Please Use the Notes Below As a Guide to Study the Material Covered in Chapter 1-5

Please Use the Notes Below As a Guide to Study the Material Covered in Chapter 1-5

MCMP 422

2007

STUDY GUIDE

Chapters 1-5

Hazbun

Please use the notes below as a guide to study the material covered in Chapter 1-5.

CHAPTER 1 (Lectures 1-3)

  1. Know the machinery of the immune system: Tissues, cells and blood proteins (e.g., complement) of the Immune System (IS) -know who are phagogcytes, APCs, killer cells (both CD8 and NK cells), helper cells (Th1 and Th2)
  2. How do we classify the immune system? Innate and Adaptive Immunity
  3. -know cells and characteristics of each (e.g. processes involving T or B cells or antibodies or cytokines secreted by T or B cells are part of the adaptive IS)
  4. Know receptors for antigen (BCRs and TCRs)
  5. -identical on a single cell, different on different cells
  6. -know the structure of the antigen bound by the TCR and bound by the BCR
  7. How does inflammation occur? Why is inflammation good but sometimes can be bad?
  8. Understand the concept of clonal amplification
  9. Know the hematopoietic system – how we can stimulate it in some cases such as neulasta
  10. Know the basic anatomy of secondary lymphoid tissue (e.g. lymph node – Tcell area, follicle, germinal center, lymphatic vessels etc)
  11. How do antibodies function?
  12. What are the basic principles of adaptive immunity – Diversity, specificity, memory and self-tolerance. How are these achieved?
  13. Basis of vaccination: understand why a secondary response (memory response) is faster and specific to one antigen
  14. What happens when the immune system is malfunctioning? For example, understand the difference between autoimmune disease and immundeficient disease.
  15. Basis of vaccination: understand why a secondary response (memory response) is faster and specific to one antigen

CHAPTER 2 (Lectures 4-6)

  1. Structure of Igs (Abs), V and C regions, complementarity determining regions (CDRs), isotypes, immunoglobulin domain
  2. How do antibodies recognize antigens? How can antibody-antigen binding be problematic?
  3. What is the difference between Polyclonal vs Monoclonal antibodies
  4. How are antibodies used in diagnostic tests? How is the principle of passive immunity used in commercial applications?
  5. Generation of diversity in the IS (when, who, where and how)
  6. Ig gene rearrangement –
  7. Ig diversity BEFORE antigen encounter: 1) random combination of V and J (light chain) and V, D, J (heavy chain) gene segments; 2) junctional diversity; 3) combinatorial association of heavy and light chains
  8. Ig diversity AFTER antigen encounter: somatic hypermutation followed by affinity maturation
  9. Isotype switching and function of individual Ig (Ab) isotypes

CHAPTER 3 (Lectures 7-10)

  1. TCR: structure, generated by random recombination
  2. What are the differences between B and T cells in development and in making their respective receptors?
  3. How does antigen processing and presentation occur?
  4. MHC I and MHC II
  5. extracellular versus intracellular pathogens
  6. remember most MHC I and MHC II bind self peptides
  7. MHC I and MHC II
  8. polymorphic (many different alleles in the human race)
  9. diverse gene families (3 genes encode MHC I, 3 genes encode MHC II α chain and at least 3 genes encode MHC II β chain)
  10. expression of MHC is co-dominant (all genes of a given class (i.e., class I or class II) are expressed simultaneously on a single cell)
  11. Exam II material commences from here at page 86 of the textbook (Section 3-14 onwards)
  12. How does one MHC molecule bind to approx. 10,000 different peptides?
  13. What do we mean by MHC restriction?
  14. Why can a haplotype be present a high rate in a population and how might it protect against a specific disease?
  15. How is a haplotype spread and/or selected in a population?
  16. What are the characteristics of balancing selection compared to driving selection?
  17. Why is the immune system primed to reject foreign organs? (this question also applies to Chapter 5)

CHAPTER 4 (Lectures 11-12) (Skip Figures 4.6, 4.10, 4.12)

  1. 4 Stages of B cell development (development in the bone marrow, elimination of self reactive B cells, activation by Ag and differentiation into plasma cells)
  2. B cell development is characterized by different Ig gene rearrangements: stem cell, pro B cell, pre B cell, immature B cell, mature B cell)
  3. Heavy chain rearranges first, surrogate light chain, then light chain rearranges (have two tries at the kappa (κ) locus, if fails, two tries at the lambda (λ) locus). How and when is chain rearrangement controlled?
  4. Role of bone marrow stromal cells – CAMs, VCAMs etc
  5. most developing B cells die: 1) fail to productively rearrange DNA, clonal deletion (recognize self antigens)
  6. Understand the link between B cell development and B cell tumors
  7. What is an anergic B cell? How is Receptor Editing linked to Anergy?
  8. Circulation - Mature B cells need survival signals from follicular dendritic cells (FDCs) (too many B cells, not enough FDCs)
  9. Germinal Centers: centroblasts, centrocytes, lymphoblasts, memory B cells, plasma cells

CHAPTER 5 (Lectures 13-14) (Skip Figure 5.15)

  1. T cell development in the thymus
  2. -αβ T cells: β rearranges first (4 tries), surrogate α chain (pre T α receptor), then α rearranges (several tries)
  3. Positive selection
  4. -happens first
  5. -double positive cells undergo positive selection
  6. -occurs in cortex of the thymus; MHC on cortical epithelial cells test developing T cells
  7. -selected to recognize self MHCs (engaging TCR is a signal to LIVE), no TCR engagement the cell dies
  8. Negative selection
  9. -happens after positive selection
  10. -double positive cells that are committed to a single lineage (either CD4 or CD8) undergo negative selection
  11. -occurs at cortical-medullary junction, self Ag is presented by bone marrow derived dendritic cells and macrophages (APCs)
  12. -selected NOT to recognize self antigen (strongly engaging TCR is a signal to DIE), no TCR engagement the cell lives
  13. Why is it ok for the thymus to involute?
  14. T cells – differences in development and function from αβ T cells
  15. What role does the thymus play in bone marrow transplantation?
  16. Why is there a high proportion of alloreactive T cells in our repertoire?
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