syndrome(APS) yes D68.8 affects the blood-clotting process. It causes blood clots to form in veins and/or arteries.
Aplastic anemiano D60 is often caused by an autoimmune attack on the bone marrow.Autoimmune hepatitisno K75.9 is a
disorder wherein the liver is the target of the body's own immune system. Autoimmune Oophoritisno N70 is a disorder in
which the immune system attacks the female reproductive organs. Celiac diseaseno K90.0 is a disease characterized by
chronic inflammation of the proximal portion of the small intestinecaused by exposure to certain dietary glutenproteins.
Crohn's diseaseno K50 is a form of inflammatory bowel diseasecharacterized by chronic inflammation of the intestinal tract.
Major symptoms include abdominal pain and diarrhea. There is also a theory that Crohn's Disease is an infectious disease
caused by Mycobacterium avium paratuberculosis. Diabetes mellitus type 1yes E10 when it is characterized by a deficiency
or absence of insulinproduction (Type I), is often the consequence of an autoimmune attack on the insulin-producing beta
cellsin the islets of Langerhansof the pancreas. Gestational pemphigoidno O26.4 is a pregnancy-related blistering condition
where autoantibodies are directed against the skin. Goodpasture's syndromeyes M31.0 is a disease characterised by rapiddestruction of the kidneys and haemorrhagingof the lungs through autoimmune reaction against an antigen found in both
organs. Graves' diseaseyes E05.0 is the most common form of hyperthyroidism, and is caused by anti-thyroid antibodies
that have the effect of stimulating (agonist) the thyroidinto overproduction of thyroid hormone. Guillain-Barr syndrome
(GBS) yes G61.0 is an acquired immune-mediated inflammatory disorder of the peripheral nervous system(i.e., notthe brain
and spinal column). It is also called acute inflammatory demyelinating polyneuropathy, acute idiopathic polyradiculoneuritis,
acute idiopathic polyneuritis and Landry's ascending paralysis. Hashimoto's diseaseyes E06.3 is a common form of
hypothyroidism, characterised by initial inflammation of the thyroid, and, later, dysfunction and goiter. There are several
characteristic antibodies (e.g., anti-thyroglobulin). Idiopathic thrombocytopenic purpurayes D69.3 is an autoimmune disease
where the body produces anti-platelet antibodies resulting in a low platelet count Kawasaki's Diseaseno M30.3 is often
caused by an autoimmune attack on the arteries around the heart. Lupus erythematosusyes L93, M32 is a chronic (long-
lasting) autoimmune disease wherein the immune system, for unknown reasons, becomes hyperactive and attacks normaltissue. This attack results in inflammation and brings about symptoms. This is a "Non-organ-specific" type of autoimmune
disease. Mixed Connective Tissue Diseasehas features of other connective tissues diseases lupus, rheumatoid arthritis,
scleroderma and polymyositis. The presence of a specific antibody called U1-RNP is needed for diagnosis. Multiple
sclerosisyes G35 is a disorder of the central nervous system(brain and spinal cord) characterised by decreased nerve
function due to myelinloss and secondary axonaldamage. Myasthenia gravisyes G70.0 is a disorder of neuromuscular
transmissionleading to fluctuating weakness and fatigue. Weakness is caused by circulating antibodies that block
(antagonist) acetylcholinereceptors at the neuromuscular junction. Opsoclonus myoclonus syndrome(OMS) n/a n/a is a
neurological disorder that appears to the result of an autoimmune attack on the nervous system. Symptoms include
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AllergiesAllergy
- An exaggerated response by the immune system to an allergen.
Allergen:a normally harmless substance that causes an allergicreaction.
ex: dust, pollen, mould, food, insect stings
Types of Allergic reactions
There are two types of allergic reactions.
a. Immediate occurs within seconds and normally lasts for about30 mins.
b. Delayed takes longer to react and can last for a much longertime.
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What happens during an allergic reaction?! During an allergic reaction antibodies cause histaminesto be
released from certain cells.
Histamines cause:
a. Swelling of tissues
b. Release of fluids (runny noses and eyes)
c. muscle spasms (some cases)
Anaphylaxis or anaphylactic shock:This is the sudden and severe allergic reaction to a substance thatcan cause death.
