Unit 8 Discussion (Zoom) Flashcards
How are lymph nodes important in the immune response?
Lymph nodes filter lymph fluid and are sites where immune cells, such as B and T lymphocytes, can encounter antigens, activate, and proliferate
How is the spleen important in the immune response?
The spleen filters blood, removing old or damaged red blood cells and pathogens, and also serves as a site for immune cell interactions and responses
How are the tonsils important in the immune response?
Tonsils are lymphoid tissues located in the throat that trap and process antigens from inhaled or ingested substances, initiating immune responses
How is MALT important in the immune response?
MALT (Mucosa-associated lymphoid tissue) includes lymphoid tissues such as Peyer’s patches in the gut, which protect mucosal surfaces by capturing antigens and promoting localized immune responses.
How are B lymphocytes important in the immune response?
B lymphocytes (B cells) are responsible for producing antibodies that bind to specific antigens, neutralizing pathogens or marking them for destruction by other immune cells
How are T lymphocytes important in the immune response?
T lymphocytes (T cells) play various roles, including directly killing infected or cancerous cells (cytotoxic T cells) and regulating immune responses (helper T cells)
Why is it advantageous for the lymphatic system to lack a pump?
The lack of a pump in the lymphatic system ensures that lymph flow is slow and steady, allowing immune cells to efficiently filter antigens and pathogens as the fluid passes through lymph nodes.
This also enables the lymphatic system to rely on muscle movement and body motion for circulation, which helps distribute immune surveillance throughout the body
When is antigen processing an essential prerequisite for an immune response?
Antigen processing is an essential prerequisite for an immune response when the adaptive immune system needs to recognize and respond to specific pathogens, as processed antigens are presented to T cells by MHC molecules to activate them
Ag are small and have no repetitive motifs
Endogenous Ag and exogenous Ag
Why does the body have both antibody and cell-mediated immune responses?
Antibody responses (humoral immunity): Target exogenous antigens
ex. bacteria, fungus, free viruses
Cell-mediated responses: Target endogenous antigens
ex. virus infected cell, cancer cell
The body has both antibody and cell-mediated immune responses to target pathogens effectively: antibodies neutralize extracellular pathogens, while cell-mediated immunity destroys infected or abnormal cells harboring intracellular pathogens
What role does NK cells play in immunity?
Natural killer (NK) cells play a critical role in immunity by targeting and destroying virus-infected cells and tumor cells without the need for prior antigen recognition, bridging innate and adaptive responses
What is exogenous? endogenous?
Exogenous: what’s happening outside the cell
Endogenous: what’s happening from inside the cell
What immune response is antigen processing?
Adaptive immune response
Differences between MHC I and MHC II
Found on what type of cells in the body?
MHC I: On all nucleated cells (no RBC)
MHC II: APC such as B cells, macrophages, and dendritic cells
Differences between MHC I and MHC II
Presents what type of epitopes?
MHC I: Processed on endogenous Ag
MHC II: Processed on exogenous Ag
Differences between MHC I and MHC II
Recognized by what receptors? On which cell?
MHC I: TCR, w/ CD8 on Tc
MHC II: TCR w/ CD4 on Th
Differences between MHC I and MHC II
How are Ag presented?
MHC I: “foreign” proteins from pathogens are broken into 8-12 amino acid pieces -> moves into ER & loaded onto MHCI on the ER membrane -> packaged in Golgi to transport vesicles to CM
MHC II: Dendritic cells phagocytize pathogen into peptides w/ in phagolysosome -> vesicles w/ MCHII fuses w/ phagolysosomes where processed Ag binds to MHCII -> vesicles fuse w/ CM
Differences between MHC I and MHC II
Does it help to activate humoral or cell-mediated response?
