Immunological Memory and Vaccination Flashcards
*Know why memory cells respond more forcefully during second infection
memory cells respond more forcefully during secondary infection b/c:
1) pathogen-specific MEMORY cells OUTNUMBER naive cells
2) Memory cells are more READILY ACTIVATED
3) Memory B-cells have already undergone ISOTYPE Switching, Somatic hypermutation and Affinity Maturation
*Know what half-life is with regard to antibodies
Half-life describes the time required for half the quantity of antibodies present in one’s body to be eliminated/diminished. Hence having lower antibody levels.
*Know why naïve B-cells do not express IgM during a secondary response
Naive B cells do NOT express Ig M during secondary response because once naive binds to pathogen with specific antibody, NEGATIVE SIGNAL is given to Naive B cell to prevent its activation.
Hence No production of Low-affinity of IgM antibodies.
*Know why memory T-cells have an increase speed of response compared to
naïve T-cells
Memory T cells have an increased speed of response compared to Naive t cells, since they are activated at site of infection already (memory cells are more abundant and react quicker to same antigen).
*Know the consequence of alternative splicing of the CD45R gene-naïve
versus memory/effector T-cells
Due to alternative mRNA splicing, the extracellular domain of CD45RO is SHORTER (less aa) and has BETTER interactions with T-cell receptor than Cd45RA
CD45RA- is LESS able to interact with TCR and activate T cell as well as CD45RO. (The signaling of CD45RA is not as robust because it has more aa, exons, and bigger)
*Know the role of L-selectin and CCR7
L-selectin and CCR7 allow central memory T cells to enter secondary lymphoid organs and be activated by antigen presenting dendritic cells.
*Understand why viruses with high mutations make it difficult to vaccinate for life
RNA Viruses like INFLUENCE have high mutation rates (making it difficult to make a vaccine to protect for life) the virus constantly replicates and forms multiple new strains. Viruses like influenza CHANGES its EPITOPES every year, so one’s immunity to the virus diminish over time and antibodies made during past infection will no longer recognize current or new viral strains.
*Know reasons why small pox was able to be eradicated
Small pox:
*Know the following regarding vaccines- killed or inactivated, live-
attenuated, sub-unit vaccine, high-affinity neutralizing antibodies, conjugate
vaccines, and adjuvants
A
What two cells result from a primary immune response?
Primary immune response results in:
- Development of EFFECTOR cells and molecules that ends infection as soon as possible
- Immunological MEMORY- long lived memory-pathogen specific B cells and T cells (due to secondary immune response)
Explain what occurs during a child’s exposure to pathogen and how antibodies aid in protection? What occurs during repeated exposures of pathogen?
High levels of antibodies are sustained for months after infection- provide PROTECTIVE immunity- made by PLASMA cells in bone marrow or tissue beneath mucosal surface
After a year, antibody levels drop
Secondary immune response- during second infection of same pathogen, memory T and B cells (pathogen specific) generate stronger/faster response
Repeated exposures to same pathogen during “seasons” (ex: during winter, repeated exposure to pathogen; antibodies made will prevent any reinfection with same virus.
What occurs when a child is exposed to pathogen during first and second time?
During child’s first infection from pathogen, primary immune response will be made, producing effector T cells (pathogen specific) and antibodies to terminate infection.
antibodies sustained for months (prevent reinfection), then after 1 year, antibodies levels drop.
3rd year after initial infection, pathogen creates second infection that induces second immune response that is faster and stronger than primary response. child has retained memory of first infection ,so secondary response eliminate pathogen before significant disruption of tissue.
Differentiate between short-lived plasma cells and long-lived plasma cells
Primary response- plasma cells are SHORT LIVED; antibody production DECREASES over the next year; MAJORITY of plasma cells (short-lived)
LONG-LIVED Plasma cells- MINORITY of plasma cells that make specific antibodies.
They are sheltered in BONE MARROW.
How do short vs long-lived plasma cells differ from one another?
short lived plasma cells- rapidly proliferate and make many antibodies; shortly die from apoptosis (due inducing cell damage and mutation)
Long-lived plasma cells- once pathogen is defeated and eliminated, clones of long-lived plasma cells made. They do not induce cell damage/mutation
Only die once pathogen clears
How do pathogen-specific memory cells resemble other cells? What occurs to B cells that become memory cells? T cells?
