Immunology- Hypersensitivity Flashcards
What is a hypersensitivity reaction
Excessive immune responses that cause damage
Can respond to different types of antigens:
- infectious agents
- environmental substances
- self antigens
Cytokines role in hypersensitivity
any of a number of substances, such as interferon, interleukin, and growth factors, which are secreted by certain cells of the immune system and have an effect on other cells eg attract leukocytes
High levels of leukocytes can cause cytokines storm
What are happens
Small molecule irritants that bind to proteins and elicit an immune response
What type of reaction in type 1 hypersensitivity
ALLergy
What cells mediate type 1 hypersensitivity
Mast cells
Eosinophils
IgE
Define atopy
Immediate hypersensitivity reaction to environmental antigens mediated by IgE
Develops within minutes of exposure
Atopy presentation
Anaphylaxis Angiooedema Urticaria Rhinitis Asthma Dermatitis Eczema
Describe the allergens peanut and penicillin
Peanut
- allergy to peanut protein ARA h2
- allergy to ARA h8
Penicillin
-allergen to B-lactam
When do B cells release IgE
When costimulated with IL-4
Mast cell roles
Degranulating cells
Mast cells initiate allergic symptoms after allergen and IgE interact
Example of type 1 hypersensitivity disease
Asthma
Rhinitis
Anaphylaxis is
What is filaggrin
Expressed by keratinocytes and involved in maintaining epithelial barriers and moisturising surfaces and controlling pH
Associated with severe eczema
Presentation of anaphylaxis
Mast cells produce prostaglandins and leukotrienes through cyclooxygenase and lipoxygenase pathways
=vasodilation
Increased vascular permeability
Fall in vascular tone
Severe blood pressure drop
Histamine release
=wellling
Fluid shift
treatment of type 1 hypersensitivity
B2-adrenergic agonists Epinephrine Antihistamines Leukotriene specific receptor blocker Corticosteroids
Investgation for type 1 hypersensitivity
Skin prick
Type 2 hypersensitivity
(B)
AntiBody mediated
IgG or IgM react with antigen present on surface of cells
Results in immune mediated haemolysis (takes several hours)
Example of type 2 hypersensitivity
Blood groups
Rhesus blood groups (IgG develops and crosses placenta= alloimmune haemolysis)
SLE
(all above = autoimmune haemolysis)
(Below= autoimmune against solid tissue)
Goodpasture syndrome (nephritis, pulmonary haemorrhage)
(Below= autoimmune against cell function)
Graves’ disease
Myasthenia gravies
What are type 3 hypersensitivity reactions
C
immune Complex disease
IgG is responsible
Immune complexes of antigen and antibody form and cause damage at site of protection or circulate and cause damage elsewhere
Complexes take some time to form
When do complexes form between antigens and antibodies?
When antibody exceeds antigen levels
How does the body clear complexes
Complement breaks down large complexes
Complement receptor 1 transfers complexes to phagocytes
Failure of clearance leads to immune complex disease and activation of innate immune system
Examples of type 3 hypersensitivity diseases?
Nephrotic syndrome, Nephritis, Glomerulonephritis , SLE, Polyarteritis nodosa, Poststreptococcal glomerulonephritis, Serum sickness
What is type 4 hypersensitivity reactions
D
Delayed hypersensitivity
T cell mediated
Tissue macrophages initiate inflammatory response
T cells stimulated
And secrete TNF
Examples of diseases caused by type 4 hypersensitivity
RA (TH1 and TH17)
(RA antigens= Citrullinated proteins)
MS
Type 1 DM
IBD
Psoriasis
Treatment of delayed hypersensitivity
Avoiding antigens Anti-inflammatory drugs: -NSAID -Corticosteroids -drugs that block TNF and IL-6 -antibodies against B cells
Immunosuppressive drugs
Mechanism of tissue injury in Type 1 hypersensitivity
Mast cells,
Eosinophils
Their mediators (vasoactive amines, lipid mediators, cytokines)
Mechanism of tissue injury in Type 2 hypersensitivity
Opsonisation and phagocytosis of cells
Complement and FC receptor medicated recruitment and activation of leukocytes (neutrophils, macrophages)
Abnormalities in cellular function eg hormone receptor, signaling, neurotransmitter receptor blockade
Mechanism of tissue injury in Type 3 hypersensitivity
Complement and Fc receptor mediated recruitment and activation of leukocytes
Mechanism of tissue injury in Type 4 hypersensitivity
1-cytokines mediated inflammation and macrophage activation
2- direct target cell killing, cytokines mediated
