L22 - immune memory
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Q: What happens toward the end of the primary adaptive immune response?
A: Memory cells are generated, allowing the immune system to respond more effectively if it encounters the same antigen again.
Q: What happens to the adaptive immune response if an antigen persists during chronic inflammation?
A: If the antigen remains present, the adaptive immune response may be continuously stimulated, causing immune cells to remain active and contribute to ongoing inflammation.
Q: What is the difference between a resolved primary immune response and a chronic immune response?
Resolved primary response: The immune response subsides, leaving behind memory cells.
Chronic response: Persistent antigen stimulation can maintain immune cell activity and ongoing inflammation.
Q: What are the three major cell types responsible for immunological memory in adaptive immunity?
Long-lived plasma cells
Memory T cells
Memory B cells
Q: What is the function of long-lived plasma cells in immunological memory?
A: Long-lived plasma cells continue producing antibodies after the primary immune response.
Q: What types of memory T cells are involved in immunological memory?
CD8+ memory T cells
Th1 memory cells
Th2 memory cells
Th17 memory cells
Tfh (follicular helper) memory cells
Q: What is the primary goal of vaccination in relation to adaptive immunity?
A: To establish immunological memory by generating memory B cells, memory T cells, and long-lived plasma cells, allowing a faster and more effective immune response upon future exposure to the antigen.
Q: Which cells are responsible for the adaptive immune memory response that vaccines aim to establish?
A: Long-lived plasma cells, memory T cells, and memory B cells.
Q: What is the function of memory T cells in immunological memory?
A: Memory T cells recognize previously encountered antigens and respond more rapidly upon re-exposure by activating T-cell immune responses.
Q: What is the function of memory B cells in immunological memory?
A: Memory B cells recognize previously encountered antigens and rapidly differentiate into antibody-producing plasma cells upon re-exposure, producing a faster and stronger antibody response.
Q: What are the two types of plasma cells produced during an immune response to infection?
Short-lived plasma cells
Long-lived plasma cells (LLPCs)
Q: What is the difference between short-lived and long-lived plasma cells?
Short-lived plasma cells: Produce a rapid, large wave of antibodies early in the immune response, then decline within a few weeks.
Long-lived plasma cells: A smaller, selected population that continues producing antibodies for months to years.
both adaptive
Q: What is the general timeline of short-lived plasma cells following infection?
Q: What is the general timeline of long-lived plasma cells following infection?
A: Short-lived plasma cells increase rapidly, peak around 2 weeks, and decline by approximately 3 weeks.
A: Long-lived plasma cells develop after the initial response and can survive for months, years, or even decades, continuing to produce antibodies.
Q: How are long-lived plasma cells associated with high-affinity antibodies and isotype switching?
A: During the adaptive immune response, some activated B cells undergo affinity maturation and isotype switching. A subset differentiates into long-lived plasma cells that continuously produce high-affinity, class-switched antibodies such as IgG.
Q: Why can antibodies from childhood vaccinations remain present into adulthood?
A: Long-lived plasma cells can survive for years or decades and continuously produce antibodies, such as IgG, against antigens encountered during childhood vaccination.
Q: What is the difference between memory B cells, memory T cells, and long-lived plasma cells?
Memory B cells: Recognize previously encountered antigens and rapidly generate new antibody-producing cells upon re-exposure.
Memory T cells: Respond rapidly to previously encountered antigens by activating T-cell immune responses.
Long-lived plasma cells: Continuously produce antibodies against previously encountered antigens.
Q: What are the steps involved in the formation of memory T cells?
A naïve T cell is activated by a dendritic cell presenting pathogen antigen.
The activated T cell undergoes clonal expansion.
Pathogen-specific effector T cells and memory T cells are produced.
Effector T cells outnumber memory T cells because they are needed to fight the current infection.
Q: What are the steps involved in the formation of memory B cells?
A naïve B cell recognizes a specific antigen.
A T follicular helper (Tfh) cell assists in B-cell activation.
The activated B cell undergoes clonal expansion.
B cells differentiate into antibody-producing plasma cells (effector cells) and memory B cells.
Plasma cells initially outnumber memory B cells to help fight the current infection.
Q: What is the difference between effector cells and memory cells during the primary immune response?
Effector cells: More numerous; actively fight and clear the current infection.
Memory cells: Less numerous; remain long-term to provide immunological memory.
Q: Do memory T and B cells require continuous exposure to an antigen to survive?
A: No. Memory cells can maintain their populations without the antigen remaining present.
Q: What cytokine supports the survival and proliferation of memory lymphocytes, and what cells produce it?
A: IL-7, which is secreted by stromal cells.
Q: When are memory T and B cells generated?