MHC I: Cell-mediated
MHC II: Humoral & cell-mediated
Scientists can develop genetically deficient strains of mice. Describe the immunological impairments that would result in mice deficient in each of the following:
MHCI
MHC I presents endogenous antigens
Affected cells: all nucleated cells
Meaning: Highly susceptible to intracellular parasites like viruses
The mice would have impaired cytotoxic T cell (CD8+) responses, reducing their ability to fight viral infections and eliminate cancerous cells
Scientists can develop genetically deficient strains of mice. Describe the immunological impairments that would result in mice deficient in each of the following:
MHC II
MHC II presents antigens to Th cells
Affected cells: On APC can’t talk to Th
Meaning: unable to develop a fully functional immune system
The mice would lack effective helper T cell (CD4+) activation, leading to weak antibody production and compromised immune responses to extracellular pathogens
Scientists can develop genetically deficient strains of mice. Describe the immunological impairments that would result in mice deficient in each of the following:
TCR
TCR helps T cells recognize presented antigens
Affected cells: T cells
Meaning: T cells are not activated, no activated Th or Tc -> no adaptive immune response
The mice would lack functional T cells, severely impairing both cell-mediated and adaptive immunity
Scientists can develop genetically deficient strains of mice. Describe the immunological impairments that would result in mice deficient in each of the following:
BCR
BCR recognizes specific epitopes
Affected cells: B cells
Meaning: B cells not activated, no antibody response
The mice would have no functional B cells, resulting in an inability to produce antibodies and a deficient humoral immune response
Scientists can develop genetically deficient strains of mice. Describe the immunological impairments that would result in mice deficient in each of the following:
IL-2 receptor
The mice would exhibit reduced T cell proliferation and immune activation, impairing both adaptive and some innate immune responses
Scientists can develop genetically deficient strains of mice. Describe the immunological impairments that would result in mice deficient in each of the following:
IFNγ
The mice would have impaired macrophage activation and reduced ability to combat intracellular pathogens, as well as weaker immune regulation
Human immunodeficiency virus (HIV) preferentially destroys CD4+ cells. Specifically, what effect does this have on antibody and cell-mediated immunity?
CD4 are on Th cells
Th cells relay information from APC like DC cells to B cells or Tc cells. Break the communication line from innate to adaptive, the B cells and Tc cells don’t know what they are supposed to do.
What cells does HIV target?
CD4 cells;
which are helper T cells
breaks down communication between B cells and Cytotoxic T cells
Does HIV infect the innate immune response?
No;
Innate trying its best to phagocytize HIV
does not infect, moves on
Has nobody to give information to because T helper cells are destroyed
In general, what sorts of pathogens would successfully attack a patient with an inability to synthesize B lymphocytes?
B cells make antibodies
Meaning: There would be no antibodies to fight against extracellular pathogens such as bacteria
What sorts of pathogens could successfully attack a patient with an inability to produce T lymphocytes?
Th cells provide information from innate to adaptive (B & Tc)
Meaning: The patient would be susceptible to all sorts of pathogens
Plasma cells are vital for protection against infection, but memory B cells are not. Why not?
Plasma cells make antibodies necessary to fight the infection (during)
Memory cells work in subsequent exposure to the antigen (later)
Compare and contrast herd immunity and contact immunity
Contact immunity = unvaccinated comes into contact w/ someone who just had an attenuated (weakened) vaccine -> immunity gained
Herd immunity = when a high % of the population is resistant to the pathogen due to such measures as vaccinations, the pathogen is unable to spread effectively within this population -> conferring protection within this community
How much of the population has to be vaccinated for herd immunity to work?
at least 75%;
for measles, greater than 95% of the population needs to be vaccinated for herd immunity
Joe Micro was hospitalized in a New York City facility with Covid-19. He was on a ventilator, steroids, and antivirals for several weeks. In August 2020, he recovered fully from this disease. He gave blood to test whether he had the antibodies against this virus.
a. What type of acquired immunity did Joe Micro have?
b. Why would scientist want to harvest Joe Micro’s antibodies? In other words, what type of acquired immunity would the scientist want to occur?
a. Natural acquired active immunity
because he got the disease
b. Artificially acquired passive immunity
because he fully recovered from the disease
Describe three ways by which genetic recombinant techniques could be used to develop safer, more effective vaccines.
- Attenuation through genetic modification: Scientists can weaken a pathogen by altering or removing virulence genes, creating a live attenuated vaccine that is safer and still triggers a strong immune response.
- Subunit vaccine production: Recombinant DNA technology can be used to produce specific antigens (e.g., proteins) of a pathogen, avoiding the use of the whole organism and reducing the risk of adverse reactions.