Treatments for Allergies
1. Avoidance of material especially food.
2. Epinephrine epi pen3. Antihistamines -- benadryl
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Autoimmune disease - MS
Multiple sclerosis (MS) is typically considered to be a disease of young
adults.
Environmental triggers Environmental exposure to a specific
infectious agent during a window of immunologic vulnerability in
childhood may predispose some individuals to the development of MS
[9] . Many viral and bacterial pathogens have been putatively linked todemyelination. Of these, the Epstein-Barr virus (EBV) has attracted
much attention.
Exposure to EBV results in persistent B-cell infection, expansion of
EBV-transformed B-cell clones, and the production of antibodies
directed against specific EBV viral antigens as well as lifelong T-cell
surveillance of infected B-cells [10] . EBV nuclear antigen has a similar
structure to myelin basic protein, a major component of central nervous
system (CNS) myelin. T-cells directed against EBV antigens may be
redirected to attack CNS myelin because of similarity between the
antigens, a process termed molecular mimicry.
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Treatment of MS
No cureOnly management tehniques
administration of high doses of intravenouscorticosteroids, such as
methylprednisolone.
(This will end the attack sooner, and prevent major damage)
Side effects include: osteoporosis, and impaired memory.
Immunosuppressantalso used in cancer chemotherapy(Approved only in the USA.)
Alternative treatments
Different alternative treatments are pursued by many patients
Dietaryregimens
Herbal medicine
On the other hand the therapeutic practice of martial artssuch as tai chi,
relaxation disciplines such as yoga, or general exercise, seem to mitigate
fatigue and improve quality of life.
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A) Axial FLAIR MRI demonstrating largetumefactive areas of demyelination. B)
Axial T1 with gadolinium contrastdemonstrating enhancement of the lesion
margins.FLAIR: fluid-attenuated inversion recovery;MRI: magnetic resonance imaging.
T1-weighted MRIscans (post-
contrast) of same brain slice
at monthly intervals. Bright
spots indicate active lesions.
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Ergo Break~~
5 minutes
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What is the Major histocompatibility complex (MHC)?
It is a native molecule
TWO main classes of MHC
Mark body cells as self
Class I MHC molecules are found on almost all
nucleated cells - that is, on almost every cell.
Class II MHC molecules are restricted to a fewspecialized cell types, including macrophages, B
cells, activated T cells, and those inside the thymus.
The MHC provides a biochemical fingerprint virtually
unique to each individual.
NUMBER ONE REASON why transplant operations
fail.
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IdentificationClass I MHC molecules, found in almost all cells,
are poised to present fragments of proteins madeby infecting microbes, usually viruses, to
cytotoxic T cells.
Cytotoxic T cells respond by killing the infected cells.
Because all of our cells are vulnerable to infection by
one or another virus, the wide distribution of class I
MHC molecules is critical to our health.
Class II MHC molecules are made by only a few
cell types, chiefly macrophages and B cells.
These cells, called antigen-presenting cells (APC
in this context, ingest bacteria and viruses and then
destroy them.
Class II MHC molecules in these cells collect peptid
remnants of this degradation and present them to
helper T cells.
In response, the helper T cells send out chemical
signals that incite other cell types to fight the
pathogen.
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Were almost done
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Contents.
! 1stdefence: Nonspecific Defences
! 2nddefence: Inflammation
! 3rddefence: Specific Immunity
! Immune Response
! Immunity in Health and Disease
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Got lazy?...
I i
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Immunity
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The Pathway of Specific Immune Response
Pathogens
Pathogens eaten by Macrophage
Displays portion of Pathogen
on surface
Helper-T cell recognizes
Pathogen
Step 1
Step 2
Step 3
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Activates B- CellActivates Cytotoxic
T- Cell
Memory B-CellMemory T-Cell
Kills Infected CellsAntibodies
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Cellular Immunity .vs. Antibody Immunity
! Carried out by T-Cells
! Infected cells are killed
by Cytotoxic T Cells.
! Carried out by B-cells
! Antibodies are produced
and dumped into blood
stream.
! Antibodies bind toantigens and deactivate
them.
