Chapter 43 Caesar Tin-U, Danh Vu
Contents.
1st defence: Nonspecific Defences
2nd defence: Inflammation
3rd defence: Specific Immunity
Immune Response
Immunity in Health and Disease
Approximate Duration:
Foreign Invaders
Called Pathogens
Viruses, bacteria or
other living thing that
causes
disease/immune
response.
Antigens
Toxins that pathogens
produce that cause
harm to an organism.
Nonspecific Defences
They dont distinguish between foreign organisms
Can be viewed in relation to a besieged city:
1st line of defence Skin
2nd line of defence Phagocytes
3rd and last defence Immune system
= City walls
= Foot soldiers
= Secret Agents
Nonspecific Defenses
Against Infection
Organisms must find a means of defence against
antigens such a viruses described on the previous
page.
If this was not the case, bacteria, fungi and viruses
would replicate out of control inside other organisms
which would most likely already be extinct.
Therefore organisms employ many types of defence to
stop this happening.
Means of defence can be categorized into first and
second lines of defence, with the first line usually
having direct contact with the external environment.
The First Line of Defence
Got own3d?
The First Line of Defence
First Lines of Defence
Skin is an excellent line of defence because it provides an almost
impenetrable biological barrier protecting the internal environment.
A Lactobacillus species, possibly
Doderlein's bacillus, in association
with a vaginal epithelial cell.
(Squamous epithelial)
Lysozyme is an enzyme found in tears and saliva that has
powerful 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 and
N-acetyl-D-glucosamine residues in a
peptidoglycan and between
N-acetyl-D-glucosamine residues in
chitodextrins.
Lysozyme
(In Plain English: It just disassembles their cell walls)
(They can also be found largely in your favorite product: egg
whites)
The primary structure of egg white
lysozyme - shown here - is a single
polypeptide chain of 129 amino acids.
There are four pairs of cysteines that
form disulfide bridges between positions
6 and 127
30 and 115
64 and 80
76 and 94
(counting from the N-terminal lysine).
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.
And the rest of the stuff
Mucus and cilia found in the nose and throat can catch foreign agents entering
these open cavities then sweep them outside via coughing, sneezing and
vomiting.
The cell wall of plants consists of fibrous proteins which provide a barrier to
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.
Contents.
1st defence: Nonspecific Defences
2nd defence: Inflammation
3rd defence: Specific Immunity
Immune Response
Immunity in Health and Disease
Approximate Duration:
The 2nd line of defence.
The Inflammatory Response
These series of slides will take you though the
basic response to outside stimuli and bodily
responses of tissue injury.
Summary
Sequence 1: Tissue injury
Injury
Tissue injury occurs
Pain inflammatory mediators
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.
Which leads to the actions of the 2nd line of defence.
Pha -> Go -> Cytosis!
Second lines of defence deal
with 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)
Neutrophil: (Video)
These phagocytes contain digestive enzymes in
their lissome (an organelle in phagocytes) such
as lysozyme.
White blood cells such as a neutrophil or a
monocyte are capable of undergoing
phagocytosis, which is illustrated below.
Monocyte:
(Video)
Pathology:
Hemophagocytosis
Associated with:
EpsteinBarr virus-Tcell lymphoma.
EpsteinBarr virus
(EBV) can infect T
lymphocytes and
manifests as
hemophagocytic
lymphohistiocytosis
(HLH), a distinct entity
of hemophagocytic
syndrome (HPS)
characterized by fever,
hepatosplenomegaly,
cytopenia,
hypercytokinemia, and
systemic macrophage Fukumoto, J. et al. ASH Image Bank 2006;2006:6-00023
activation with
hemophagocytosis.
Copyright 2006 American Society of Hematology. Copyright restrictions may apply.
Figure 1. Histiocytes ingesting red cell precursors may be seen in response to certain
infections
Maslak, P. et al. ASH Image Bank 2002;2002:100540
Copyright 2002 American Society of Hematology. Copyright restrictions may apply.
Pyrogens- High-molecular-weight substances of
polymerous nature, like lipopolysacharids.
