Hyper sensitivities Flashcards
(48 cards)
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