Cellular Immunity Antibody or Humoral Immunity
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Immune Response Explained
1. Antigen infects cells.
2. Macrophage ingests antigen and displays portion on itssurface.
3. Helper T- Cell recognizes antigen on the surface of themacrophage and becomes active.
4. Active Helper T-Cell activates Cytotoxic T-Cells and B-Cells.5. Cytotoxic T-Cells divide into Active Cytotoxic T-cells andMemory T Cells.
6. Active Cytotoxic T-Cells kill infected cells.
7. At the same time, B-Cells divide into Plasma Cells andMemory B- Cells.
8. Plasma cells produce antibodies that deactivate pathogen.
9. Memory T and Memory B cells remain in the body to speedup the response if the same antigen reappears.
10. Supressor T-Cells stop the immune response when allantigens have been destroyed.
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Immune Response Summary
Antigen
Macrophage
Helper T - Cell
Active Cytotoxic T-Cell Active B - Cell
Kills Infected Cells Memory T- Cell Plasma Cell Memory B-Cell
Antibodies
Deactivates Antigens
Displays copy of antigen
on surface of cell
Cellular ImmunityAntibody Immunity
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Primary .vs. Secondary Immune Response
! Primary Immune Response
" This is a response to an invader the First time the
invader infects the body.
! No measurable immune response for first few days.
! Next 10 15 days antibody production grows steadily
! Secondary Immune Response
" A more rapid response to an invader the 2ndtime it
invades the body.! Antibody production increases dramatically and in a much
shorter time period..
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Primary .vs. Secondary Immune Response
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Passive .vs. Active Immunity1. Active Immunity
This is immunity where the body is actively producing antibodies
to fight infection.Ex: You have a throat infection and you are actively creating
antibodies to fight it.
Vaccination: An injection of a weakened strainof aninfectious microbe (pathogen) that causes the body to undergoactive immunity (produce antibodies).
2. Passive Immunity
This is immunity where antibodies are given to aperson from the blood of another person or animal.
This immunity only lasts for a short period of time.
ex: Breastfeeding mothers pass antibodies to theirchildren through the milk.
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! HIV is a retrovirus.
! A more specific name is Lentivirus.
! Retroviruses have an RNA genome that isreplicated via a DNA intermediate in infected
cells. DNA also integrates in the hostgenome to form provirus.
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Structure of HIV
Sarcophagus-shaped capsid
contains 2 copies of RNA genome
(SS (+) strand), a reversetranscriptase, integrase, and
protease.
P7 coats the RNA, and P24 forms
the nucleocapsid structure, which
is enclosed by a lipid bilayer.
Lipid bilayer comes from the host
cell, but contains two viral-
encoded glycoproteins, gp41 (41
kDa) and gp120 (120 kDa).
gp120 binds the CD4 receptor on
helper T cells.
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Infection
gp120 and gp41 associate with one
another. The complete complex is
probably trimeric (3 copies of each
protein).
Beta turns in C3 and C4 regions are
important for binding to the cell-
surface CD4 receptor.
Primary Target: CD4 helper T cells.
The normal role of these cells is to stimulate macrophages to destroy
pathogens, and coordinate the immune response. They have on their
surface, a glycoprotein called CD4. The viral protein gp120 binds CD4.
Gp120 also binds the chemokine co-receptor. gp41 causes membrane
fusion (between virion and cell).
H d HIV kill ll ?
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How does HIV kill cells?
Virus budding from cell membrane is not lethal. Cells die by autofusion, syncytial
formation, and apoptosis. Other mechanisms?
1. Autofusion
CD4 and gp120/41 proteins
mediate fusion and intracellular
vesicle formation.
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2. Syncytium formation
gp120/41 proteins on
infected cells bind to CD4
receptors on normal cells,
causing cell fusion. Thegiant multi-nucleated
syncytium dies before
long.
3.Apoptosis
An infected helper T cell can direct an uninfected T helper cell to undergo
apoptosis (programmed cell death). Apoptosis can be normal, forexample, to eliminate auto-reactive T lymphocytes to establish self-
tolerance.
Normal cell
Infected cell
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Current Therapies
1. Nucleoside analogues and other RT
inhibitors.