They increase the temperature of the body contributing to
defence.
Inhibits growth of some microorganisms.
Facilitates phagocytosis
Catalyses bodily reactions (tissue synthesis)
Sometimes responsible for septic shock
Body temperature exceeds normal fever.
The phagocytes:
Eosinophils
Natural killer (NK) (T
cells)
Monocytes
Neutrophils
Natural Killer (T-Cell)
Maslak, P. ASH Image Bank 2005;2005:101382
Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Monocytes may be increased in chronic infections, chronic inflammatory disorders and
some forms of MDS and myeloid leukemia
Maslak, P. ASH Image Bank 2005;2005:101369
Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Plasmacytoid lymphocyte has an oval nucleus with condensed
chromatin
Maslak, P. ASH Image Bank 2005;2005:101375
Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Figure 1. Peripheral smear from a 17 year old female with Chediak-Higashi syndrome is
shown
Lazarchick, J. et al. ASH Image Bank 2005;2005:101296
Copyright 2005 American Society of Hematology. Copyright restrictions may apply.
Figure 1. Lymphoblasts in the peripheral blood
Maslak, P. ASH Image Bank 2004;2004:100992
Copyright 2004 American Society of Hematology. Copyright restrictions may apply.
Contents.
1st defence: Nonspecific Defences
2nd defence: Inflammation
3rd defence: Specific Immunity
Immune Response
Immunity in Health and Disease
Approximate Duration:
Immune Biology
Cytokines
Low molecular weight protein mediators involved
in cell growth, inflammation, immunity,
differentiation and repair
Production triggered by presence of foreign
particles
Autocrine agent Act on cell that produced it
Types
Interleukins (ex. IL-2)
Meaning: They are chemical messengers between (inter)
Leukocytes
Interferons
Intefere with viral reproduction
Secreted by infected dying cells.
Cytokines (chemokines)
Structure of interleukin 2
Fig. 1
Schematic overview of the highaffinity
interleukin2 receptor complex, including
the receptor chains, downstream signaling
components and target genes
Fig. 2
exposed surface
Kappa
hidden surface
Previously
hinge region
hidden surface
carbohydrate
Lambda
Intact Immunoglobulin
Free Light Chain
Bradwell, Serum free light chain assay
Chemokines:
-50 different proteins
-Induces inflammation
-Induces toxin production in lymphocytes
Called
chemo-taxis.
(like taxiing)
Contents.
1st defence: Nonspecific Defences
2nd defence: Inflammation
3rd defence: Specific Immunity
Immune Response
Immunity in Health and Disease
Approximate Duration:
The last line of defence.
How Specific Immunity Arises
Lymphocytes are the key cells to immunity
and bodily defence.
They generate the key responses that
eliminate infections.
Antibodies
Interferons
Third Line of Defense Specific Immune Response
This is a specific response to a specific
pathogen/antigen.
The response involves the creation of Antibodies.
Antibodies
Y-shaped protein
molecule.
Made up of variable and
constant regions.
Made up of Heavy and
Light chains.
Produced by BLymphocytes
Function: Recognize
antigens, bind to and
deactivate them.
Note: Variable region
recognizes the anitgens.
How an antibody operates/works?
Deactivation of a bacterium by an antibody.
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 specificity only targeting foreign cells
Lymphocytes detect foreign molecule marker
Antigen
Countered with Antibodies.
generator)
Created by B Cells
(Antigen = Short for Antigen-
Video
Origin of lymph
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 by
apoptosis
Normally has lymphocytes that react against its
self
Failures of selftolerance leads to
autoimmune diseases.
Autoimmune Disease
Autoimmune diseases are diseases where the
immune 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 treated
with drugs.