- DNA or RNA vaccines: Genetic techniques enable the creation of vaccines that deliver nucleic acids encoding pathogen antigens, allowing the host’s cells to produce these antigens and stimulate immunity without using live or killed pathogens
For helper T cells, why are we not sure if they differentiate into memory Th cells?
Memory Th cells don’t exist in a large enough population that indicated that it’s a memory T helper cell
What are some cytokines?
Humoral
IL-4
Stimulates differentiation of naïve T cells into Th2 cells & promotes B-cell activation & antibody production, especially IgE.
Cell-mediated
IL-2
Encourages growth, proliferation, and activation of T cells, particularly regulatory and cytotoxic T cells
IL-12
Promotes differentiation of naïve T cells into Th1 cells & enhances activity of NK cells & cytotoxic T lymphocytes
BCR can recognize how many epitopes?
Only 1
What are the 5 classes of antibodies?
IgM
IgG
IgA
IgE
IgD
What do each of the 5 classes on antibodies do?
- IgM: The first antibody produced during an immune response, IgM is effective at forming antigen-antibody complexes and activating the complement system.
- IgG: The most abundant antibody in blood and extracellular fluid, IgG provides long-term immunity and can cross the placenta to protect the fetus. neutralizes toxins, & opsonizes pathogens for phagocytosis.
- IgA: Found primarily in mucosal areas (e.g., respiratory and gastrointestinal tracts) and secretions like saliva and breast milk, IgA plays a key role in protecting mucosal surfaces from infection.
- IgE: Involved in allergic reactions and responses to parasitic infections, IgE binds to allergens and triggers histamine release from mast cells and basophils.
- IgD: Found in small amounts, IgD is primarily located on immature B cell surfaces and helps initiate B cell activation during immune responses.
BCR _____________ to find the pathogen
Made _______ to any interaction of a foreign antigen
BCR are the eyes of the B cells to find the pathogen
Made prior to any interaction of a foreign antigen
TCR ______ of T cells
The recognize ________ that are being reflected to them by _____
TCR are the eyes of T cells
They recognize processed antigens that are being reflected to them by MHC types
Isotope switching: where do I go?
Start off at IgM or IgD
then switched depending on where it needs to go (what response)
ex. IgE for allergic reactions and responses to parasitic infections
Clonal Deletion with B cells
Prevents autoimmune disease buy killing cells that recognize “self”
because if it recognizes it can attack the body
If doesn’t recognize “self” goes out to spleen
Clonal deletion with T cells
Do I recognize processed antigen (epitope) on MHC?
No: apoptosis
Yes: go to part 2
Part 2;
Do I recognize “self” on MHC?
Yes: apoptosis
No: can go out
Regulatory T cells (T reg cells):
Recognize self and are allowed to
They:
- prevent autoimmune disease
- suppress allergies and asthma
- fetal maternal tolerance
fetus can grow without being attacked by mothers immune cells
Clonal selection:
When the BCR or TCR binds to a specific antigen
by binding they are being selected
BCR will bind directly to antigens
TCR binds to APC given to them on/by MHC’s
That is selection
Clonal expansion then happens:
- more is made
- increasing number of particular immune cells for a specific antigen
The differentiate into
- plasma cells: make antibodies
and
- memory B and T cells: used for any subsequent encounter with that specific pathogen, used later on
Steps of B cell activation:
- B cells attached to epitope with BCR
- B cell engulfs & presents epitope with MHC II
- The cell’s TCR and CD4 match up with B cell presentation
- Second signal & cytokines released from Th
- B cell divides and differentiates
- Plasma cells make antibodies
Steps of T cell activation?
- DC engulfs virus & presents pieces with MHC II
- TCR & CD8 on Tc recognize epitope presented by MHC I on DC
- Cross presentation of epitope by DC where Th1 recognizes antigen on MHC II and Tc recognizes antigen on MHC I. Only then does Th1 release cytokines to Tc
- Tc divides & differentiates in response to cytokines from Th1
- Mature Tc does surveillance for epitope presenting cells to target
Explain how a pregnancy test works at the molecular level.
A pregnancy test works by detecting the presence of human chorionic gonadotropin (hCG), a hormone produced by the placenta shortly after a fertilized egg attaches to the uterine lining.
The test uses antibodies that specifically bind to hCG; if hCG is present, it triggers a visible reaction on the test strip, indicating pregnancy.
