Hypersensitivity Flashcards
What is hypersensitivity?
- Group of disorders
- normally beneficial components of the immune system response act
- in an exaggerated or inappropriate fashion to environmental antigens which don’t normally cause tissue damage.
- Exaggerated response itself is actually responsible for the tissue damage.
What is the ACID Pneumonic and how does it relate to Hypsensitivty?
- A - Allergic (Atophy/Anaphalxis) - Type 1
- C - Cytotoxic - Type 2
- I - Immune Complex - Type 3
- D - Delayed - Type 4
Generally, outline Type 1 Hypersensitivity
- The type of reaction involved in (most) allergies
- Mediated by IgE immunoglobulins.
- Resulting in an immediate reaction
- Associations are also seen to hypersensitive T Helper Cells.
What are the 2 phases of Type 1 Hypersensitivity?
Sensitisation Phase
Reaction Phase
Describe what is occurring in the sensitisation phase of Type 1 Hypersensitivity.
- APC (Antigen Presenting Cell) - picks up a hapten (non-human protein source/allergen)
- Activated APC
- Go to the lymph nodes where they see T Helper Cells
- These recognise the foreign antigen - and bind to the abnormal HLA
- Interleukins are released.
- IL-4 - encourage B cell activation - IgM -> IgE
- IL-5 Granulcyte Activation
- B cells change to produce IgE rather than IgM
- Changes also seen in Basophils, Eoisinophils and mast cells.
What happens in the reactive phase of a Type 1 Hypersensitivity Reaction?
Mass cells degranulate
- Histamine release
- Inflammation seen (- Oedema and Urticaria)
Other + inflammatory mediators released too
- Basophils
- Th2
- Eosinophils etc.
- Interleukins released
- bringing more WCs & Basophils
What is Atophy?
Genetic predisposition to develop allergic diseases.
- Eczema
- Hayfever
- Asthma
Bascially outline Atopic Dermatitis in terms of a Type 1 Hypersensitivity?
Eczema
- Common in children
- Seen on exposed and flexor surfaces
- Degranulation of basophils and mast cells in response to sensitised IgE.
- Leaky skin allows more allergen in.
What are the treatment options for Type 1 Hypersensitivity?
- Antihistamines
- Corticosteroids
- Adrenaline (anaphlaxis)
- Allergen avoidance
What is Type 2 Hypersensitivity?
Also known as Cytotoxic Hypersensitivity.
- Antibody-mediated destruction of cells, by tissue-specific antibodies.
- Antigen-antibody complexes lead to activation of the complement system.
- Neutrophil degranulation
- MAC formed
- NK degranulation - apoptosis of marked cells.
What is Intrinsic and Extrinsic causes of Type 2 Hypersensitivity?
- Intrinsic - Reacting to HLA (human cells)
- Extrinsic - Reacting to something not normally found in the body - such as penicillin.
What is Type 3 Hypersensitivity?
“Complex”
- Antigen-Antibody/Immune complex formation.
- With soluble antigens
- Deposition in tissues and BV
- Activating phagocytes and causing damage in these areas
- Complement activation causes inflammation
Tends to be systemic.
An example of Type 3 Hypersensitivity is in Lupus.
Briefly outline how Lupus is a type 3 Hypersensitivity
Systemic Lupus Erythematosis
- Failure of Tolerance, allowing ”self-reactive” B/T cells to circulate
- Leaked auto-antigen is presented to B-cell, passed to T Helper cells and antibodies to DNA made
What is Type IV Hypersensitivity?
- “Delayed” - reaction to none harmful hapten.
- T Cell Mediated
- Cytotoxic (CD8+) and Helper (CD4+)
- Quite similar to Atophic disease - but occurs much slower because there is a lack of genetic disposition
- Activation of the Complement cascade happens too.
- Tc Cells themselves also at atach MHC1 (foreign)
- Release perfroins - directly damages surface.
Generally outline Contact Dermatitis.
Type 4
- Haptens cross stratum corneum of skin
- Langerhans cells present to TH1 cells
- TNF alfa and IL 1, 13 and 18
- LCs become differentiated Dendritic cells presenting allergenic epitope and multiply
- More aggressive response 2nd time
