6 Hypersensitivity Flashcards
Define hypersensitivity
Undesirable and damaging reactions produced by the normal immune system, directed against innocuous antigens in a pre-sensitised host.
What are the clinical features or a Type 1 hypersensitivity?
Common antigens?
Anaphylaxis.
Fast onset. Weal and flare. My have 2nd phase response.
Pollen, bee venom, animal dander.
How is IgE produced?
By B cells under the control off IL-4 and CD40L-CD40 interaction
What is the early phase response of a Type 1 reaction?
IgE binds to FcR1 on mast cell. Activation leads to degranulation and synthesis of lips mediators.
Which molecules are released in mast cell degranulation and what are their roles?
Histamine - sm contraction, increase vascular permeability, stimulate nerve receptors.
Kallikrein - activates bradykinin.
Tryptase
Which lipid mediators are synthesised by mast cells? How are they synthesised?
Leukotrienes.
Prostaglandins. (TxA etc)
Both derived from arachidonic acid via 5-lipoxygenase and cyclo-oxygenase respectively.
What role do eosinophils play in the late phase response of a Type 1 reaction?
Attracted by chemokine (eotaxin), release granule contents.
Cytotoxic proteins e.g. eosinophil cationic protein.
Source of major tissue damage.
What role do T cells play in the late phase response of a Type 1 reaction?
Cytokine production drives activity.
Give some examples of Type 1 allergic disease. (4).
Asthma.
Rhinitis.
Dermatitis.
Food Allergy.
What occurs in a type 2 hypersensitivity reaction?
Antibody mediated cytotoxicity.
Complement cascade results in cell lysis. Aggregation of Fc and C3b with their receptors results in opsonisation and phagocytosis.
What are type 2 reactions mostly ignited by and why?
IgM - pentavalent so most efficient at binding.
IgG requires multiple binding.
Give some examples of Type 2 allergic disease. (2).
Blood group incompatibility.
Autoimmune haemolytic anaemia.
Affecting neutrophils and platelets.
Explain the process of Type 3 hypersensitivity reactions.
Antibody mediated.
IgG+Ag forms AgAB complex. FcR bind to C1q. Complement activation. C5a attracts neutrophils. C3b - opsonin. Attempted phagocytosis of complexes releases enzymes and radicals, damaging tissues.
Explain the process of Type 4 hypersensitivity reactions.
T cell mediated (MHC class 2).
Tuberculin skin reaction.
Perivascular infiltration of lymphocytes and monocytes. Langerhans cells present neo-antigen to T cells which release cytokines, which recruit macrophages. Activation of macrophages causes tissue damage.
Describe the process of contact dermatitis.
CD8 T cell mediated (MHC I).
Nickel/poison ivy acts as hapten with epidermal proteins. Antigen presentation.