ASSIGNED READING CHAPTER 18: pp 443-458 OUTLINE/SUMMARY
- Active vs Passive Immunization
- Vaccines for Active Immunization
- Whole Organism Vaccines
- Attentuated viral or bactrial vaccines
- Inactivated viral or bactrial vaccines
- Purified macromolecules as vaccines
- polysaccharides
- toxoids
- Recombinant antigens
- Recombinant Vector Vaccines
- DNA Vaccines
- Synthethetic Peptide Vaccines
- Multivalent Subunit Vaccines
- Anti-Idiotype Vaccines
- Vaccines for Passive Immunization
- Applications
- Humanized antibodies
PERFORMANCE OBJECTIVES
DEFINE THE FOLLOWING KEY TERMS:
passive immunization [444] |
active immunization [445] |
vaccine[445] |
boosters[445] |
herd immunity [446] |
attenuated vaccines [448] |
inactivated vaccines[448] |
reversion [449] |
toxoid[451] |
vector [451] |
vector vaccines [451] |
antiidiotype vaccine [455] |
Immunostimulating Complexes (ISCOMS) [454 |
|
|
solid matric antibody antigens (SMAA) [454 |
|
|
ON COMPLETION OF THIS SECTION THE STUDENT SHOULD BE ABLE TO:
- Compare the acquisition passive and active immunization
and give specific examples of each [444]
- Discuss the recommended program for Childhood
immunizations.[445]
- Construct a table to compare the advantages and
disadvantages of attentuated vs inactivated vaccines.
- compare the risks associated with attenturated or
inactivated vaccines vs specific purified macromolecular
vaccines.
- Compare the three general forms of purified
macromolecular vaccines; polysaccharide, toxoid, and
recombinant antigens
- Draw a diagram to show the steps in the production of a
vaccina virus vector vaccine[452]
- Draw a diagram to show the uses of an
anti-idiotypeantibody as a vaccine.
- Discuss the advantages of anti-idiotype vaccines[455]
- Compare solid matrix antibody-antigen complexes with
immunostimulating complexes in the development of
multivalent subunit vaccines. [455]
SHORT ANSWER QUESTIONS
- Differentiate between variolation and vaccination.
- Define vaccine. Name fouR types of vaccines and give
examples of each.
CHAPTER 19: Immune Response to Infectious Disease
THIS CHAPTER WILL NOT BE DEALT WITH IN THIS COURSE AS IT
IS THE FOCUS OF THE INFECTIOUS DISEASE COURSE AND THE MEDICAL
MICROBIOLOGY COURSE
ASSIGNED READING
CHAPTER 20: pp 485-505
- Organ Specific Autoimmune Diseases
- Direct cellular damage
- Hashimoto's thyroiditis
- autoimmune anemias
- Goodpasture's syndrome
- insulin dependent diabetes mellitus (IDDM)
- Antibody effects
- Grave's disease
- myasthenia gravis
- Systemic Autoimmune Diseases
- systemic lupus erythematous (SLE)
- multiple sclerosis (MS)
- rheumatoid arthritis (RA)
- Animal Models
- Spontaneous autoimmunity
- Experimentally induced
- TCR & MHC in Autoimmunity
- Induction of Autoimmunity
- Relase of sequestered antigen
- molecular mimicry
- Wrong expression of MHC-II
- Polyclonal B cell activation
- Experimental Treatment
- T cell vaccination
- Peptide blockage
- MABs
- Tolerance induction
PERFORMANCE OBJECTIVES
DEFINE THE FOLLOWING KEY TERMS:
autoantigens |
autoimmunity |
autoimmune hemolytic diseases |
cold antibody |
Graves disease |
autoimmune hemolytic anemia |
Warm antibody |
Hasimoto's thyroiditis |
thrombocytopenic purpura |
glomerulonephritis |
myasthenia gravis |
autoimmune hemolytic anemia |
rheumatic fever |
Horror Autoxicus |
Insulin dependent diabetes millitus ( Type I) |
rheumatoid arrthritis |
allergic encephalomyeltis |
Organ specific autoimmune diseases |
|
systemic lupus erythematosis |
systemic autoimmune diseases |
ON COMPLETION OF THIS SECTION THE STUDENT SHOULD BE ABLE TO:
- Show how the origins of autoimmune disease may lie in the
immune process, the self antigens or both.