Attenuated vs. Inactivated vs. Toxoid vaccines
- Attenuated vaccines use live pathogens that have been weakened to provoke a strong immune response without causing disease.
- Inactivated vaccines contain pathogens that have been killed, offering immunity without the risk of infection.
- Toxoid vaccines use inactivated toxins from bacteria to stimulate immunity against the harmful effects of the toxin without causing disease. rather than the whole pathogen
During the war in Iraq in 2010, an Army corporal with type AB blood received a life-saving blood transfusion from his sergeant who had type O blood. Later, the sergeant was involved in a traumatic accident and needed blood desperately. The corporal wanted to help but was told his blood was incompatible. Explain the immunological reasons the corporal could receive from but could not give to the sergeant
The Army corporal with type AB blood can receive blood from the sergeant with type O because type O blood lacks A and B antigens, making it universally compatible for transfusion recipients
However, the corporal’s AB blood contains both A and B antigens, which the sergeant’s immune system would recognize as foreign, potentially triggering a dangerous immune response
A patient arrives at the doctor’s office with a rash covering her legs. How could you determine if the rash were a type I or a type IV hypersensitivity?
A type I hypersensitivity (e.g., an allergic reaction) would occur rapidly after exposure to an allergen, involving IgE-mediated mast cell degranulation and symptoms like itching or swelling.
In contrast, a type IV hypersensitivity (e.g., contact dermatitis) would develop hours to days later, driven by T-cell-mediated inflammation without immediate allergic symptoms.
An expectant mother has a blood type A+. Why is a child born to this mother not susceptible to Rh-related hemolytic disease of the newborn?
A child born to an A+ mother is not susceptible to Rh-related hemolytic disease of the newborn because the mother is Rh-positive, meaning her immune system does not produce antibodies against the Rh antigen
Hemolytic disease of the newborn occurs when an Rh-negative mother produces anti-Rh antibodies that attack the Rh-positive red blood cells of her baby, a scenario not possible in this case.
Why is a person who produces a large amount of IgE more likely to experience anaphylactic shock than a person who instead produces a large amount of IgG?
A person who produces a large amount of IgE is more likely to experience anaphylactic shock because IgE binds to mast cells and basophils, triggering the release of histamine and other inflammatory mediators upon allergen exposure
In contrast, IgG does not activate mast cells or basophils in this manner, making it less likely to provoke the widespread, severe allergic reaction seen in anaphylaxis
Two boys have autoimmune diseases: one has Bruton-type agammaglobulinemia (lacks B cells), and the other has DiGeorge syndrome (lacks T cells). On a camping trip, each boy is stung by a bee, and each falls into poison ivy. What hypersensitivity reactions might each boy experience because of his camping mishaps?
- The boy with Bruton-type agammaglobulinemia may not experience a type I hypersensitivity reaction to the bee sting because he lacks B cells needed to produce IgE antibodies. However, he could still experience non-allergic effects from the venom, such as local pain and swelling.
- The boy with DiGeorge syndrome may not develop a type IV hypersensitivity reaction to poison ivy due to his lack of T cells, which are essential for this delayed immune response. However, he could still experience other non-immune effects, such as skin irritation caused by the plant’s oils.
What are the differences and similarities between the four types of hypersensitivities? Name an example of each type.
- Type I hypersensitivity involves immediate allergic reactions mediated by IgE and mast cells, such as in anaphylaxis (e.g., peanut allergy).
- Type II hypersensitivity occurs when IgG or IgM antibodies target cells for destruction, such as in hemolytic anemia caused by mismatched blood transfusions.
- Type III hypersensitivity results from immune complex deposition causing inflammation, such as in systemic lupus erythematosus (SLE).
- Type IV hypersensitivity is a delayed T-cell-mediated response, such as in contact dermatitis from poison ivy exposure.
All types involve immune system overreactions but differ in mediating components (antibodies vs. T cells) and timing (immediate vs. delayed).
What is the difference between autoimmune disease and hypersensitivity?
Autoimmune diseases occur when the immune system mistakenly attacks the body’s own tissues, treating self-antigens as foreign.
In contrast, hypersensitivity refers to an exaggerated or inappropriate immune response to external or internal antigens, which may or may not involve self-tissues.