Autoimmune diseases
Acute disseminated encephalomyelitis (ADEM) yes G04.0 is a form of encephalitis caused by an autoimmune reaction and
typically occurring a few days or weeks after a viral infection or a vaccination. Addison's disease yes E27 is often caused by
autoimmune destruction of the adrenal cortex. Ankylosing spondylitis yes 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 anemia no D60 is often caused by an autoimmune attack on the bone marrow. Autoimmune hepatitis no K75.9 is a
disorder wherein the liver is the target of the body's own immune system. Autoimmune Oophoritis no N70 is a disorder in
which the immune system attacks the female reproductive organs. Celiac disease no K90.0 is a disease characterized by
chronic inflammation of the proximal portion of the small intestine caused by exposure to certain dietary gluten proteins.
Crohn's disease no K50 is a form of inflammatory bowel disease characterized 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 1 yes E10 when it is characterized by a deficiency
or absence of insulin production (Type I), is often the consequence of an autoimmune attack on the insulin-producing beta
cells in the islets of Langerhans of the pancreas. Gestational pemphigoid no O26.4 is a pregnancy-related blistering condition
where autoantibodies are directed against the skin. Goodpasture's syndrome yes M31.0 is a disease characterised by rapid
destruction of the kidneys and haemorrhaging of the lungs through autoimmune reaction against an antigen found in both
organs. Graves' disease yes E05.0 is the most common form of hyperthyroidism, and is caused by anti-thyroid antibodies
that have the effect of stimulating (agonist) the thyroid into 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., not the 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 disease yes 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 purpura yes D69.3 is an autoimmune disease
where the body produces anti-platelet antibodies resulting in a low platelet count Kawasaki's Disease no M30.3 is often
caused by an autoimmune attack on the arteries around the heart. Lupus erythematosus yes L93, M32 is a chronic (longlasting) autoimmune disease wherein the immune system, for unknown reasons, becomes hyperactive and attacks normal
tissue. This attack results in inflammation and brings about symptoms. This is a "Non-organ-specific" type of autoimmune
disease. Mixed Connective Tissue Disease has 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
sclerosis yes G35 is a disorder of the central nervous system (brain and spinal cord) characterised by decreased nerve
function due to myelin loss and secondary axonal damage. Myasthenia gravis yes G70.0 is a disorder of neuromuscular
transmission leading to fluctuating weakness and fatigue. Weakness is caused by circulating antibodies that block
(antagonist) acetylcholine receptors 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
opsoclonus, myoclonus, ataxia, intention tremor, dysphasia,
Allergies
Allergy
- An exaggerated response by the immune system to an allergen.
Allergen: a normally harmless substance that causes an allergic
reaction.
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 about
30 mins.
b. Delayed takes longer to react and can last for a much longer
time.
What
happens during an allergic reaction?
During an allergic reaction antibodies cause histamines to 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 that
can cause death.
Treatments for Allergies
1. Avoidance of material especially food.
2. Epinephrine epi pen
3. Antihistamines -- benadryl
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 to
demyelination. 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.
Treatment of MS
No cure
Only management tehniques
administration of high doses of intravenous corticosteroids, such as
methylprednisolone.
(This will end the attack sooner, and prevent major damage)
Side effects include: osteoporosis, and impaired memory.
Immunosuppressant also used in cancer chemotherapy
(Approved only in the USA.)
Alternative treatments
Different alternative treatments are pursued by many patients
Dietary regimens
Herbal medicine
On the other hand the therapeutic practice of martial arts such as tai chi,
relaxation disciplines such as yoga, or general exercise, seem to mitigate
fatigue and improve quality of life.
A) Axial FLAIR MRI demonstrating large
tumefactive areas of demyelination. B)
Axial T1 with gadolinium contrast
demonstrating enhancement of the lesion
margins.
FLAIR: fluid-attenuated inversion recovery;
MRI: magnetic resonance imaging.
T1-weighted MRI scans (postcontrast) of same brain slice
at monthly intervals. Bright
spots indicate active lesions.
Ergo Break~~
5 minutes
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 few
specialized 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.
Identification
Class I MHC molecules, found in almost all cells,
are poised to present fragments of proteins made
by 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 (APCs)
in this context, ingest bacteria and viruses and then
destroy them.
Class II MHC molecules in these cells collect peptide
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.
Were almost done
Contents.
