Hyper sensitivities Flashcards
what are Hypersensitivity reactions
Immune responses that cause tissue injury
Hypersensitivity reactions arise from?
uncontrolled or Abnormal responses to foreign Ags
or Autoimmune responses against self Ags
General characteristics of: Type 1 hypersensitivity
mediated by IgE and results from actions of mediators secreted by mast cells
General characteristics of: Type II hypersensitivity
Mediated by Abs that bind tissue Ags and cause complement dependent tissue injury
General characteristics of: Type III hypersensitivity
Circulating Ag-Ab complexes that deposit in vessels and cause complement-dependent injury in the vessel wall (vasculitis)
General characteristics of: Type IV hypersensitivity
Mediated by T cells and results form inflammation caused by cytokines produced by CD4 Th1 and Th17 cells, macrophages, or killing of host cells via CD8 CTLs
What triggers Type 1 Hypersensitivity
Enviromental Ags whitch activate mast cells in an IgE manner
Atopy
genetic tendency to develop allergic diseases and are said to be atopic
Mediators of Type 1 Hypersensitivity
Mast cell: responsible for the acute reactions and inflammation
Histamine: dilation of small vessels and increase permeabillity
Proteases: local tissue damage
Prostaglandins: vascular dilation
Leuokotrienes: stimulate smooth muscle contraction
Cytokines: induce local inflammation (late phase reaction)
Initial Allergen encounter
Th2 cells and IL-4 create adaptive immune response by B cells that mature into plasma cells to make IgE to allergen
IgE bind to FcRe (CD23) on mast cells
Patient is now sensitized
Subsequent Allergen Encounter
Allergen cross-liking binds IgE on Mast Cells and cause degranulation of all type 1 mediators
Immediate Phase Type I Hypersensitivity
vascular and smooth muscle reactions within minutes
Vasodilation, congestion, and Edema
Late Phase Reaction Type I Hypersensitivity
2-24 hours later
inflammatory infiltrate rich in eosinophils, neutrophils, and T cells
Asthma
Airway obstruction via release of inflammatory mediators via the allergen
increased capillary permeabillity and spasmodic contraction of smooth muscle around bronchi
decrease size of bronchial lumen and shortness of breath
can happen via cold and exercise
Anaphylaxis
ecposure to food allergen cause massive release of Vasoactive Amines and cytokines
contraction of smooth muscle and Vasodilation of capillary endothelium
Blood pressure drops that results in vascular shock
Allergen testing
Type 1 Hypersensitivity and is performed on Arm or back if babies
injected in Dermis and wait 30 minutes to see the results
Allergen Specific Immunotherapy (SIT)
single curative approach by administration of increasing doses of Allergen
- Induce peripheral T cell tolerance
- Increase thresholds of mast cell and basophil activation
- Decrease IgE mediated Histamine release (increased IgG and IgG)
Generation of induced regulatory Treg cells is the key mechanism
fix the Th1/Th2 ratio
Activation of Type II Hypersensitivities
via IgG and IgM activates Complement resulting in production of C3a and C5a to induce inflammation and recruiting
What are the 2 mechanisms of Type II Hypersensitivity
Complement mediated Cytotoxicity
Ab-dependent Cellular Cytotoxicity (CDCC)
Graves Disease Type II hypersensitivity
Ab stimulates the activity of the thyroid stimulating hormone receptors causing Hyperthyroidism
Myasthenia Gravis: Type II hypersensitivity
Abs may inhibit binding of Acetylcholine neurotransmitter to ACh receptor
ABO blood Transfusion Reaction
Type II hypersensitivity
have Antigen A means you produce Antibody B
Hemolytic disease of Newborn: Type II hypersensitivity
if Mother is Rh- and kid is Rh + then the Antibodies of Mom will attack the fetus in the subsequent pregnancy
Drug Induced Hemolytic Anemia Type II hypersensitivity: Hapten Model
Penicillin
Drug binds directly to the erythrocyte surface and induces an anti-drug antibody
Drug Induced Hemolytic Anemia Type II hypersensitivity: Immune complex formation
quinidine
Autoantibodies from immune complexes with the drug
erythrocytes bind Immune complexes through CR1 and cause killing of the erythrocyte by complement
Drug Induced Hemolytic Anemia Type II hypersensitivity: Auto immune model
Methyldopa-induced anemias
drug induces an antidrug antibody that cross reacts with an Rh antigen
Type II Hypersensitivity Diseases: Autoimmune Hemolytic anemia
Opsonization and phagocytosis of erythrocytes due to Rh blood group
Type II Hypersensitivity Diseases: Autoimmune idiopathic thrombocytopenic purpura
Platelet membrane proteins that cause opsonization and phagocytosis of platelets
Type II Hypersensitivity Diseases: Goodpastures syndrome
non-collagenous protein in basement membranes of kidney glomeruli and lung alveoli cause complement activation and Fc receptor mediated inflammation
Type II Hypersensitivity Diseases: Pemphigus Vulgaris
proteins in intercellular junctions of epidermal cells cause antibody mediated activation of proteases
Type II Hypersensitivity Diseases: Rheumatic fever
Steptococcal cell wall antigen creates and antibody cross reaction with mycardial tissue.
Major mechanism of triggering tissue damage in Hypersensitivity III
Ab-Ag complexes formed in the Blood in circulation deposit and recruit CP of complement and recruitment of leukocytes
Type III Hypersensitivity Diseases: SLE
antibody binds on DNA, nucleo proteins and others and causes nephritis, vasculitis, and arthiritis
Type III Hypersensitivity Diseases: Polyarteritis nodosa
antibody binds microbial antigens causes vasculitis
Type III Hypersensitivity Diseases: Post-streptococcal glomerulonephritis
antibody binds on Streptococcal cell wall antigens and causes nephritis
Type III Hypersensitivity Diseases: Serum sickness
systematic reaction and usually involves a toxin
Type III Hypersensitivity Diseases: Arthus Reaction
involves a subcutaneous administration of a protein Ag to a previously immunized animal and is a local vasculitis usually at site of injection
Major Triggers of Type IV Hypersensitivity
Autoimmunity, exaggerated response to environmental Ags or microbial Ags (TB)
Delayed Hyper Hypersensitivity (DTH)
Type IV Hypersensitivity, mediated by T cells
Type IV Hypersensitivity inflammation caused by:
Th1 and Th17 secret the cytokines that recruit the macrophage and neutrophils
Type IV Hypersensitivity injury caused by:
Macrophages, neutrophils, and the lysosomal enzymes, reactive oxygen species, nitric oxide and pro-inflammatory cytokines
Type IV Hypersensitivity diseases: Multiple Sclerosis
Attacking of the Mylein proteins
Type IV Hypersensitivity diseases: Rheumatoid arthritis
Attacking of the antigens in the joints
Type IV Hypersensitivity diseases: Type 1 diabetes
attacking of the Pancreatic islet antigens
Type IV Hypersensitivity diseases: Crohns disease
Attacking of the intestine microflora which have an autoimmune component
Type IV Hypersensitivity diseases: Contact sensitivity
DTH reaction on skin can be from metals or poison Ivy
Type IV Hypersensitivity diseases: Chronic infections
Microbial proteins including TB
Common metals to respond with Allergic Contact dermatitis
costume jewlery increases sensitization to nickel and cobalt
and leather sensitization of chromium