A: During the primary adaptive immune response, when activated T and B cells undergo clonal expansion and differentiation.
Q: Does the body continue generating memory T and B cells throughout life?
Yes. Memory cells continue to be generated throughout life as long as normal T-cell and B-cell responses occur.
Certain medications or diseases can interfere with this process.
Q: What is the role of T follicular helper (Tfh) cells in memory B-cell formation?
A: Tfh cells assist in activating B cells, allowing them to proliferate and differentiate into plasma cells and memory B cells.
Q: What type of immune response begins the primary immune response?
A: Innate immunity, which responds rapidly but is not antigen-specific.
Q: What are the benefits of the innate immune response during the primary immune response?
Rapidly clears pathogens.
Helps prevent the spread (dissemination) of pathogens.
Produces inflammatory signals that initiate adaptive immunity.
Q: How does innate immunity help activate adaptive immunity?
A: Innate immune cells, such as dendritic cells, present antigens to T cells, initiating the adaptive immune response.
Q: When does the adaptive immune response typically peak during the primary immune response?
A: Approximately 7–14 days after initial exposure.
Q: Why does high-affinity IgG take longer to develop during the primary immune response?
A: B cells must undergo activation, class switching, and affinity maturation to produce high-affinity IgG.
Q: What is generated during the primary immune response as pathogens are eliminated?
A: Immunological memory, which allows the immune system to respond faster upon future exposure to the same pathogen.
Q: How does the secondary immune response differ from the primary immune response?
Primary: Slower, typically peaks in 7–14 days.
Secondary: Faster, often responds within a few days.
The secondary response produces a greater number of effector T cells and a stronger antibody response, particularly IgG.
Q: What is the function of memory lymphocytes during the secondary immune response?
A: Memory lymphocytes rapidly activate and differentiate into new effector cells to fight the pathogen.
These are newly generated effector cells, not the original effector cells from the primary response.
Q: Why is immunological memory important for vaccines?
A: Vaccines generate immunological memory so that future exposure to a pathogen produces a faster and stronger immune response, reducing disease severity, morbidity, and mortality.
Q: Why is the secondary immune response more effective than the primary immune response?
A: It uses previously generated memory T cells, memory B cells, and long-lived plasma cells, allowing a faster, stronger, antigen-specific response.
Q: Does innate immunity occur during the secondary immune response?
A: Yes. Innate immunity is activated during the first few days of the secondary immune response.
Q: How quickly does the antigen-specific lymphocyte response occur during the secondary immune response?
A: Within 1–3 days, much faster than the primary immune response.
Q: How does the peak of the secondary immune response compare to the primary immune response?
A: The secondary immune response has a larger peak response than the primary immune response.
Q: What types of antibodies are already present during the secondary immune response?
A: Pre-existing, high-affinity, isotype-switched antibodies, including IgG, IgA, and IgE.
Q: What is the advantage of having effector lymphocytes during the secondary immune response?
A: Effector lymphocytes can rapidly enter infected tissues and begin fighting the infection.
Q: How does the secondary immune response affect morbidity and mortality?
A: It reduces morbidity and mortality by providing a faster and stronger immune response.
Q: Why do memory B cells have higher-affinity antigen receptors?
A: Somatic hypermutation leads to affinity maturation of B-cell receptors, allowing them to bind antigens more effectively.
Q: Does the secondary immune response require more or less antigen stimulation than the primary immune response?
A: Less antigen stimulation is required to activate the secondary immune response.
Q: When are long-lived memory B and T cells generated, and what do they do?
A: They are generated during the late stages of the primary immune response.
They recirculate throughout the body, surveying for their specific antigen.
Q: What are the major advantages of the secondary immune response compared to the primary immune response?
Faster: Antigen-specific response within 1–3 days.
Stronger: Larger peak immune response.
Higher affinity: B cells have undergone affinity maturation.
Less stimulation: Requires less antigen.
Greater protection: Reduces morbidity and mortality.
Q: How does the number of pathogen-specific cells differ between the primary and secondary immune responses?
Primary: Small number of pathogen-specific cells.
Secondary: Large number of pathogen-specific cells.
Q: How does the timing of antibody production differ between the primary and secondary immune responses?
Primary: There is a delay before specific antibodies are produced.
Secondary: Specific antibodies are already present.
Q: How do antibody isotype and affinity differ between the primary and secondary immune responses?
Primary: Starts with IgM antibodies of low to medium affinity.
Secondary: Antibodies are already isotype-switched and have high affinity.
Q: How does the threshold for immune cell activation differ between the primary and secondary immune responses?
Primary: High activation threshold (requires more stimulation).