- Describe two major events that may lead to autoimmune
disease
- Distinguish between cell mediated and antibody mediated
autoimmune diseases, give two specific examples of each
and discuss these examples.
- Discuss the treatment of autoimmune diseases
SHORT ANSWER QUESTIONS
- The idea of clonal deletion suggests that self reactive
cells are eliminated (no cells to react to self antigens;
therefore, we tolerant self antigens), yet autoimmune
diseases occur (react to self antigens). Explain.
- The idea of "Horror autotoxicus" was proposed
in 1901 to suggest that reactions against self could not
occur.
- Current evidence suggests otherwise. Explain.
- Other than the characteristic of foreigness, self
antigens and exogenous antigens are not inherently
different. Explain?
- What are Witebsky's postulates?
- Why are they important in describing autoimmune disease?
- The origin of an autoimmune disorder may lie in the
immune process, the self antigens, or both. Explain.
- What are the two major events that could lead to an
autoimmune disease?
- List some other possibilities.
- The description of SLE includes three mechanistic
elemtns; What are they?
- In Hashimoto's disease, high levels of antibodies against
thyroglobulin are found. Yet these antibodies do not seem
to cause the disease. Explain.
- Compare and contrast the three lines of treatment for RA.
- Briefly discuss some autoimmune disease that can follow
bacterial infections.
- Why would the induction of tolerance to an autoantigen,
which is causing disease, be one of the most effective
treatment approaches for autoimmunity?
- Phagocytic Deficiencies
- Reduced Neutrophils
- Defective phagocytes
- adherence defects
- chemotactic defectgs
- killing defects
- Humoral Deficiencies
- X-linked agammaglobulinemia
- X-linked hyper-IgM Syndrome
- Common variable hypogammaglobulinemia
- Selective immunoglobulin deficiences
- Cell mediated Deficiences
- DiGeorge sysndrome
- Nude mice
- Combined Immunodeficiences
- Reticular dysgenesis
- Bare lymphocyte syndrome
- SCID
- Wiskott-Aldrich Syndrome
- Complement Deficiences
PERFORMANCE OBJECTIVES
DEFINE THE FOLLOWING KEY TERMS:
immunodeficiency [507] |
Wiskott-Aldrich syndrome (WAS)[519] |
neutropenia[508] |
congenital agranulocytosis [508] |
granulocytopenia[508] |
leukocyte-adhesion deficiency [508] |
agranulocytosis[508] |
lazy leukocyte syndrome [510] |
selective Iga Deficiency [ 514] |
chronic granulomatous disease (CGD)[510], |
nude mice [515] |
X linked agammaglobulinemia [511], |
reticular dysgenesis [516 |
X-linked hyper IgM (XHM) syndrome [512] |
bare lymphocyte syndrome [516] |
common variable hypogammaglobulinemia(CVH) [513 |
X linked SCID [518] |
DiGeorge Syndrome (Congential thymic aplasia) [515] |
|
severe combined immunodeficiency disease (SCID)[517] |
ON COMPLETION OF THIS SECTION THE STUDENT SHOULD BE ABLE TO:
- construct a table comparing four different
- phagocytic deficiency diseases [510]
- Construct a table comparing 4 different humoral
deficiences;
- X linked agammaglobulinemia [511],
- X-linked hyper IgM (XHM) syndrome [512],
- common variable hypogammaglobulinemia(CVH) [513],
- selective Iga Deficiency [514]
- Draw a diagram of hematopoiesis and indicate congential
defects that impair the immune response for
- phagocytic deficiences,
- humoral deficiences
- cell mediated deficiciences
- combined immunodeficiencies
- Discuss the impact of T cell deficiencies
- Construct a table of the combined immunodeficiences that
shows the disease, the immune system deficiency and the
possible mechanism [517]
- Discuss the use of CB-17 SCID mice as a model system
SHORT ANSWER QUESTIONS
- How does immunodificiency differ from immunotolerance?
