Immunology Exam 3 part 2 Flashcards
types of molecules that stimulate immune response
antigen
hapten
toxin
superantigen
antibody isotypes involved in a secondary immune response
high affinity of…
IgG - neutralization/opsonization
IgA- neutralization/opsonization
IgE - activates mast cells/eosinophils
list characteristics of lymphocytes involved in maintaining immunologic memory
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
describe how pathogens evolve to evade immunologic memory
- antigenic variation
- latency
- exploitation of immune cells
- resistance to immune effector mechanisms
- immunosuppression
antibody functions
- agglutination
- toxin neutralization
- block attachment
- complement fixation
- opsonization
- antibody-dependent cell-mediated cytotoxicity
role of IgA
mucosal immunity (respiratory/GI)
role of IgG
systemic immunity
role of cytotoxic T cells
cellular immunity
minimize spread of disease, prevent viremia
how long do viral vaccines last? bacterial vaccines? toxin vaccines?
3 years
12 months
4-6 months
why do virus vaccines last longer than bacterial?
less complex and have fewer epitopes
what is a vaccine titer
concentration of serum antibodies produced
describe the different types of the T helper responses for appropriate immune response
Th1 for cell-mediated responses
- activates macrophages
Th2 for humoral immunity
what are the components of vaccines
antigen
adjuvant
pH buffers
colorants
stabilizers
cellular debris
describe routes of immunization and which ones are better for specific immune response
intranasal/intradermal good for mucosal routes and quicker immunity (days)
intramuscular/subcutaneous good for systemic routes, slower (weeks)
types of antigens
- live organism = cause disease
- modified live = replicates but does not cause disease
- inactivated (killed) = great for humoral response, safer (e.g. rabies)
- inactivated subunit - often have problems with efficacy, but could be good for cats and young animals
why is FELV/FIV not used as modified live
because modified live is a retrograde virus and alters DNA
why is Rabies not used as modified live
due to the potential of reversion
why is coronavirus not used as a modified live
it can cause active distemper
what are types of adjuvants
inorganic compounds
liquid base
bacterial products
cytokines
how do you minimize vaccine failure
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
role of cytotoxic T cells
cellular immunity
minimize the spread of disease, prevent viremia
what pathogens does IgE remove?
why?
what T helper cell is involved?
what cytokines?
parasites
too big to phagocytize and need physical repulsion
Th2 cell
IL 4,5,9,13,25,33
how does Th2-mediated response help with the elimination of parasites
isotype switch to IgE
mast cell infiltration
increased epithelial cell turnover on mucosal surfaces
how are mast cells involved with IgE
-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
function of histamine & eicosanoids
muscle contraction
airway constriction
mucus production
vasodilation
function of IL4
drives Th2 response
function of TNF-alpha
adhesion molecules and leukocyte migration
function of tryptases
breakdown of extracellular matrix
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
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
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
how can maternal contribution cause allergic reactions
if the baby is exposed to IgE without antigen from colostrum, could result in allergic reaction
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
what are some general treatments of allergies
epinephrine
steroids
B-adrenergic receptor agonists
desensitization
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
what are some allergen specific treatments of allergies
induction of anergy of Th2
allergen + Th1 cytokines
allergen + recombinant microorganism
plasmid DNA
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)
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
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)
what is an example of type II hypersensitivity
autoimmune diseases
-immune-mediated hemolytic anemia
- mysthenia gravis
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)
examples of type III hypersensitivity
arthritis
dermatitis
glomerulonephritis
polyarthritis
feline infectious peritonitis
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
examples of Type IV hypersensitivity
delayed hypersensitivity
- contact dermatitis (e.g. poison ivy)
- tuberculosis from chronic CD4+ activation from circus
symptoms of anaphylaxis
bronchospasm
pulmonary edema
bradycardia
hypotension
diarrhea
vomiting
urticaria
angioedema