Secondary: Low activation threshold (requires less stimulation).
Q: How does effector T-cell activation differ between the primary and secondary immune responses?
Primary: There is a delay before effector T cells are activated and enter infected tissues.
Secondary: Effector T cells are present and can rapidly become activated in infected tissues.
Q: How does cooperation between innate and adaptive immunity differ between the primary and secondary immune responses?
Primary: Innate immunity initially works alone until adaptive immunity becomes activated.
Secondary: Innate and adaptive immunity cooperate closely from the beginning of infection.
Q: What are the six major differences between the primary and secondary immune responses?
Primary | Secondary |
|---|---|
Few pathogen-specific cells | Many pathogen-specific cells |
Delay in antibody production | Antibodies already present |
IgM, low–medium affinity | Isotype-switched, high affinity |
High activation threshold | Low activation threshold |
Delayed effector T-cell activation | Rapid effector T-cell activation |
Innate immunity initially works alone | Innate and adaptive immunity cooperate immediately |
Q: Where do naïve T cells migrate?
A: Peripheral lymph nodes.
Q: What level of IL-2 receptors do naïve T cells express on their surface?
A: Low levels of IL-2 receptors.
Q: What CD45 markers are expressed on the surface of naïve T cells?
CD45RA: High expression.
CD45RO: Little to no expression.
Q: Why do naïve T cells require a higher threshold of activation during the primary immune response?
A: Because CD45RA functions poorly during T-cell activation, requiring greater stimulation to activate naïve T cells.
Q: What are the major characteristics of naïve T cells?
Migrate to peripheral lymph nodes.
Express low levels of IL-2 receptors.
Express high CD45RA and little to no CD45RO.
Require a high activation threshold during the primary immune response.
Q: How can CD45RA and CD45RO be used to differentiate naïve and memory T cells?
A:
CD45RA: High on naïve T cells.
CD45RO: High on many memory T cells.
Memory trick:
RA = Adolescent (naïve)
RO = Old (memory)
Q: Why do naïve T cells require a higher threshold for activation?
A: Naïve T cells express high levels of CD45RA, which functions less efficiently during activation, requiring stronger costimulation through CD28–B7.
Q: What happens to CD45RA expression after naïve T cells become activated?
A: CD45RA decreases, while CD45RO typically increases as T cells differentiate into memory cells.
Q: Why are CD45RA and CD45RO important when evaluating T cells in transplantation?
A: They help distinguish naïve T cells from memory T cells, which is useful when evaluating T-cell populations in transplant recipients.
Q: What CD45 markers are expressed on memory T cells?
D45RO: High expression.
CD45RA: Low expression.
Q: What happens to CD45RA and CD45RO expression when naïve T cells become activated?
CD45RA decreases.
CD45RO increases and is expressed on activated effector and many memory T cells.
Q: Why do memory T cells have a lower activation threshold than naïve T cells?
A: CD45RO functions more efficiently during T-cell activation, allowing memory T cells to respond faster with less stimulation.
Q: What are the three major types of memory T cells?
Central memory T cells (TCM)
Effector memory T cells (TEM)
Resident memory T cells (TRM)
Q: Where do central memory T cells (TCM) circulate, and what is their function?
Circulate between the blood, lymph, and secondary lymphoid tissues.
Have a low activation threshold.
Produce high levels of IL-2 after activation.
Differentiate into effector T cells.
Maintain a population of TCM cells for future responses.
Q: Why is IL-2 production important in central memory T cells (TCM)?
A: TCM cells produce high levels of IL-2 after activation, promoting rapid T-cell proliferation and differentiation into effector T cells.
Q: Where do effector memory T cells (TEM) circulate, and what is their function?
Circulate between the blood, non-lymphoid tissues, and lymph.
Migrate into inflamed tissues.
Respond rapidly to infections directly at the tissue site.
Q: Where are resident memory T cells (TRM) located, and what is their function?
Remain in non-lymphoid tissues.
Rapidly respond to local infections.
Q: What is the major difference between TCM, TEM, and TRM cells?
Memory T cell | Location | Main function |
|---|---|---|
TCM | Secondary lymphoid tissues | Proliferate and generate effector T cells |
TEM | Circulate through blood and non-lymphoid tissues | Rapidly respond at inflamed tissues |
TRM | Reside in non-lymphoid tissues | Provide rapid local protection |
Q: Why do memory T cells respond faster than naïve T cells?
Higher CD45RO expression improves activation efficiency.
Lower activation threshold.
Rapid IL-2 production promotes T-cell proliferation.
