Hypersensitivity Flashcards
Th2 produces these cytokines which stimulates B cells to produce IgE
IL4,5,13
this cytokine stimulates eosinophils for worm killing
IL-5
synonym to allergy
hypersensitivity
define hypersensitivity
refers to undesirable reactions produced by a normal but overreacting immune system
hypersensitivity rxns requires this
a pre-sensitized immune system
- prior exposure to antigen augments hypsersensitivity rxns
how are the types of hypersensitivities distinguised?
based on the mechanisms involved and the time required for the rxn to occur
immediate hypersiytivity responses
antibody-mediates
I-III
5 mins to 10 hrs
delayed hypersensitivity
T cell mediated
type IV
24-48 hrs
common sources of allergens
inhaled = pollen, mold
injected = insect venom, vaccines, etc.
ingested = food, etc.
contact = plant leaves ,etc.
IgE-mediated hypersens response
imediate; type I
- range symptoms = minor inconvenience like itching to death
- 15-30 mins following exposure
- mast cell or absophil
- rxn may involve one or more areas of body = skin, eyes, nasopharynx, lungs, GI tract
this is a requirement for type I hypersens
preference in IgE production
this antibody has a very high affinity for Fc receptors on mast cells and basophils
IgE = connects with FcERI
= IgE bound to Fc receptor and awaits secondary exposure
- IgE low half-life in circulation so binds to Fc receptor of mast and baso
- changes the echanism of cell; optimizes it to recgonize a specific antigen
what happens when IgE binds to mast/baso?
second exposure to same antigen cross-links cell bound IgE
- triggers the release of substances from mast cells inducing them to degranulate
- includes vasoactive amines and potent inflammatory mediators
T or F. A single mast cell could have different targets when bound with IgE
T! if different isotypes of IgE are bound
influx of this causes mast cells to degranulate after crosslinking of IgE
intracellular Calcium
Why is IgE produced?
- nature of antigen
- history of exposure
- heredity
- TH2 cells and IL-4 = IgE production
IL-4
important for B cells to make memory and proliferate
roles of the mast cell granule mediators
constricts smooth muscle in lung and GI
vasodilation
increase permeability of small blood vessels = leaky, tissue swells
increases mucus secretion
prevents clotting
generally = pro-inflam mediators produced
mast cell granule mediators
histamine = preformed and short-lived
lipid mediators = synthesized and longer lasting = leukotrienes, prostaglandins
role of PAF
- platelet activating factor
- attracts leukocytes, amplifies production of lipid mediators, and activates neuts, macs, platelets
these cytokines amplifies Th2 response (humoral)
IL 4,13
IL-5
promotes eos = amplifies inflam response = tissue destruction
TNFa
promotes inflammation and stimulates cytokine production in many cell types
a sudden, severe, potentially fatal, allergic rxn
anaphylaxis
- can involve various areas of body
- symptoms within minutes
- reaction = mild to life-threatening
asthma vs allergic rhinitis
asthma = lower airwys = danders, pollens, dust mite feces
allergic rhin = nasal passages = pollen (ragweed, oak, etc.), dust mite feces
treatment of anaphylaxis
nullify effects of mast cells
- anti-histamines, epinephrine
what does epinephrine do?
reduce perm of blood vessels
diminish tissue swelling
raise BP
relax constricted smooth muscles
stimulates heart
for more systemic/significant rxns
the treatment of choice to save life of person experiencing severe systemic anaphylactic shock
epinephrine
T or F. Type IV hypersensitivity is rooted in the normal anti-helminth immune response
F! type I
Th1 vs Th2 in allergies
Th1 = healthy immune response when exposed to helminths early in life
Th2 response = skewed immune response = allergies when growing in uran centrres, only child, etc.
Type II hypersens
- antibodies generated to antigens found on cell surfaves
- antibodies are then recognized by Fc receptors of immune cells
- promotes destruction by ADCC
= macs, granulocytes and NK cells - can activate complement
- variety of oragns; minutes to hours
T or F. In Type II Hypersens, Ab-Ag interact first then Fc receptors recognizes them
T!
drug rxns hypersens
type II
- penicillin covalently bind to RBCs surface = proteins altered = targets for Abs
rheumatic fever
type II
- antibodies formed against bacteria (GAS) but cross react with antigens found on heart valves
HDN
type II hypersens
blood transfusion rxns
type II hypersens
T or F. Type III hypersens also Ab based
T
when IgG and IgM react with soluble antigens and form immune complexes
type III
failure to remove immune complexes leads to…
Type III Hypersensitivity
immune complexes can be deposited in _________ ____________and ______
blood vessels and organs
T or F. Immune complexes activate complement and immune cells (neuts) resulting in tissue damage/destruction
T
in order for type III hypersensitivity this must occur
point of equivalence = equal Ags and Abs
type III hypersensitivity conditions
autoimmune = rhematoid arthritis
SLE
persisitent infections = leprosy
bacterial endocrditis
malaria
hepatitis
trypanosomiasis
immune response does not completely clear antigens = persistent antigens = lon-gterm stimulation of immune response = immune complexes
Farmer’s lung = moldy hay
birds fancier’s disease = fecal antigens
type IV hypersens
delayed hypersens
= 24hrs for rxn to occur or later
this hypersens is mediated by activated immune cells only
delayed
= no antibodies
this hypersens is often intiated by CD4+ Th cells
delayed
similar to type III, this hypsersens also requires persistent antigen exposure
type IV
mechanism of T4 hypersens
- antigen exposed to Th cells = active
- CD4+ Th cells secrete cytokines that activate and recruit other immune cells such as macrophages and neutrophils
- products released from activated macrophages and neutrophils cause the majority of the tissue damage and symptoms of type IV hypersensitivity
