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What is the function of the Fab region of an antibody?
(antigen-binding) fragment confers specificity to its target by binding to antigens.
What is the function of the Fc region of an antibody?
(crystallizable) fragment drives the biological function of the antibody, such as interacting with immune cells and activating the complement system.
STEAM
How many polypeptide chains make up an antibody?
four polypeptide chains:
Two heavy chains
Two light chains
What are the two main regions in each antibody chain?
Variable region (V region): Determines antigen specificity.
Constant region (C region): Determines the antibody's class and function.
How many antigen-binding sites does an antibody have?
two antigen-binding sites, located at the tips of the Fab regions.
What is the structural difference between the heavy and light chains in an antibody?
Heavy chains are longer and contain both variable and constant regions.
Light chains are shorter and also have variable and constant regions.
What is the function of neutralization of microbes and toxins?
Antibodies block pathogens from attaching to cells, preventing infection and toxin effects.
How does opsonization of pathogens help in immune defense?
Antibodies coat pathogens, marking them for easier phagocytosis by immune cells like macrophages and neutrophils.
What happens when antibodies activate the complement system?
Antibodies trigger a complement cascade, leading to membrane attack complex (MAC) formation and cell lysis.
What is ADCC (Antibody-Dependent Cell-Mediated Cytotoxicity)?
Antibodies bind to infected cells and signal immune cells (like NK cells) to release toxic molecules that destroy the target cell.
What are the four major mechanisms of antibodies?
neutralization of microbes and toxins
opsonize pathogens
activate compliment system
bind to infected cells and activate ADCC (Antibody-Dependent Cell-Mediated Cytotoxicity)
B cell + microbe → antibodies → antibody with microbe →
neutralization of microbes and toxins
B cell + microbe → antibodies → Phagocyte →
opsonization and phagocytosis of micobes
B cell + microbe → antibodies → NK cell attached to Fc gamma receptor →
antibody-dependent cellular cytotoxicity
B cell + microbe → antibodies → C3b receptor macrophage attached to microbe →
phagocytosis of microbes opsonized with complement fragments (e.g. C3b). 2nd function of complementary activation
B cell + microbe → antibodies → Neutrophil →
inflammation 2nd functions of complementary activation
B cell + microbe → antibodies → complement activation → microbes
lysis of microbes 2nd functions complementary activation
IgG
opsonization of antigens for phagocytosis by macrophages and neutrophils
activation of the classical pathway of complement
antibody-dependent cell-mediated cytotoxicity mediated by natural killer cells
neonatal immunity: transfer of maternal antibody across the placenta and gut
feedback inhibition of B cell activation
Neutralization of microbes and toxins
IgM
activation of classical pathway of complement
neutralization of microbes and toxins
IgA
Mucosal immunity: secretion of IgA into the lumens of the gastrointestinal and respiratory tracts
Neutralization of microbes and toxins in lumens of mucosal organs
IgE
Mast cell degranulation (immediate hypersensitivity reactions)
Defense against helminths
How do antibodies neutralize microbes and toxins?
The Fab region of antibodies blocks binding sites on microbes and toxins, preventing them from attaching to cellular receptors.
What is steric hindrance in neutralization?
Antibodies physically interfere with microbial binding to host receptors, preventing infection.
Can antibodies induce conformational changes in microbes?
Yes, antibody binding can alter microbial surface molecules, stopping their interaction with host receptors.
How does IgG promote phagocytosis?
IgG antibodies coat (opsonize) microbes and bind to Fc receptors (FcR) on phagocytes, enhancing phagocytosis.
Which immune cells have Fc receptors (FcR) for IgG?
Mononuclear phagocytes (macrophages) and neutrophils express Fcγ receptors that bind antibody-coated microbes.
What is opsonization?
A process where microbes are coated with antibodies (IgG) or complement proteins (C3b) to enhance phagocytosis.