Type | Main function |
|---|---|
? | Reactivate in lymphoid tissues, produce IL-2, and generate effector T cells |
? | Circulate to inflamed tissues and respond rapidly |
? | Remain in tissues and provide rapid local protection |
Type | Main function |
|---|---|
TCM | Reactivate in lymphoid tissues, produce IL-2, and generate effector T cells |
TEM | Circulate to inflamed tissues and respond rapidly |
TRM | Remain in tissues and provide rapid local protection |
Q: What is CD45, and what is its role in T-cell activation?
A: CD45 is a transmembrane tyrosine phosphatase involved in T-cell activation.
Q: Which CD45 isoforms are expressed on naïve versus memory T cells?
Naïve T cells: CD45RA
Memory/effector T cells: CD45RO
Q: Why is CD45RA less efficient at activating T cells than CD45RO?
A: CD45RA is larger and interacts less efficiently with the T-cell receptor (TCR) complex, resulting in a higher activation threshold.
Q: Why does CD45RO allow memory T cells to activate more easily?
A: CD45RO has a shorter extracellular domain, allowing better interactions with the TCR complex and a lower activation threshold.
Q: What process produces the structural differences between CD45RA and CD45RO?
A: Alternative mRNA splicing, which produces different CD45 isoforms.
Q: What is the structural difference between CD45RA and CD45RO?
CD45RA: Larger extracellular domain containing additional amino acid sequences encoded by exons A, B, and C.
CD45RO: Shorter extracellular domain due to alternative splicing.
Q: What mnemonic helps distinguish CD45RA from CD45RO?
RA = Adolescent: Naïve T cells, higher activation threshold.
RO = Older: Memory T cells, lower activation threshold.
Q: Why do effector and memory T cells have a lower activation threshold than naïve T cells?
A: They typically express CD45RO, which interacts more efficiently with the TCR complex, allowing faster and easier activation.
Q: How can CD45RA and CD45RO be used to differentiate T cells?
A: Their expression levels help distinguish naïve, effector, and memory T cells.
Q: What are the expression levels of CD45RA and CD45RO on naïve T cells?
CD45RA: High (+++)
CD45RO: Low (+)
Q: What are the expression levels of CD45RA and CD45RO on effector T cells?
CD45RA: Low (+)
CD45RO: High (+++)
Q: What are the expression levels of CD45RA and CD45RO on memory T cells?
CD45RA: Absent (−)
CD45RO: High (+++)
Q: What happens to CD45RA and CD45RO expression as naïve T cells differentiate into effector and memory T cells?
CD45RA decreases.
CD45RO increases.
Q: Which T-cell populations express high levels of CD45RO?
A: Effector and memory T cells both express high levels of CD45RO (+++).
Q: What antibodies do naïve B cells express on their surface?
A: IgM and IgD, which initially have low antigen-binding affinity.
Q: Where do naïve B cells migrate to become activated?
A: Secondary lymphoid tissues.
Q: What is the first antibody produced during the primary immune response?
A: Low-affinity IgM.
Q: What three processes occur during T-dependent B-cell activation to produce high-affinity antibodies?
Somatic hypermutation
Affinity maturation
Isotype switching
These processes help generate high-affinity plasma cells and memory B cells.
Q: What is the significance of somatic hypermutation, affinity maturation, and isotype switching?
A: They allow B cells to produce more specialized, high-affinity antibodies that bind antigens more effectively.
Q: What antibody classes are usually expressed by activated, class-switched B cells?
A: IgG, IgA, or IgE.
Q: How does the antibody affinity of activated B cells compare to naïve B cells?
A: Activated B cells generally have higher-affinity antigen receptors, which may continue increasing through affinity maturation.
Q: What do activated effector B cells differentiate into?
A: Antibody-secreting plasma cells, which are large cells with abundant cytoplasm.
Q: What two major cell populations are generated during T-dependent B-cell activation?
lasma cells: Secrete antibodies.
Memory B cells: Provide long-term immunological memory.
Q: Why does the body invest significant time and energy into B-cell activation and maturation?
A: To generate specialized, high-affinity antibodies that bind more effectively to specific antigens and improve immune protection.
Q: What antibody classes can memory B cells express on their surface?
A: IgG, IgA, or IgE.
Q: Do memory B cells secrete antibodies?
A: No. Memory B cells express surface antibodies, while plasma cells secrete antibodies.
Q: How are memory B cells selected during the primary immune response?
A: They are derived from B-cell clones with the highest affinity for the antigen through affinity maturation.
Q: What is affinity maturation?
A: The process by which B cells with higher-affinity antigen receptors are selected, producing B cells that bind more effectively to their specific antigen.
Q: During the secondary immune response, which B cells are preferentially activated?
A: Memory B cells are preferentially activated, while naïve B-cell responses are inhibited.