2. Active site inhibitors of the HIV
protease (part of the Pol gene).3. Interferon (stimulates anti-viral
response)
4. Cocktails of all 3.
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Whole virus vaccines
Attenuated viruses: Essentially intact, living HIV virions that havebeen chemically or genetically damaged.
Whole killed virus: Intact virions that have been damaged so badly
that they are completely nonfunctional (dead).
Subunit vaccines
Clone one gene from HIV, express the protein and use it to vaccinate
patients. The disadvantage is that the person only raises antibodies
against one target. With free virus, the targets are mainly the
envelope proteins; however, these are extremely variable proteins.
Six amino acids of the V3 loop of gp120 appear to be relatively
constant (some variability exists but most antibodies cross react with
the variants). Antibodies against cocktails of different V3's are being
tried.
Nucleic Acid Vaccines
Gene gun, muscle expression.
Vaccines?
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A Major Challenge in Maintaining
Control of HIV! HIV evolves rapidly! The RT is error-prone (no proof-
reading)
! ~ 1-2 mutations in each cDNA copy ofthe 9.8 kb RNA genome
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! Caesars little cancer cell fighting theory
applied to HIV / AIDS.
The Immune PathwayThink Michaelis-
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The Immune PathwayEffector Cell IL-2 Molecules
IL-2 ReceptorTumor
recognition site
Tumor
cells
Step 1
Step2
1. IL-2 binds IL-2 Receptor
2. Effector Cell with
bound IL-2
3. Effector Cell Activated
And Multiply
4. Tumor Eating
Site Activated
6. Attack Mode!
c ae s
Menton
5. Locates Tumor
Step 3Step 4
Step 5
Step 6
Calculus
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Calculus.
Change in
Effector cells
over time
Antigenicity
and size of
tumor
Death
rate
Death
rate
IL-2
StimulationEffector Cell
Injection
Change in
Tumor cells
Logistic
growth rate
of Tumor
Killing rate
by Effector
cellsChange in IL-2
Natural
production of IL-2IL-2
Injection
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Lupus
Lupus is a long-term autoimmune disease.
Immune system attacks body
causing inflammation and tissue
Symptoms:
Fatigue, fever, skin rashes, and muscle
and joint pain.
Some people may have severe episodes;
others have a milder form of the disease.
There is no cure for lupus.
More common in women than men.
The Epstein-Barr virushas been linked to lupus in children.
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References:
1. Kandel ER, Schwartz JH, Jessell TM, editors. Principles of
Neural Science (Fourth Edition). New York: McGraw Hill (Health
Professions Division). 2000;472-491.
2. Millan MJ. Progress in Neurobiology 1999;57:1-164.
3. Dickenson AH. Brit J Anaesthesia 1995;75:193-200.
4. Suzuki R and Dickenson AH. Neuroreport 2000;11:R17-21.
5. Waxman S. Pain 1999;6:S133-140.
References
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Works cited / Sources
! Kumar and Clark Clinical Medicine, 5thed.
! Campbell Reece Biology 6th& 7thed.
! Steven Zumdahl Chemistry 6thed.
! http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/L/Lysozyme.html
! http://www.textbookofbacteriology.net/normalflora.html
! https://reader008.{domain}/reader008/html5/0313/5aa7c1a67a4cd/5aa7c1d027586.jpg! http://www.georgiapainphysicians.com/l2_edu_pharma_mod2_slides.htm
! www.worldofteaching.com! www.hopkins-aids.edu/hiv_lifecycle/! www.who.int/hiv/en! hivinsite.ucsf.edu/InSite.jsp?doc=kb-02-01-02
! Chris Cunningham & Asad Usman Adoptive Immunotherapy
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And more sources
! Rosenberg, SA, Yang, JC, White, DE, et al. Durability of complete responses in patients with metastatic cancertreated with high-dose interleukin-2: Identification of the antigens mediating response. Ann Surg 1998; 228:307.
! Rosenberg, SA, Yang, JC, Topalian, SL, et al. Treatment of 283 consecutive patients with metastatic melanoma orrenal cell cancer using high-dose bolus interleukin-2. JAMA 1994; 271:907.
! Nicola NA (ed) (1994) Guidebook to Cytokines and their Receptors. Oxford: Oxford University Press.