Leukocyte Fc Receptors activate
FcgammaR1 (CD64) affinity- high binds IgE1 and IgG3 can bind to monomeric IgG ; cell distribution- macrophages, neutrophils, eosinophils ; function- phagocytosis activation of phagocytes
FcgammaRIIIA (CD16) affinity- low ; cell distribution: NK cells, macrophages, dendritic cells ; function: antibody-dependent cell-mediated cytotoxicity (NKs)
FCepsilonRI affinity-high binds monomeric IgE ; cell distribution- Mast cells, basophils ; function- cell activation (Degranulation)
Leukocyte Fc Receptors inhibited
FcgammaRIIB: affinity-low ; cell distribution- B lymphocytes, macrophages, dendritic cell other cells ; function- feedback inhibition of various cellular responses
binds with CD32
antibody-mediated opsonization and phagocytosis
opsonization of microbe by IgG
Binding of opsonized microbes to phagocyte Fc receptors (FcgammaRI)
Fc receptor signals activate phagocyte
Phagocytosis of microbe
Killing of ingested microbe
What is Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)?
NK cells and macrophages bind to antibody-coated cells via Fc receptors, leading to target cell destruction.
Which immune cells are primarily responsible for ADCC?
Natural Killer (NK) cells and macrophages.
What is the role of FcγRIIIA in ADCC?
low-affinity receptor on NK cells that binds clustered IgG molecules on antibody-coated target cells
What happens when NK cells recognize antibody-coated target cells?
ctivated to secrete IFN-γ and release cytotoxic granules, killing the target cell.
Why can’t phagocytes engulf helminths?
Helminths (worms) are too large to be engulfed by phagocytes, requiring an alternative immune response
Which immune components are involved in helminth clearance?
IgE antibodies, eosinophils, and mast cells work together to mediate helminth killing and expulsion.
How do eosinophils kill helminths?
release a toxic cationic protein called major basic protein (MBP) from their granules, which damages helminths.
What role do Th2 cells play in helminth defense?
Th2 cells activate IgE production and eosinophilia, enhancing the immune response against helminths.
What triggers the classical complement pathway?
Antigen-bound IgG or IgM initiates the C1 complex activation.
Does soluble IgG activate complement?
No, soluble IgG does not activate complement because Fc portions are not adjacent—it requires at least two Fc regions.
Why does antigen-bound IgG activate complement?
When IgG binds to an antigen, Fc regions are close together, allowing C1q binding and complement activation
What structural change allows IgM to activate complement?
Soluble IgM (planar form) cannot activate complement, but when IgM binds an antigen, it shifts to the staple form, enabling C1q binding.
What is the role of C1q in complement activation?
C1q binds to Fc regions of antigen-bound IgG or IgM, initiating the C1 complex (C1r₂s₂) activation cascade.
What is the shape and size of the COVID-19 virus as revealed by electron microscopy?
spherical with a diameter of 60–140 nm and has 9- to 12-nm–long spikes that give it a solar corona-like appearance.
What are the four major structural proteins of the COVID-19 virus?
Spike (S)
Nucleocapsid (N)
Membrane (M)
Envelope (E)
What is the function of the Spike (S) protein in COVID-19?
facilitates viral entry into the host cell by binding to the ACE2 receptor.
What does the Nucleocapsid (N) protein do in COVID-19?
encapsulates the viral RNA genome, protecting and stabilizing it.
What is the role of the Membrane (M) protein in COVID-19?
viral assembly and maintaining the virus's shape.
How does the Envelope (E) protein contribute to the COVID-19 virus?
involved in virus assembly and release from the host cell.
What is the primary immunogenic target for COVID-19 virus neutralization and vaccine design?
transmembrane spike (S) glycoprotein, specifically the S1 subunit and its Receptor Binding Domain (RBD).
What is the function of the S1 subunit of the COVID-19 S protein?
contains the Receptor Binding Domain (RBD), which allows the virus to attach to the ACE2 receptor on host cells.
What is the role of the S2 subunit of the COVID-19 S protein?
promotes membrane fusion, allowing viral entry into the host cell.
Why are the S1 subunit and RBD key targets for vaccines and therapeutic antibodies?