Pathogen-specific MEMORY cells mirrors that of pathogen-specific EFFECTOR cells.
Components:
CD8 T cells
TFH, TH1, TH2, TH17, CD4 T- cells
B cells are programmed to become plasma cells secreting IgA, IgG, and Ig E
What kind of cells are made during primary immune response?
Both EFFECTOR and MEMORY cells are made during primary respnse
differentiate between how T cells and B cells become memory and effector T cells.
T cell:
1. A naive T cell is activated by pathogen
2. a clone of pathogen-specific effector and memory T cells are produced (majority- effector)
3. Effector T cells outnumber memory T cells
B cell:
1. A naive B cells is activated by pathogen and TFH cells
2. a clone of pathogen-specific B cells is produced
3. Effector cells outnumber B cells (only 1 memory cell)
Describe the two phases in primary response, as well as the phase in secondary immune response. Also include what is created as a result.
Primary response:
1. Early phase: naive B cell binds pathogen, and be activated to become antibody-producing plasma cell. This plasma cells will secrete low-affinity Ig M.
2. Late phase: Naive B cell binds to pathogen coated with HIGH-AFFINITY Ig G and Naive B cell will receive a NEGATIVE signal from Fc receptor, leading to B cell induced to die (apoptosis)
Secondary response: Memory B cell is activated to become an antibody-producing plasma cell. This plasma cell secretes HIGH-AFFINITY IgG.
What occurs when memory cells are activated during a second infection? What process leads to improved antibody response?
once memory cells are activated, Pathogen is usually cleared with NO sign of DISEASE
Affinity Maturation- during each subsequent infection continues to IMPROVE Antibody response.
What is the first disease that has been completely eradicated in the world. How did this occur? When did it happen?
SMALL POX- 1st disease eradicated via VACCINATION
from 1850s- 1979- 1 billion people died from disease
1972, small pox eradicated worldwide
50% US population has immunity, 50% do not (poses vulnerability for population, since everyone not vaccinated)
What is the role of Vaccinia? How long do antibodies last? How long are pathogen-specific memory B and t cells maintained?
Vaccinia- a similar, benign version of small pox vaccine that is sufficient enough to induce a secondary immune
response with an immunological memory to small pox (helps work against small pox)
Vaccinia- specific antibody titres that decrease 99%, but is maintained greater than or equal to 75 years.
Antibody- lasts 6 weeks (memory cells must replenish)
Pathogen-specific Memory B and T cells: maintained for greater or = to 75 years.
many vaccinated individuals still retain populations of Vaccinia- specificCD4 and CD8 T cells
Specify the half life of antibodies for anti-diphtheria vs anti-measles.
Half-life of antibodies varies;
Anti-Diptheria- 19 years
Anit-Measles- 200 years
Explain why memory lymphocytes are more resistant to apoptosis than their native counterparts. What are the memory T cells for CD4 and CD8 cells?
Memory lymphocytes are more resistant to apoptosis:
1. Individual memory cells have limited-life span, but a small portion DIVIDE and REPLENISH the population
Memory cells for CD4 and CD8 cells:
CD4 T cells: IL-7
CD8 T cells: IL-15
Where does renewal and replenishment of memory cells occur, and what drives the process?
Renewal and replenishment occurs in BONE MARROW and is likely driven by interactions with STROMAL Cells and Cytokines produced by Stromal cells.
Differentiate between an unimmunized donor of primary response and immunized donor of secondary response. How does frequency of B cells, isotype, and affinity of antibody differ?
UNIMMUNIZED donor of primary response
-LOWER frequency of antigen-specific B cells
-Isotype of antibodies: Ig M, IgG, IgA, and Ig E
LOW Affinity of antibody
-LOW Somatic Hypermutation
IMMUNIZED donor of secondary response -HIGHER frequency of antigen-specific B cells(1 in 10^2-1in 10^3) -Isotype of antibodies: IgG, IgA and IgE HIGH AFFINITY of antibody HIGH Somatic Hypermutation.