! OstrandRosenberg S (1994) Tumor immunotherapy:the tumor cell as an antigenpresenting cell. CurrentOpinionin Immunology 6: 722727.
! Rosenberg SA. Lotze MT. Muul LM. Chang AE. Avis FP. Leitman S. Linehan WM. Robertson CN. Lee RE. RubinJT. et al. A progress report on the treatment of 157 patients with advanced cancer using lymphokine-activated killercells and interleukin-2 or high-dose interleukin-2 alone. [Journal Article] New England Journal of Medicine.316(15):889-97, 1987 Apr 9.
! Kirschner D. Panetta JC. Modeling immunotherapy of the tumor-immune interaction. [Journal Article] Journal ofMathematical Biology. 37(3):235-52, 1998 Sep.
! J.C. Arciero, T.L. Jackson, and D.E. Kirschner. A mathematical model of tumor-immune evasion and siRNAtreatment. [Journal Article] Discrete and Continuous Dynamical Systems: Series B. 4(1) 39-58, 2004 Feb.
! Dudley ME. Rosenberg SA. Adoptive-cell-transfer therapy for the treatment of patients with cancer. [Review] [97refs] [Journal Article. Review. Review, Tutorial] Nature Reviews. Cancer. 3(9):666-75, 2003 Sep.
! Chang W., Crowl L., Malm E.,Todd-Brown K., Thomas L., Vrable M. Analyzing Immunotherapy and Chemotherapyof Tumors through Mathematical Modeling. [Book] Department of Mathematics: Harvey-Mudd University, 2003Summer.
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Nonspecific Specific Immune ArisingImmunity In
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2 pt
3 pt
4 pt
5pt
1 pt
2 pt
3 pt
4 pt
5 pt
1 pt
2pt
3 pt
4pt
5 pt
1pt
2pt
3 pt
4 pt
5 pt
1 pt
2 pt
3 pt
4pt
5 pt
1pt
Nonspecific
Defense
Specific
Defense
Immune
Responses
Arising
ImmunityHealth and
Disease
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The ingestion ofinvading organisms by
certain type of white cells
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What is Phagocytosis?
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These are thephagocytic cells.
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What are neutrophils?
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The skin, mucous,membranes, and
secretions of skinand
mucous membranes.
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What is the firstline of defense?
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Phagocytic white bloodcells, antimicrobial
proteins theinflammatory response.
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What is the secondline of defense?
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This sets the bodys
thermostat at
a higher temperature.
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What are Pyrogens?
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White blood cells.
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What areLymphocytes?
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An antigen-bindingimmunoglobulin that functions
as the effector in an
immune response.
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What are antibodies?
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Lymphoctyes andAntibodies
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What is the thirdline of defense?
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Molecules secreted by blood
vessel endothelial cells
and monocytes.
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What are chemokines?
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A group of at least20 blood proteins that
cooperate withother defense mechanisms.
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What is thecomplement system?
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A protein that forms
pores in the target
cells membrane.
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What is perforin?
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A localized regionon the surface of an
antigen that ischemically recognized
by antibodies.
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What is a epitope?
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Can simulate antibody
production only withhelp from T helper cells
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What are T-dependentantigens?
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A process by which the
antibody binds to
and blocks the activity
of the antigen
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The activation of the complement
system by antigen-antibodyComplexes.
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What is complementfixation?
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A foreign molecule that
elicits a specific response
by lymphocytes.
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What are antigens?
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Short-lived cells that combat the
same antigen.
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What are effector cells?
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Long-lived cells bearing
receptors specific for
the same antigen.
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What are memory cells?
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Another term for
membrane antibodies.
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What is an antigenreceptor?
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The selective proliferationand differentiation of
lymphocytes that occurs thefirst time in the body is
exposed to an antigen.
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What is the PrimaryImmune Response?
A h f
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Another term for
immunization.
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What is vaccination?
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Another red blood cell antigen.
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What is the Rh factor?
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A life-threatening reaction
to injected or ingested
allergens.
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What is
anaphylactic shock?
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Temporary immunity obtained byacquiring ready-made antibodies
or immune cells.
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What is PassiveImmunity?
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The causative agent of AIDS.
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What is HumanImmunodeficiency
Virus (HIV)?