VBS 2032 Exam 3 learning guides Questions And Answers
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Course
VBS
Institution
VBS
What cells participate in the process of antibody production? Where are they located? - ANS naive B cells produce the plasma cells, the plasma cells then make the antibodies
plasma cells are found in the bone marrow
B cell sits around largely in lymph nodes?
In what ways do the complem...
VBS 2032 Exam 3 learning guides
Questions And Answers
What cells participate in the process of antibody production? Where are they located? - ANS
naive B cells produce the plasma cells, the plasma cells then make the antibodies
plasma cells are found in the bone marrow
B cell sits around largely in lymph nodes?
In what ways do the complement pathways and humoral immunity interact? - ANS the
classical pathway in complement is activated by antibody-antigen dependent binding
Where are lymphoid cells produced? - ANS bone marrow
Draw the structure of IgG. What part recognizes the epitope? What part interacts with
phagocytic cells? What are the parts called? - ANS the variable region recognizes and
binds the epitope
the Fc region interacts with phagocytic cells
How do antibodies promote phagocytosis? Which antibody class functions as an opsonin? -
ANS Complement system activation via classical pathway
Cross-linking makes phagocytosis more efficient
IgG functions as an opsonin and facilitates phagocytosis
Compare and contrast the terms "antigen" and "epitope". What types of molecules are best at
stimulating antibody production? - ANS Antigen - big, bind to antibodies and antigen
receptors and stimulate antibody production. composed of epitopes.
Epitopes- small, specific to antibody. region on antigen that is recognized by antibodies and
antigen receptors
proteins are best for stimulating antibody production
List and describe the various functions of antibodies. Which class(es) of antibody participate in
each? - ANS neutralization- IgG, IgM, IgA
cross-linking- IgG, IgM
antibody-dependent cellular cytotoxicity- IgG
opsonization- IgG
complement system activation- IgG, IgM immobilization and prevention of adherence- IgG, IgM,
IgA
, IgM antibodies - ANS Pentamer, first antibody produced in primary response
principle antibody produced by T-independent antigens
activates complement
better for crosslinking
IgG antibodies - ANS monomer, most abundant in blood and tissues
facilitates phagocytosis
activates complement
IgA antibodies - ANS Dimeric, most abundant antibody in the body, present in secretions,
protects mucous membranes
IgE - ANS Fc binds to basophils and mast cells (and eosinophils?) involved in allergic
reactions - release of histamine
Neutralization - ANS viruses and toxins prevented from binding to their targets: IgG, IgM,
IgA
Cross-linking - ANS phagocytosis is more efficient: IgG and IgM
Antibody-dependent cellular cytotoxicity - ANS NK cells release toxic products: IgG
Opsonization - ANS Phagocytes have Fc receptors, similar to C3 opsonization. Antibodies
act like opsonins "velcro" : IgG
complement system activation - ANS classical pathway: IgG and IgM
Immobilization and prevention of adherence - ANS interferes with motility and attachment:
IgG, IgM, IgA
How do TH cells participate in B cell activation? Why might a second signal act as a safety
mechanism to protect the host? - ANS T h cells act as a second signal, scan B cells
presenting antigens. The binding of the T cell receptor to the peptide presented by B cell, it
activates B cell by delivering cytokines and initiate clonal expansion. A second signal can
protect the host responses against self and harmless antigens
What kind(s) of antigens can stimulate T-independent B cell activation? Why might these
antigens be inferior in producing a host protective response? - ANS T-independent
antigens such as a polysaccharide with multiple repeating subunits and Lipopolysaccharide
(LPS) can stimulate T-independent B cell activation. These are not very immunogenic in
children, who cannot produce antibodies that bind to the capsules on polysaccharides. We do
not get the same immunogenic memory in T-independent B cell activation, leaving us more
susceptible to pathogens with those features.
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