1st defence: Nonspecific Defences
2nd defence: Inflammation
3rd defence: Specific Immunity
Immune Response
Immunity in Health and Disease
Approximate Duration:
Got lazy?...
Immunity
The Pathway of Specific Immune Response
Step 1
Pathogens eaten by Macrophage
Step 2
Displays portion of Pathogen
on surface
Step 3
Pathogens
Helper-T cell recognizes
Pathogen
Activates B- Cell
Activates Cytotoxic
T- Cell
Memory T-Cell
Kills Infected Cells
Memory B-Cell
Antibodies
Cellular Immunity .vs. Antibody Immunity
Cellular Immunity
Antibody or Humoral Immunity
Carried out by T-Cells
Carried out by B-cells
Infected cells are killed
by Cytotoxic T Cells.
Antibodies are produced
and dumped into blood
stream.
Antibodies bind to
antigens and deactivate
them.
Immune Response Explained
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Antigen infects cells.
Macrophage ingests antigen and displays portion on its
surface.
Helper T- Cell recognizes antigen on the surface of the
macrophage and becomes active.
Active Helper T-Cell activates Cytotoxic T-Cells and B-Cells.
Cytotoxic T-Cells divide into Active Cytotoxic T-cells and
Memory T Cells.
Active Cytotoxic T-Cells kill infected cells.
At the same time, B-Cells divide into Plasma Cells and
Memory B- Cells.
Plasma cells produce antibodies that deactivate pathogen.
Memory T and Memory B cells remain in the body to speed
up the response if the same antigen reappears.
Supressor T-Cells stop the immune response when all
antigens have been destroyed.
Immune Response Summary
Displays copy of antigen
on surface of cell
Antigen
Macrophage
Antibody Immunity
Helper T - Cell
Cellular Immunity
Active Cytotoxic T-Cell
Kills Infected Cells
Memory T- Cell
Active B - Cell
Plasma Cell
Antibodies
Deactivates Antigens
Memory B-Cell
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 2nd time it
invades the body.
Antibody production increases dramatically and in a much
shorter time period..
Primary .vs. Secondary Immune Response
Passive .vs. Active Immunity
1. 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 strain of an
infectious microbe (pathogen) that causes the body to undergo
active immunity (produce antibodies).
2.
Passive Immunity
This is immunity where antibodies are given to a
person from the blood of another person or animal.
This immunity only lasts for a short period of time.
ex: Breastfeeding mothers pass antibodies to their
children through the milk.
HIV is a retrovirus.
A more specific name is Lentivirus.
Retroviruses have an RNA genome that is
replicated via a DNA intermediate in infected
cells. DNA also integrates in the host
genome to form provirus.
Structure of HIV
Sarcophagus-shaped capsid
contains 2 copies of RNA genome
(SS (+) strand), a reverse
transcriptase, 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 viralencoded glycoproteins, gp41 (41
kDa) and gp120 (120 kDa).
gp120 binds the CD4 receptor on
helper T cells.
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 cellsurface 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).
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.
2. Syncytium formation
gp120/41 proteins on
infected cells bind to CD4
receptors on normal cells,
causing cell fusion. The
giant multi-nucleated
syncytium dies before
long.
Infected cell
Normal cell
[Link]
An infected helper T cell can direct an uninfected T helper cell to undergo
apoptosis (programmed cell death). Apoptosis can be normal, for
example, to eliminate auto-reactive T lymphocytes to establish selftolerance.
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.
Vaccines?
Whole virus vaccines
Attenuated viruses: Essentially intact, living HIV virions that have
been 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.
A Major Challenge in Maintaining
Control of HIV
HIV evolves rapidly
The RT is error-prone (no proofreading)
~ 1-2 mutations in each cDNA copy of
the 9.8 kb RNA genome
Caesars little cancer cell fighting theory
applied to HIV / AIDS.