Because they play a crucial role in viral infection, making them ideal targets for neutralizing the virus through vaccines and antibody therapies.
Which is the first antibody isotype to be secreted in response to an infection?
IgM
What is the structural configuration of IgM?
pentameric structure, consisting of five antibody molecules linked together.
What advantage does IgM’s pentameric structure provide?
allows IgM to bind multiple antigens simultaneously, enhancing its effectiveness in immune responses.
What is the molecular weight of IgM?
greater than 900 kDa.
What is the primary effector function of IgM?
activates the classical complement pathway, which promotes:
Inflammation
Opsonization (marking pathogens for phagocytosis)
Cell lysis (destruction of pathogens)
What is affinity in immunology?
strength of interaction between a single antibody binding site and its specific antigen.
🧲 (Like how strongly a single magnet sticks to a fridge)
What is avidity in immunology?
total strength of all non-covalent interactions between an antibody with multiple binding sites and its antigen(s).
🧲🧲🧲 (Like five small magnets together—they hold much stronger than just one!)
How does IgM exhibit affinity and avidity?
IgM has low affinity (each individual bond is weak).
IgM has high avidity (because its pentameric structure allows multiple bindings, making the overall interaction very strong).
What type of immunity does convalescent plasma provide?
Passive immunity (receiving ready-made antibodies instead of producing them).
From who is the convalescent plasma obtained?
patients who have recovered from COVID-19 and contain antibodies against SARS-CoV-2.
What is the primary protective mechanism of convalescent plasma?
Pathogen neutralization, where antibodies block the virus from infecting cells.
What additional immune mechanisms may be involved in convalescent plasma therapy?
Antibody-Dependent Cellular Cytotoxicity (ADCC) (immune cells destroy infected cells).
Opsonization (antibodies mark the virus for phagocytosis).
Is convalescent plasma a natural or artificial form of passive immunity?
Artificial passive immunity (since antibodies are transferred from another person through medical intervention).
What is autoimmunity after COVID-19 infection?
After COVID-19, the immune system can mistakenly attack the body's own cells, leading to autoimmune-like reactions
What is molecular mimicry in the context of autoimmunity?
occurs when a lymphocyte receptor recognizes both a foreign pathogen antigen and a self-protein due to structural similarities, causing immune cross-reactivity.
What is bystander activation in autoimmunity?
happens when infection-induced inflammation damages cells, releasing hidden self-antigens. This can accidentally activate autoreactive immune cells, leading to an attack on healthy tissue.
How does the immune system normally fight viral infections?
B cells produce antibodies that attach to the virus.
Infected cells display viral pieces on MHC I, signaling cytotoxic T cells to destroy them, preventing virus spread.
How can molecular mimicry lead to autoimmune diseases?
If the immune system mistakes human proteins for viral proteins, it can attack healthy cells, potentially leading to autoimmune diseases.
How does bystander activation cause immune system overreaction?
The inflammatory response to infection releases hidden self-antigens, which may cause T cells to mistakenly attack normal tissues.
What are monoclonal antibodies?
are identical antibodies produced from a culture of antibody-producing cells that generate a large quantity of antibodies with a specific function.
What is the function of Bamlanivimab?
binds with high affinity to an epitope within the receptor binding domain (RBD) of the SARS-CoV-2 spike protein, preventing the virus from attaching to ACE2 receptors on human cells and blocking infection
Where does Bamlanivimab bind on the SARS-CoV-2 virus?
to an epitope within the receptor binding domain (RBD), which overlaps with the binding site of angiotensin-converting enzyme 2 (ACE2).
How does Bamlanivimab prevent SARS-CoV-2 infection?
blocking the SARS-CoV-2 virus from attaching to ACE2 receptors on human cells, thus preventing the virus from infecting the host.
What is Bamlanivimab specifically designed to target?
lab-made monoclonal antibody designed to target a specific part of the virus, specifically the receptor binding domain (RBD) on the SARS-CoV-2 spike protein.
