PCB 3233
PCB 3233 EXAM 6 QUESTIONS AND
ANSWERS 2026 UPDATE
If you got multiple immunizations with the same antigen, what would you find
with regard to Ab levels (IgG) and antibody affinity?
-IgG would increase
-affinity would be high
What is the difference between protective immunity and secondary immune
response?
Primary response:
-small number of pathogen-specific cells respond at the start
-delay before pathogen-specific antibodies are produced
-non-isotype-switched antibody having a mixture of affinities for the pathogen is
produced at the start
-high threshold of activation
-delay before effector T cells are generated and are able to enter infected tissues
-innate immunity works alone until an adaptive response is generated
Secondary response:
-large numbers of pathogen-specific cells respond immediately
-pathogen-specific antibodies already present
-antibodies are isotope-switched and have high affinity for the pathogen
-lower threshold for activation
-effector T ells are present and can enter infected tissue immediately
-close cooperation between innate and adaptive immunity from the start
What cells/molecules are used in each?
primary- naive cells
secondary- memory cells (not naive)
Do B-cells go through the same types of processes during a secondary immune
response as they do during a primary immune response?
yes
PCB 3233
, PCB 3233
Do we typically have more memory B-cells specific for antigen in a secondary IR
than we had naïve B-cell (antigen specific) in the primary response?
more memory cells in 2 response
Know what original antigenic sin is and how to use the concept if you are asked a
clinical type of question.
a phenomenon whereby the first influenza strain to infect a person constrains the
future response to the other strains
Can a naive B cell be activated in a secondary immune response?
No
Can we use this knowledge to help us in things like hemolytic disease of the
newborn (how does RhoGAM work)?
-Yes
-RhoGAM tricks mom's immune response into thinking that it is a 2 immune
response
-First pregnancy of RhD- mother carrying a RhD+ fetus-->primary immune
response, IgM plus low amounts of low-affinity IgG-->minor destruction of fetal
erythrocytes by anti-RhD IgG--> healthy newborn baby
-Second and subsequent pregnancies of RhD- mother carrying a RhD+ fetus-->
secondary immune response abundant, high-affinity IgG transcytosed to fetal
circulation-->massive destruction of fetal erythrocytes triggered by anti-RhD IgG--
>Anemic newborn babies
-First and subsequent pregnancies of RhD- mother carrying a RhD+ fetus and
infused with anti-Rh IgG-->primary immune response to RhD is inhibited by the
presence of RhD-specific IgG--> fetal erythrocytes are not destroyed-->healthy
newborn babies
Understand figure 11.12
Highly mutable viruses such as infuenza gradually escape from immunological
memory without stimulating a compensatory immune response. A person's
history of infection with infuenza is shown here. The first infection is with a strain
of influenza virus that elicits a primary antibody response to viral epitopes A, B, C,
PCB 3233
PCB 3233 EXAM 6 QUESTIONS AND
ANSWERS 2026 UPDATE
If you got multiple immunizations with the same antigen, what would you find
with regard to Ab levels (IgG) and antibody affinity?
-IgG would increase
-affinity would be high
What is the difference between protective immunity and secondary immune
response?
Primary response:
-small number of pathogen-specific cells respond at the start
-delay before pathogen-specific antibodies are produced
-non-isotype-switched antibody having a mixture of affinities for the pathogen is
produced at the start
-high threshold of activation
-delay before effector T cells are generated and are able to enter infected tissues
-innate immunity works alone until an adaptive response is generated
Secondary response:
-large numbers of pathogen-specific cells respond immediately
-pathogen-specific antibodies already present
-antibodies are isotope-switched and have high affinity for the pathogen
-lower threshold for activation
-effector T ells are present and can enter infected tissue immediately
-close cooperation between innate and adaptive immunity from the start
What cells/molecules are used in each?
primary- naive cells
secondary- memory cells (not naive)
Do B-cells go through the same types of processes during a secondary immune
response as they do during a primary immune response?
yes
PCB 3233
, PCB 3233
Do we typically have more memory B-cells specific for antigen in a secondary IR
than we had naïve B-cell (antigen specific) in the primary response?
more memory cells in 2 response
Know what original antigenic sin is and how to use the concept if you are asked a
clinical type of question.
a phenomenon whereby the first influenza strain to infect a person constrains the
future response to the other strains
Can a naive B cell be activated in a secondary immune response?
No
Can we use this knowledge to help us in things like hemolytic disease of the
newborn (how does RhoGAM work)?
-Yes
-RhoGAM tricks mom's immune response into thinking that it is a 2 immune
response
-First pregnancy of RhD- mother carrying a RhD+ fetus-->primary immune
response, IgM plus low amounts of low-affinity IgG-->minor destruction of fetal
erythrocytes by anti-RhD IgG--> healthy newborn baby
-Second and subsequent pregnancies of RhD- mother carrying a RhD+ fetus-->
secondary immune response abundant, high-affinity IgG transcytosed to fetal
circulation-->massive destruction of fetal erythrocytes triggered by anti-RhD IgG--
>Anemic newborn babies
-First and subsequent pregnancies of RhD- mother carrying a RhD+ fetus and
infused with anti-Rh IgG-->primary immune response to RhD is inhibited by the
presence of RhD-specific IgG--> fetal erythrocytes are not destroyed-->healthy
newborn babies
Understand figure 11.12
Highly mutable viruses such as infuenza gradually escape from immunological
memory without stimulating a compensatory immune response. A person's
history of infection with infuenza is shown here. The first infection is with a strain
of influenza virus that elicits a primary antibody response to viral epitopes A, B, C,
PCB 3233