Effector Cell
The Immune Pathway
Think MichaelisMenton
IL-2 Molecules
1. IL-2 binds IL-2 Receptor
Step 1
Tumor
recognition site
Tumor
cells
Ste
p2
IL-2 Receptor
4. Tumor Eating
Site Activated
6. Attack Mode!
Step 6
Step 4
2. Effector Cell with
bound IL-2
Step 3
Step 5
5. Locates Tumor
3. Effector Cell Activated
And Multiply
Calculus.
Change in
Effector cells
over time
Antigenicity
and size of
tumor
Death
rate
IL-2
Stimulation
Effector Cell
Injection
Logistic
growth rate
of Tumor
Change in
Tumor cells
Killing rate
by Effector
cells
Change in IL-2
Natural
production of IL-2
Death
rate
IL-2
Injection
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 virus has been linked to lupus in children.
References
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.
Works cited / Sources
Kumar and Clark Clinical Medicine, 5th ed.
Campbell Reece Biology 6th & 7th ed.
Steven Zumdahl Chemistry 6th ed.
[Link]
[Link]
[Link]
[Link]
[Link]
[Link]/hiv_lifecycle/
[Link]/hiv/en
[Link]/[Link]?doc=kb-02-01-02
Chris Cunningham & Asad Usman Adoptive Immunotherapy
And more sources
Rosenberg, SA, Yang, JC, White, DE, et al. Durability of complete responses in patients with metastatic cancer
treated 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 or
renal 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. Current Opinion
in Immunology 6: 722727.
Rosenberg SA. Lotze MT. Muul LM. Chang AE. Avis FP. Leitman S. Linehan WM. Robertson CN. Lee RE. Rubin
JT. et al. A progress report on the treatment of 157 patients with advanced cancer using lymphokine-activated killer
cells 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 of
Mathematical 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 siRNA
treatment. [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] [97
refs] [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 Chemotherapy
of Tumors through Mathematical Modeling. [Book] Department of Mathematics: Harvey-Mudd University, 2003
Summer.
Nonspecific
Defense
Specific
Defense
Immune
Responses
Arising
Immunity
Immunity In
Health and
Disease
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The ingestion of
invading organisms by
certain type of white cells
What is Phagocytosis?
These are the
phagocytic cells.
What are neutrophils?
The skin, mucous
,membranes, and
secretions of skin
and
mucous membranes.
What is the first
line of defense?
Phagocytic white blood
cells, antimicrobial
proteins the
inflammatory response.
What is the second
line of defense?
This sets the bodys
thermostat at
a higher temperature.
What are Pyrogens?
White blood cells.
What are
Lymphocytes?
An antigen-binding
immunoglobulin that functions
as the effector in an
immune response.
What are antibodies?
Lymphoctyes and
Antibodies
What is the third
line of defense?
Molecules secreted by blood
vessel endothelial cells
and monocytes.
What are chemokines?
A group of at least
20 blood proteins that
cooperate with
other defense mechanisms.
What is the
complement system?
A protein that forms
pores in the target
cells membrane.
What is perforin?
A localized region
on the surface of an
antigen that is
chemically recognized
by antibodies.
What is a epitope?
Can simulate antibody
production only with
help from T helper cells
What are T-dependent
antigens?
A process by which the
antibody binds to
and blocks the activity
of the antigen
What is
neutralization?
The activation of the complement
system by antigen-antibody
Complexes.
What is complement
fixation?
A foreign molecule that
elicits a specific response
by lymphocytes.
What are antigens?
Short-lived cells that combat the
same antigen.
What are effector cells?
Long-lived cells bearing
receptors specific for
the same antigen.
What are memory cells?
Another term for
membrane antibodies.
What is an antigen
receptor?
The selective proliferation
and differentiation of
lymphocytes that occurs the
first time in the body is
exposed to an antigen.
What is the Primary
Immune Response?
Another term for
immunization.
What is vaccination?
Another red blood cell antigen.
What is the Rh factor?
A life-threatening reaction
to injected or ingested
allergens.
What is
anaphylactic shock?
Temporary immunity obtained by
acquiring ready-made antibodies
or immune cells.
What is Passive
Immunity?
The causative agent of AIDS.
What is Human
Immunodeficiency
Virus (HIV)?