What is the function of Imdevimab and Casirivimab?
are monoclonal antibodies that bind to the receptor binding domain (RBD) of the SARS-CoV-2 spike protein, blocking the virus from attaching to ACE2 receptors on human cells and preventing infection.
How do Bamlanivimab and Etesevimab function to prevent viral attachment?
are monoclonal antibodies that bind to different but overlapping epitopes on the RBD of the SARS-CoV-2 spike protein, blocking viral attachment to the ACE2 receptors and reducing the risk of viral resistance.
What is the overall role of monoclonal antibodies like Imdevimab,Casirivimab, Bamlanivimab, and Etesevimab in COVID-19 treatment?
monoclonal antibodies prevent viral entry into the host cell by neutralizing the virus, which reduces the severity of infection and prevents fusion with the host cell.
What do the monoclonal antibodies Imdevimab, Casirivimab, Bamlanivimab, and Etesevimab target on the SARS-CoV-2 virus?
target the receptor binding domain (RBD) of the SARS-CoV-2 spike protein, blocking the virus from binding to ACE2 receptors on human cells.
how do monoclonal antibodies reduce the risk of viral resistance in COVID-19?
binding to overlapping epitopes on the RBD of the spike protein, they reduce the risk of viral resistance to treatment.
What is Antibody-Dependent Enhancement (ADE)?
occurs when antibodies increase the severity of a viral infection instead of providing protection.
How does Antibody Dependent Enhancement (ADE) enhance virus uptake into cells?
can lead to enhanced virus uptake into Fc gamma receptor IIa (FcγRIIa)-expressing phagocytic cells, which results in increased viral replication and worsens the infection.
How does ADE cause excessive inflammation?
can lead to excessive Fc-mediated antibody effector functions or immune complex formation, causing enhanced inflammation and immunopathology, which worsens the infection.
What happens when antibodies in ADE help the virus enter immune cells?
can help the virus enter immune cells (phagocytes) more easily, leading to increased viral replication and worsening of the infection.
What are the two main mechanisms of Antibody-Dependent Enhancement
a. Macrophage tropic viruses
b. Non-macrophage tropic respiratory viruses
What is the ADE mechanism for macrophage tropic viruses (e.g., dengue, FIPV)?
Non-neutralizing or weakly neutralizing antibodies enhance infection by helping the virus enter monocytes or macrophages through FcγRIIa receptors, leading to increased viral replication and more severe disease.
What is the ADE mechanism for non-macrophage tropic respiratory viruses (e.g., RSV, measles)?
Non-neutralizing antibodies bind to viral antigens in airway tissues, forming immune complexes that trigger inflammatory responses, including cytokine release, immune cell recruitment, and complement system activation, causing excessive inflammation and severe respiratory distress.
How does ADE contribute to severe COVID-19 disease?
COVID-19 does not effectively infect macrophages, but ADE mechanisms involve immune complex formation, complement activation, and local immune responses, contributing to severe inflammation in the lungs.
Where is the vaccine inserted, and what does it contain?
inserted into the skin or muscle, and it contains antigens that trigger an immune response.
What is the role of dendritic cells (DCs) in the immune response after vaccination?
recognize the antigens from the vaccine using pattern recognition receptors (PRRs), pick them up, and travel to the lymph nodes to activate T cells.
How are CD8+ T cells activated after vaccination?
are activated when dendritic cells present the antigen via MHC I molecules, leading to the activation of CD8+ effector T cells (trained killers) and CD8+ memory T cells (long-term immunity).
What do CD8+ effector T cells do after activation?
destroy infected cells that present the antigen via MHC
How are CD4+ T cells activated and what is their role?
are activated when dendritic cells present the antigen via MHC II, helping to activate B cells and assist CD8+ T cells in responding to the infection.
What happens to B cells after they receive signals from helper T cells?
recognize the antigen, receive signals from helper T cells, and start to proliferate. They can then differentiate into memory B cells (long-term immunity) or plasma cells (which produce antibodies).
What is the role of bone marrow in immunity after vaccination?
produces long-lived plasma cells that continue to produce antibodies, providing extended protection against future infections.
