Immunology Exam 3 part 2 Flashcards

1
Q

types of molecules that stimulate immune response

A

antigen
hapten
toxin
superantigen

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2
Q

antibody isotypes involved in a secondary immune response

A

high affinity of…
IgG - neutralization/opsonization
IgA- neutralization/opsonization
IgE - activates mast cells/eosinophils

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3
Q

list characteristics of lymphocytes involved in maintaining immunologic memory

A

respond quickly
present in large numbers
easier to activate
affinity maturation already occurred
B cells - Ab on surface
B cells - Ag:MHC II complexes on their surface
T cells - don’t require costimulation through CD28

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4
Q

describe how pathogens evolve to evade immunologic memory

A
  1. antigenic variation
  2. latency
  3. exploitation of immune cells
  4. resistance to immune effector mechanisms
  5. immunosuppression
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5
Q

antibody functions

A
  1. agglutination
  2. toxin neutralization
  3. block attachment
  4. complement fixation
  5. opsonization
  6. antibody-dependent cell-mediated cytotoxicity
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6
Q

role of IgA

A

mucosal immunity (respiratory/GI)

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7
Q

role of IgG

A

systemic immunity

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8
Q

role of cytotoxic T cells

A

cellular immunity
minimize spread of disease, prevent viremia

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9
Q

how long do viral vaccines last? bacterial vaccines? toxin vaccines?

A

3 years
12 months
4-6 months

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10
Q

why do virus vaccines last longer than bacterial?

A

less complex and have fewer epitopes

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11
Q

what is a vaccine titer

A

concentration of serum antibodies produced

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12
Q

describe the different types of the T helper responses for appropriate immune response

A

Th1 for cell-mediated responses
- activates macrophages
Th2 for humoral immunity

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13
Q

what are the components of vaccines

A

antigen
adjuvant
pH buffers
colorants
stabilizers
cellular debris

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14
Q

describe routes of immunization and which ones are better for specific immune response

A

intranasal/intradermal good for mucosal routes and quicker immunity (days)
intramuscular/subcutaneous good for systemic routes, slower (weeks)

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15
Q

types of antigens

A
  1. live organism = cause disease
  2. modified live = replicates but does not cause disease
  3. inactivated (killed) = great for humoral response, safer (e.g. rabies)
  4. inactivated subunit - often have problems with efficacy, but could be good for cats and young animals
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16
Q

why is FELV/FIV not used as modified live

A

because modified live is a retrograde virus and alters DNA

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17
Q

why is Rabies not used as modified live

A

due to the potential of reversion

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18
Q

why is coronavirus not used as a modified live

A

it can cause active distemper

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19
Q

what are types of adjuvants

A

inorganic compounds
liquid base
bacterial products
cytokines

20
Q

how do you minimize vaccine failure

A

proper storage
proper administration
full dose
series of vaccines to overcome neutralization by maternal antibodies
do not freeze
once reconstituted use within an hour or throw away

21
Q

role of cytotoxic T cells

A

cellular immunity
minimize the spread of disease, prevent viremia

22
Q

what pathogens does IgE remove?
why?
what T helper cell is involved?
what cytokines?

A

parasites
too big to phagocytize and need physical repulsion
Th2 cell
IL 4,5,9,13,25,33

23
Q

how does Th2-mediated response help with the elimination of parasites

A

isotype switch to IgE
mast cell infiltration
increased epithelial cell turnover on mucosal surfaces

24
Q

how are mast cells involved with IgE

A

-mast cells bind IgE and when an antigen is encountered by IgE and IgE crosslinks, mast cell degranulates
- releases histamine & eicosanoids
- release of IL4
- release of TNF-alpha
- release of tryptases

25
function of histamine & eicosanoids
muscle contraction airway constriction mucus production vasodilation
26
function of IL4
drives Th2 response
27
function of TNF-alpha
adhesion molecules and leukocyte migration
28
function of tryptases
breakdown of extracellular matrix
29
how are eosinophils involved with IgE
-FceR bind IgE which cause eosinophil to degranulate and secrete major basic protein to kill parasites and activates mast cells -attracted by IL5 and CCL11 -stimulated by inflammation/highly toxic pathogens and tissues
30
how are basophils involved with IgE
- help drive Th2 - CD40L on basophil binds CD40 on B cells to stimulate IgE switch - if FceR binds IgE, baso degranulates
31
describe the hygiene hypothesis
high hygiene, low pathogen/adjuvant burden = unbalanced expression in absence of Treg cells; prone to immunopathology (autoimmune or allergy) low hygiene, high pathogen/adjuvant burden = Treg cells, no immunopathology
32
how can maternal contribution cause allergic reactions
if the baby is exposed to IgE without antigen from colostrum, could result in allergic reaction
33
Th2 IL that affect atopy what do they cause
IL4,5,9,10,13,31 result in IgE upregulation, eosinophil/mast cell development, airway hyper responsiveness, mucous production, and chronic inflammation
34
what are some general treatments of allergies
epinephrine steroids B-adrenergic receptor agonists desensitization
35
what are some non-allergen-specific treatments for allergies
target Th2 transcription redirection of Th2 response target IL4 and or 5 target IgE target IL31
36
what are some allergen specific treatments of allergies
induction of anergy of Th2 allergen + Th1 cytokines allergen + recombinant microorganism plasmid DNA
37
type I hypersensitivity pathogenesis triggers cells involved reactions initiated
anibody-mediated (IgE) insect bites, food, drugs, inhaled or contact allergens mast cells, eiosinophils, Th2, B cell localized (dermal, GI, resp) or systemic (anaphylaxis)
38
what are some examples of type I hypersensitivity in dermis, GI, and respiratory system?
dermis: atopy, hives, urticaria, angioedema GI: gastroenteritis respiratory: asthma, allergic rhinitis, allergic bronchitis
39
type II hypersensitivity pathogenesis triggers cells involved reactions initiated
antibody mediated (IgG) self-directed antibodies opsonize cells & target them for destruction neutrophils and macrophages complement activation (cell lysis and inflammation)
40
what is an example of type II hypersensitivity
autoimmune diseases -immune-mediated hemolytic anemia - mysthenia gravis
41
type III hypersensitivity pathogenesis triggers cells involved reactions initiated
antibody-antigen complex/immune complex mediated complex deposits in tissues neutrophils proinflammatory response (neutrophils, complement, vasculitis)
42
examples of type III hypersensitivity
arthritis dermatitis glomerulonephritis polyarthritis feline infectious peritonitis
43
type IV hypersensitivity pathogenesis triggers cells involved reactions initiated
CD4+ and CD8+ T cell mediated (independent of antibodies) chronic infection or allergen exposure or contact allergens CD4+, cytotoxic T lymphocytes (CD8+), neutrophils, macrophages, eosinophils inflammation (Th1, 2, 17) and direct cell lysis
44
examples of Type IV hypersensitivity
delayed hypersensitivity - contact dermatitis (e.g. poison ivy) - tuberculosis from chronic CD4+ activation from circus
45
symptoms of anaphylaxis
bronchospasm pulmonary edema bradycardia hypotension diarrhea vomiting urticaria angioedema