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Flashcards in 6 Hypersensitivity Deck (17)
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1
Q

Define hypersensitivity

A

Undesirable and damaging reactions produced by the normal immune system, directed against innocuous antigens in a pre-sensitised host.

2
Q

What are the clinical features or a Type 1 hypersensitivity?

Common antigens?

A

Anaphylaxis.
Fast onset. Weal and flare. My have 2nd phase response.
Pollen, bee venom, animal dander.

3
Q

How is IgE produced?

A

By B cells under the control off IL-4 and CD40L-CD40 interaction

4
Q

What is the early phase response of a Type 1 reaction?

A

IgE binds to FcR1 on mast cell. Activation leads to degranulation and synthesis of lips mediators.

5
Q

Which molecules are released in mast cell degranulation and what are their roles?

A

Histamine - sm contraction, increase vascular permeability, stimulate nerve receptors.
Kallikrein - activates bradykinin.
Tryptase

6
Q

Which lipid mediators are synthesised by mast cells? How are they synthesised?

A

Leukotrienes.
Prostaglandins. (TxA etc)
Both derived from arachidonic acid via 5-lipoxygenase and cyclo-oxygenase respectively.

7
Q

What role do eosinophils play in the late phase response of a Type 1 reaction?

A

Attracted by chemokine (eotaxin), release granule contents.
Cytotoxic proteins e.g. eosinophil cationic protein.
Source of major tissue damage.

8
Q

What role do T cells play in the late phase response of a Type 1 reaction?

A

Cytokine production drives activity.

9
Q

Give some examples of Type 1 allergic disease. (4).

A

Asthma.
Rhinitis.
Dermatitis.
Food Allergy.

10
Q

What occurs in a type 2 hypersensitivity reaction?

A

Antibody mediated cytotoxicity.

Complement cascade results in cell lysis. Aggregation of Fc and C3b with their receptors results in opsonisation and phagocytosis.

11
Q

What are type 2 reactions mostly ignited by and why?

A

IgM - pentavalent so most efficient at binding.

IgG requires multiple binding.

12
Q

Give some examples of Type 2 allergic disease. (2).

A

Blood group incompatibility.
Autoimmune haemolytic anaemia.
Affecting neutrophils and platelets.

13
Q

Explain the process of Type 3 hypersensitivity reactions.

A

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.

14
Q

Explain the process of Type 4 hypersensitivity reactions.

A

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.

15
Q

Describe the process of contact dermatitis.

A

CD8 T cell mediated (MHC I).

Nickel/poison ivy acts as hapten with epidermal proteins. Antigen presentation.

16
Q

Describe the cells and cytokines in granulomas.

A

Macrophages, epithelioid cells, giant cells, lymphocytes.
T cells (Th1) secrete IL2 and IFN𝛾.
IL12 release by macrophage initiates response.

17
Q

Name four granulomatous diseases.

A

Mycobacterial - TB/atypical/Leprosy.
Sarcoidosis.
Wegener’s Granulomatosis.
Crohn’s disease.