ASSIGNED READING Chapter 22: pp 523-554 OUTLINE/SUMMARY
- Discovery
- Human Immunodeficiency Virus (HIV)
- Retroviruses
- Structure of HIV
- HIV Infection of Targety Cells
- Transmission of HIV
- HIV Genome
- Activation of HIV Provirus
- Expression of HIV proviral DNA
- Genetic variation
- Diagnosis of HIV
- Diagnosis of AIDS
- Destruction of CD4+ T cells
- CD4+ T cells infected with HIV
- Destruction of CD4+ T cells uninfected with HIV
- Anti GP120
- GP120
- Syncytia
- Maturation inhibition
- Immunologic Abnormalities in Aids
- Lymph node pathology
- Reduced response to antigen
- Ineffective antibody
- Cytokine imbalance
- Decreased DTH response
- Impaired CTL activity
- Development of AIDS Vaccine
- Obstacles
- glycoproteins
- Attenutated viruses
- Recombinant viruses
- Synthetic peptides
PERFORMANCE OBJECTIVES
DEFINE THE FOLLOWING KEY TERMS:
long terminal repeats[531 |
Acquired immunodificiency syndrome(AIDS) [524] |
fusin[529] |
HIV-1 |
Human immunodeficiency virus (HIV)[524] |
integrase[530] |
HIV-2 |
simian immunodificiency virus (SIV) [526] |
budding[530] |
HIV-0 |
cytopathic retroviruses[524] |
syncytium[]542] |
retroviruses [524] |
transforming retroviruses [524] |
Karposi's sacrcoma |
V3 loop[536] |
reverse transcriptase [526] |
fusogenic domain[528] |
seroconversion[536] |
opportunistic infections [524] |
crown region[536] |
D ON COMPLETION OF THIS SECTION THE STUDENT SHOULD BE ABLE TO:
- Draw and label cross sectional diagram of an HIV virion
- Draw and label a diagram of the genome of HIV-1
- Discuss the factors that contribute to the genetic
variation of HIV
- Construct a table of the cell types that can be infected
by HIV[530].
- Draw and label a diagram show the steps in the infection
of a target cell by HIV[528]
- Draw and label a diagram that shows activation of HIV
provirus [528]
- Discuss the origins of HIV-1, HIV-2 and HIV-0.
- Draw a diagram to show the early and late stages in the
expression of HIV-1 proviral DNA [534]
- Label a diagram of HIV-1 envelope glycoproteins.
- Describe the screening tests for HIV infection [537].
- Describe the clinical symptoms of AIDS[537]
- Describe the various mechanisms for the depletion of CD4+
cells in AIDS patients[538-543]
- Construct a Table summarizing the immunologic
abnormalities associated with HIV infection.
- Construct a table showing the estimated incidence of AIDS
around the world[525]
SHORT ANSWER QUESTIONS
- Immunological Basis of Graft Rejection
- Specificity & memory
- Cell mediated responses
- Transplantation antigens
- Mechanisms of graft rejection
- Sensitization stage
- Effector stage
- Clinical Manifestions of Graft Rejection
- Hyperacute rejection
- Acute Rejection
- Chronic rejection
- Tissue Typing
- General Immunosupressive Therapy
- Mitotic inhibitors
- Corticosteroids
- Cyclosporin A
- Total irradiation
- Specific Immunosupressive Therapy
- MABs to T cells
- Block co-stimulatory signal
- Microchimeras
- Clinical Transplantation
- Bone marrow transplants
- Organ transplants
- Xenotranplants
- Immunologically priveleged sites
PERFORMANCE OBJECTIVES
DEFINE THE FOLLOWING KEY TERMS:
allogtraft |
alloreactivity |
autograft |
chronic rejection |
Class I MHC |
Class II MHC |
first set rejection |
graft |
grafting |
Graft vs host reaction |
privileged sites |
privileged tissues |
mixed lymphocyte reaction |
syngraft |
transplant |
second set rejection |
transplantation |
xenograft |
transplantation immunity |
|
|
ON COMPLETION OF THIS SECTION THE STUDENT SHOULD BE ABLE TO:
- Show that the cell mediated response to transplants in
the same as the immune response to any other foreign
antigen
- Describe four types of grafts
- Describe the five transplantation laws
- Distinguish among first set rejection, second set
rejection and chronic rejection;
- Differentiate between host versus graft reaction and
graft versus host reaction.
- Compare the contribution of Class I and Class II MHC to
graft rejection.
- Comment on which T cells are responsible for graft
rejection
- Describe serologic tissue typing.
- Describe the mixed lymphocyte reactions and why you would
want to use the MLR in tissue typing
- Rank the success rate for transplants of different
tissues and organs
SHORT ANSWER QUESTIONS
- What do we mean when we say that the immune system is the
greatest obstacle to most transplants?
- What is the difference between autograft and syngraft?
