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23 Cards in this Set
- Front
- Back
What sustains immunological memory?
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Clones of long-lived memory T and B cells (NOT antibody); constant exposure to low antigen levels
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What is the difference in the amount of time between primary and secondary immune response?
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Primary response takes a long time, up to a week, allowing the organism to get sick. Secondary response is almost immediate.
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What is the role of existing antibodies in immunological memory?
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Antibody levels can be maintained for several months after infection by plasma cells. Reinfection during this time will be destroyed very quickly thru neutralization, opsonization, and complement activation.
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Of neutralization, opsonization, and complement activation, which is a) independent of Ig class and b) Fc region dependent?
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A)Neutralization
B) Complement activation (can sometimes punch hole in antigen) and opsonization |
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Most activated T and B cells become ___________ while fewer become ___________.
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short-lived effector cells; long-lived memory cells
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Properties of 2ndary immune response:
1) Memory lymphocytes (more or less) abundant than naive 2) Memory lymphocytes have (higher or lower) affinity antigen receptors than naive. |
1) More
2) Much higher. This allows them to act to a lower concentration of pathogen. They've already undergone isotype switching and affinity maturation. |
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Are memory cells more likely to be IgM or IgG? Why?
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IgG. It has undergone isotype switching and affinity maturation. It works better than IgM.
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Only memory B cells, and not naive B cells, participate in the secondary immune response. WHY?
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Immune complexes bind to the BCR of pathogen-specific naive B cells and also to inhibitory Fc receptor (FcγRIIB1) which is expressed by naive B cells but not memory B cells.
This cross-linking <b>transmits a negative signal that inhibits activation of the naive B cell, even though it is pathogen-specific.</b> |
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What is FcγRIIB1?
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A receptor that is only expressed by naive B cells. When it binds complexes composed of pathogen coated with a more specific antibody (from the memory B cell), it sends negative signals that inhibits activation of the naive B cell, even though it is pathogen-specific.
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What is the benefit of negative regulation/suppression of activation of naive B cells?
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Prevents production of low-affinity IgM antibodies that would be a wasteful and interfering recapitulation of the primary response.
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What is hemolytic disease of the newborn? How does it result?
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Occurs when father is Rh+ and mother is Rh- during <b>second or later pregnancy.</b>
During the first Rh+ pregnancy, fetal RBCs cross the placenta, get into mother's blood, and stimulate anti-Rh antibodies. These are low affinity and so cause little harm to fetus. During a second pregnancy that's Rh-, fetal red cells cross the placenta and induce a secondary response to Rh which is now high-affinity IgG. These coat fetal RBCs and cause them to be cleared. Babies have severe anemia when born. |
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How is hemolytic disease of the newborn prevented?
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<b>Trick mother's immune system into responding to the primary exposure as if it were a secondary exposure. </b>During 28th week of pregnancy, give the mother a shot of anti-Rh IgG (before they've had a chance to make anti-Rh IgG). This is sufficient to coat all the fetal red cells that cross placenta to enter maternal circulation. Activation of mother's Rh-specific naive B cells is prevented!
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When Rh- woman is ABO compatible with Rh+ fetus, there is increased risk to develop Rh alloimmunization to fetus. Why?
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ABO incompatible RBCs that sneak over from fetus to mother don't survive long. ABO compatible, in contrast, have a better chance of staying around long and thus inducing antibody production.
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What are some drawbacks of suppressing naive B cells activation during 2ndary immune response?
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If you get a pathogen that is similar but not exactly the same (e.g., a flu virus that has mutated), a potentially higher-affinity antibody-producing B cell may be suppressed.
(this is the original antigenic sin) |
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What is original antigenic sin?
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The phenomenon whereby the first flu strain to infect a person constrains/prevents development to future response to OTHER (similar) strains
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What cell surface markers distinguish memory T cells from naive T cells?
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CD45<b>RO</b> made by memory T cells, CD45<b>RA</b> made by naive T cells.
Memory cells express different cytokines, in general, that naive cells (don't need to memorize list). |
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What are two types of memory T cell function?
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1) Effector memory T cells: quickly differentiate into potent effector T cells making lots of cytokines, and depending on the cytokine envt, can differentiate into Th1, Th2, or Th17.
2) Central Memory T cells: specialized towards entering T cell zones of secondary lymphoid tissue. rapidly express CD40L and itneract with B cells. Some become follicular helper cells. |
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What are Central Memory T cells?
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specialized towards entering T cell zones of secondary lymphoid tissue. rapidly express CD40L and itneract with B cells. Some become follicular helper cells.
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What are Effector memory T cells?
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quickly differentiate into potent effector T cells making lots of cytokines, and depending on the cytokine envt, can differentiate into Th1, Th2, or Th17.
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What does CCR7 do in terms of memory T cells?
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Central memory T cells express it and remain in lymphoid tissue. Effector memory T cells lack it and migrate out to other tissues.
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Is maintenance of immunological memory dependent on antigen?
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This is controversial.
Quite low levels of antigen can remain in germinal centers attached as immune complexes on follicular dendritic cells (FDCs). These could periodically restimulate. |
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What are FDCs?
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follicular dendritic cells (NOT same as dendritic cells that activate T cells). They activate B cells.
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How are antigens retained for long periods of time on FDCs? What are implications of this?
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in form of immune complexes.
FDCs express high levels of Fc and C3 (complement) receptors that bind Antigen/Antibody complexes for a long time. Implications are allowance for continual restimulation of B cells. B cells can restimulate Ts as well. |