Download microbio 7 [4-20

Chapter 7
Learning Objectives
1.
2.
What is the difference between epitopes and antigens?
 Epitopes are the smallest structures that the immune system can recognize
 Antigens are collections of epitopes that are either unique or repeating
What is the Fab? How about F(ab’)2?
Fab is the antigen binding Fragment of an immunoglobulin, formed when papain cleaves an
immunoglobulin into smaller pieces with only a single epitope-binding site each
 F(ab’) 2 is formed when pepsin cleaves Fab into a larger fragment that retains 2 binding sites
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3.
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What genetic components does chromosomal rearrangement bring together for light chains?
Light chains are a union of VL, JL, and CL genes (Variable, Joining, and Constant segments)
4.
What kind of genes are brought together for heavy chains? Which determines the isotype of
the immunoglobulin?
 Heavy chains require VH, DH, JH, and CH (D = Diversity; CH determines μ, δ, γ, α, or ε isotype)
[C gives us such a wonderful Combination of isotypes]
5.
What enzyme increases junctional diversity?
 Terminal deoxyribonucleotidyl transferase (TdT) mashes nucleotides between V, D, and J
genes
6.
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Which immunoglobulins are confined to the bloodstream, and which can enter tissues?
IgG and IgE can leave the vasculature and enter peripheral tissue

Which isotype is secreted, especially in breast milk?
IgA can be transported across cells and provides supplemental immunity to babies along with
maternal IgG that had previously crossed the placental barrier
7.
8.
How are TCRs genetically constructed? How is junctional diversity created in TCRs? What
difference between TCRs and immunoglobulins causes TCRs to have fewer possible specificities?
 TCRs are made of either α and β chains, or γ and δ chains
i. β and δ chains are sourced from the VH, DH, and JH genes
ii. α and γ chains come from VH and JH genes
 DNA rearrangements via TdT also occur in TCRs
 However, the genes for TCRs do not undergo somatic hypermutation
9.

What molecules support the TCR?
The CD3 complex provides ITAMs for the use of the TCR, which otherwise has none
10. Rule of 8?
 4 * II = 8 = 8 * I
[CD type * MHC class = 8]
11. Order the events in T Cell maturation:
 Double negative stage
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Double positive stage
Thymocytes with γδ TCRs exit the thymus early for unknown reasons
Positive selection
Negative selection (interaction with self antigens)
12. What enzyme do cytotoxic T cells use to kill other hots cells?
 Granzyme & perforins
13. What are B-1 cells?
 B-1 cells seem to bridge innate and adaptive immunity by producing a limited series of
antibodies that react with carbohydrates of infectious origin
14. What defines the first two stages of B-2 cell development? What are the final two stages?
 Pro-B cells produce Recombination activation genes (Rag-1 and Rag-2)
 Pre-B cells synthesize a surrogate light chain
 Mature B cells express surface IgD and IgM monomers
 Plasma cells are the end-stage differentiation, and they secrete immunoglobin
15. What are the two methods of dendritic cell sampling?
 Dendritic cells sample the environment via phagocytosis with clathrin-coated pits
 Or via macropinocytosis and the formation of phagolysozomes
16. What dendritic surveilance system are pathogen-associated molecular patterns (PAMPs)
associated with?
 PAMPs are recognized as part of direct sensing in dendritic cells
17. What heterodimer transports peptides that result from proteasome digestion? What’s their
destination?
 TAP-1 and TAP-2 transport future MHC I peptides only
i. Transporter associated with Antigen Processing
18. How do helper T cells differentiate? [the book is confused on this point]
 Helper T cells (Thp cells) can differentiate into Th1 or Th2 cells
i. IL-12 causes Th1 differentiation, these produce IFN-y
ii. IL-4 causes Th2 differentiation, these make more IL-4
[four eyes has 2 eyes with a B (glasses)]
19. What acts as a second signal for B cell activation besides CD4+ T cells?
 Engaging the C3b complement receptor also works as a B cell second activator
20. Which antibody isotypes are most/least effective at agglutination?
 IgM is best, IgG is the worst at agglutination
21. What system synergizes with the humoral immune system?
 The classical pathway of complement works together with free antibodies to kill microbes
22. What is delayed-type hypersensitivity (DTH)?

DTH occurs when a CD4+ cell is reactivated by pMHC II, causing macrophage RAGE by
releasing tons of cytokines
23. What happens when a lymphocyte doesn’t receive a second signal to activate?
 Anergy ensues, stupifying the lymphocyte forever
24. What effect doe IFN-γ and IL-4 have on helper T cell differentiation?
 IL-4 inhibits the Th1 pathway, and IFN-y inhibits the Th2 pathway
[they inhibit each other]
25. What is type II hypersensitivity? Is this an autoimmune reaction? Example? Time table?
 Activation of complement by antibodies attached to surfaces
 Sometimes autoimmunity
i. Ex) Goodpasture syndrome
 Hours => 1 day
26. Type III? Can this be an autoimmune reaction? Examples?
 Activation of complement by antibody-antigen complexes
 NOT autoimmunity
i. Ex) immune complex deposition in kidneys
ii. Ex) rheumatoid arthritis
27. Type IV? Example? Time table?
 Inflammation following CD4+/CD8+ mediated Delayed Type Hypersensitivity responses
i. Ex) Mantoux test
 Generally 48 hours
Clinical shizznit:
28. How do Coxsackie virus or cytomegalovirus autoimmunity cause diabetes?
 Antibodies cross-react with glutamate decarboxylase (pancreatic β-cell enzyme)
29. What are the symptoms when a Klebsiella infection causes autoimmunity (2)?
 Ankylosing spondylitis
 Reiter syndrome
30. What immune response kills fungi?
 DTH, although radical, clears infectious fungi
31. What’s the difference between antigenic shift and drift?
 Shift occurs when two viruses from different sources infect the same cell and recombine
i. This is how we get swine flu et cetera