Flashcards in Hypersensitivities Type I-IV Deck (51):
above and beyond normal response
how many types of hypersensitivities?
type IV hypersensitivity
T cell mediated diseases
type I hypersensitivity
aka immediate hypersensitivity
caused by Type I hypersensitivity
big player in type I hypersensitivity**
extra constant region domain
-allows it to bind Fc on mast cells
three properties controlling IgE?
1 half life of IgE
2 T cell control (need isotype switching)
3 cross-linking of IgE on surface of mast cells and basophils
half life of IgE?
2 days in serum (very short)
produced in response to allergens
half life increased when binds to mast cells and basos
receptor for IgE on mast cells and basos?
half-life of IgG
3 weeks woah!
receptors for IgE on B cells?
Th1 activation leads to?
IFN-gamma and IL-12
no upregulation of IgE
**suppressive the atopic reaction
Th2 activation leads to?
IL-4, IL-5 IL-13
leads to class switching (via IL-4) to IgE
**increases the atopic reaction
stimulates maturation of eosinophils
antigen that gives rise to immediate hypersensitivity
-most are proteins
-usually taken in very small quantities that is sustained throughout life (ex/ dust)
food - large dose
mediators of IgE (intermediate) response in mast cells?
histamine, heparin, and tryptase (5 minutes)
also, newly generated (5-30 minutes)
**vasoactive amines and lipid mediators
late phase reaction of mast cells immediate hypersensitivty?
2-10 hours later
-cyrokines, IL-4, TNF-alpha
released by eosinophils?
cationic granule proteins and eosinophil peroxidase
**to kill worms, but can kill self cells
what must occur for mast cell activation?
binding of IgE and must be CROSS-LINKED**
increased mucus secretion
extravasation of sera
late phase reaction ?
4-6 hours after type I reaction
-can persist 1-2 days
infiltration of PMNs, eosinophils, macrophages, lymphocytes, basophils
occurs bc mast cells produce TNF-alpha and IL-1 which leads to increased extravasation
mast cells also produce neutrophil chemotactic factor
on-site release of IL-3, IL-5, IL-8, and GM-CSF
normal function of IgE
protection against parasites
Type II Hypersensitivity
initiating antigen is a surface
antibodies bind FcR on tissue surface initiating effector cells
binding of C1 to IgG or IgM activates C' cascade
damages target cells
-locallized to cells bearing antigens
antibodies against cell surfaces are usually pathogenic
antibodies against internal antigens are usually not pathogenic
C3a and C5a?
chemotaxis of PMNs, basophils, and eosinophils
normal phagocyte activation?
machophage binds Fc receptor and C3 receptor
-results in phagocytosis and lysosomal fusion
cannot internalize complex
instead, releases all of its enzymes to intravascular space and degrades tissue
**occurs in hypersensitivity type II
hemolytic disease of the newborn (HDNB)
when mother Rh- and baby is Rh+
aka erythroblastosis fetalis
during birth, mother will make IgM antibodies against Rh+ (there is some blood exchange during birth)
-makes memory which will respond to next pregnancy if baby is Rh+
how to avoid erythroblastosis fetalis?
binds the Rh antigens and inhibits the mothers immune response from being exposed to it
antigens involved in HDNB?
Rhesus D most positive
also Kell (K) antigen
using whole blood during transfusion?
giving someone serum (no good)
donated blood is what?
separated to serum and cells first
autoimmune hemolytic anemia
warm antibodies - different epitopes than transfusion rxn. (Rhesus)
cold antibodies - high titer IgM
-usually in old people during winter
can be spontaneous or drug caused
self-antibodies to AcH receptors
extreme muscle weakness**
Type III Hypersensitivity
involve immune complexes
normally, taken care of by waste management
-if not, lead to pathology
can have interlacing collection with increased pathology
three groups of type III hypersensitivity
inhalation of antigen
normal waste management?
CR1 receptor on RBCs bind to immune complexes
taken to spleen and liver where they are degraded
when immune complexes settle out?
in very small vessels
-bring in baspohils, mast cells, macrophages results in leakiness (great area for immune complex)
platelet aggregation occurs
increase in BP, vascular turbulence, and complex deposition
presensitized with IgG
so that it won't bind IgE
get localized hemorrhage in 4-10 hours
can lead to allergic alveolitis
induced by large injection of foreign antigen
complexes deposit in blood vessels and tissues
leads to arthritis and glomerulonephritis
complication of equine serum therapy (horse) or antigen excess (acute infectious disease)
mechanisms of Type II and III
inflammatory pathways are identical
-difference is initiator
type II - fixed surface
type III - soluble
complement major mediator
delayed type hypersensitivity?
Type IV hypersensitivity
T cells are mediator
-effector T cells are stimulated
-can lead to granulomas from macrophages
three types of DTH?
tuberculin (ex/ PPD test)
granulomatous (clinically most important)
-usually 28 days out
contact sensitivity stages?
sensitization and elicitation
sensitization - 10-14 days in epidermis
-ex/ poison oak/ivy (require haptens)
-build memory cells
elicitation - recruit CD4 T cells to site of contact
pro-inflammatory cytokine driven
-mainly CD4 T and small number of CD8
tuberculin type DTH?
looking for a recall - to see if you have been sensitized to it
ex/ tuberculin skin test
usually persistance of macrophages
-microbes that can resist killing
-other cells cell can't destroy
occurs with Th1 response
basis for classification of hypersensitivity?
Coombs and Gell
what immune complexes deposited the most?
small positively-charged ones