Give examples of both.
- How do we know that the immune system is involved in
allograft rejection?
- Are antibodies or T cells the main mediators of
rejection?
- ompare and contrast first set rejection and second set
rejection.
- What does second set rejection suggest about the
similiarity of transplantation antigens?
- What conditions could lead to a graft vs host response
(GvHR)?
- Even though class II antigens are found mainly on immune
cells, they can still contribute to graft rejection. How?
- What may be the biologic significance of alloreactivity?
- Describe serologic tissue typeing.
- Describe the MLR. Why is this test done in addition to
serologic tissue typing?
- Differentiate between privileged sites and privileged
tissues.
- Origins & Terms
- Malignant Transformation
- Oncogenes
- Induction of cell proliferation
- Inhibition of cell proliferation
- Regulation of apotosis
- Tumours of the Immune System
- Tumour Antigens
- Tumour specific Antigens
- chemically induced
- virally induced
- Tumour associated antigens
- oncofetal tumour antigens
- oncogene proteins
- TATAs on human melanomas
- Immune Response to Tumours
- NK cells & macrophages
- Immune surveillance theory
- Tumour Evasion of Immune Response
- Immunologic enhancement
- Modulation of tumour antigens
- Reduce MHC-I
- No co-stimulatory signal
- Cancer Immunotherapy
- Modify Co-stimulatory signal
- Enhance APC activity
- Cytokine therapy
- MABs
- Tumour cell vaccines
PERFORMANCE OBJECTIVES
DEFINE THE FOLLOWING KEY TERMS:
Antibody dependent cell mediated cytotoxicity (ADCC) |
benign tumour |
carcinogens |
tumour specific transplantation antigens |
natural killer cells (NK) |
immunotoxins |
immalignancymune surveillance |
Specific immunotherapy |
neoplasm |
non specific immunotherapy |
tumour specific antigens |
oncogens |
Lymphokine activated killer cell(LAK) |
malignant tumour |
tumour |
tmour associated transplantation antigens |
oncofetal antigens |
cancer |
tumour associated antigens |
proto oncogens |
metastasis |
ON COMPLETION OF THIS SECTION THE STUDENT SHOULD BE ABLE TO:
- Differentiate between a benign tumour and a malignant
tumour.
- Describe the concept of immunosurveillance
- Describe the different ways that tumours can camouflage
themselves to evade immune defenses,
- Discuss the advantages of immunotherapy over other forms
of cancer therapy.
- Distinguish between specific and nonspecific
immunotheraphy with the use of specific examples.
- Describe immunotoxins.
- Describe the development of humanized antibodies to
tumour antigens
- Evalulate the contribution of T cells, NK cells,
Macrophages, and B cells to tumour immunity.
- Distinguish between tumour specific transplantation
antigens and tumour assoicated transplantation antigens.
- Describe oncofetal antigens.
SHORT ANSWER QUESTIONS
- Explain how some cancer cells that can make TGF-beta are
immunosuppressive.
- Tumours and transplants are similar to one another,yet
very different. Explain this observation in the context
of what the immune system recognizes and the result of
this recognition.
- The qualities of proliferation and differentiation are
essentially all that distinguishes a normal cell from a
cancer cell. Explain.
- Design an experiment using mice that proves that the
immune system provides immunity against tumours.
- Distinguish between tumour-specific transplantation
antigens (TSTA) and tumour associated transplantation
antigens (TATA).
- Design an experiment to show Tumour associated
Transplantation Antigens (TATA).
- What is the main difference separating cell surface
antigens from chemically induced and virually induced
cancers? Speculate on why this difference leads to
difficulty in designing anticancer vaccines.
- What are oncofetal antigens? Are they important in tumour
immunity? Why?
- What is immune surveillance? All evidence for immune
surveillance is indirect. Speculate on how you could get
direct evidence.
- What immune cells play a role in tumour rejection?
Briefly describe how each accomplishes this task. Include
such things as cytokines, perforins, ADCC etc.
- Cancers camouflage themselves to evade antitumour
defenses. Pick three possible forms of camouflage that
you think are most important, describe them and state why
you think they are most important.
- What are immunotoxins?
- Surgery, radiation and chemotherapy are the methods most
widely used to treat cancer patients. What are the
problems with this regimen, and how could immunotherapy
overcome these problems. Distinguish between specific and
nonspecific immunotherapy.