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Clinical immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

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1
Q

What are the definitions for hypersensitivity

A

Type-I reactions – when the immune system causes more damage than an antigen or pathogen would normally cause

Immune reaction is out of proportion to the damage caused by the antigen

Immune reaction to a harmless antigen (food molecule)

Type II – when the immune system reacts but the immune response is inappropriate (not needed)

Transfusion reactions

Drugs

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2
Q

What are type I reactions

A

Immediate

Mediated by IgE

Anaphylaxis, angioedema and urticaria

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3
Q

What are Type II reactions

A

Cytotoxic

IgM or IgG, complement and phagocytosis

Cytopenia and nephritis

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4
Q

What are type III reactions

A

Immune complexes

IgM, IgG, complement and precipitins

Serum sickness and vasculitis

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5
Q

What are type IV reactions

A

Delayed

T cell and macrophage

Contact dermatitis

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6
Q

How are type I reactions induced

A

by certain types of antigens known as allergens

Allergens induce an humoral response similar to that generated by other antigens

The immunoglobulin generated is IgE

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7
Q

What secretes IgE

A

IgE secreting plasma cells
towards the allergen are created
Memory B cells created also

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8
Q

What cells mediate type I reactions

A

mediated by plasma cells that secrete IgE exclusively

default B cell Ig is IgM

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9
Q

Where do IgE bind to in order to induce a type I reaction

A

IgE binds (with high affinity) to FcεR (Fc-
epsilon receptors) expressed on tissue
mast cells and peripheral blood basophils

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10
Q

What happens after IgE binds

A

The IgE coated mast cell / basophils
become sensitised

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11
Q

What follows mast cell/basophil sensitisation

A

High affinity binding of IgE to FcεR-I (and FcεR-II; lower affinity) on initial exposure to allergen results in sensitisation (last months or years)

Subsequent exposure to the same allergen ‘cross-links’ IgE on sensitised cell surface causes mast cell / basophil degranulation

Degranulation releases pharmacologically active compounds

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12
Q

What do mast cells and basophils contain

A

contain numerous cytoplasmic vesicles

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13
Q

What do mast cells do

A

Mast cells travel to tissues (integrate) and mature – connective tissue
close to blood supply, skin, mucosa of respiratory tract
& gut

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14
Q

How do mast cells trigger anaphylaxis

A

Release of vesicles upon activation (response is out of
proportion to relative cell number) which in certain
cases can lead to anaphylaxis (systemic HSR)

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15
Q

What is required to initiate the signal transduction cascade

A

Cross-linking of sensitised Fcε-R

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16
Q

What does the degranulation signal involve

A

Degranulation signal involves PLCγ activation and PIP2 cleavage into IP3 and DAG → Ca2+ influx and PKC activation
Cytoskeletal changes
and release of vesicles

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17
Q

What peaks with Fcε-R cross-linking

A

Ca2+ level peak within 2 minutes

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18
Q

What are converted into prostaglandins and leukotrienes

A

Eicosanoids (arachidonic acid)

are inflammatory mediators

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19
Q

What second messenger also plays a role

A

cAMP also plays a role
through PKA activation
promoting vesicle
release

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20
Q

What are clinical manifestations due to and how do they act

A

the biological effects of the
mediators released by activated basophils / mast cells

Which act locally and on secondary effector cells such as
neutrophils, eosinophils T cells, monocytes and platelets
(beneficial during parasitic invasion)

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21
Q

How is the local action inappropriate

Study These Flashcards
A

increased vascular
permeability / inflammation (detrimental & can be fatal)

22
Q

What are the difference between primary and secondary mediators

Study These Flashcards
A

Primary mediators are pre-formed and released at degranulation

Secondary mediators are synthesised in response to primary signals,
such as the eicosanoids (prostaglandins / leukotriens)

23
Q

What are the primary mediators

Study These Flashcards
A

Histamine - increases vascular permeability and smooth muscle contraction

Serotonin - same as histamine

Eosinophil chemotactic factor (ECF-A) - esinophil chemotaxis

Neutrophil chemtactic factor (NCF-A) - neutrophil chemotaxis

Proteases - Bronchial secretion; degradation of blood vessel basement membrane; cause complement protein cleavage and activation

24
Q

What are the secondary mediators

Study These Flashcards
A

Platelet activating factor - platelet aggregation and degrnaulation, contraction of smooth muscle (pulmonary)

Leukotrienes (slow reactive substances of anaphylaxis) - Increased vasculature permeability and contraction of pulmonary smooth muscles (eg Asthma)

Prostalgandins - Vasodilation; contraction of pulmonary smooth muscles; platelet aggregation

Bradykinin - Increased vasculature permeability; smooth muscle contraction

Cytokines (IL-1 and TNFα): proinflammatory - Systemic anaphylaxis; increased expression of adhesion molecules on venular endothelial cells (caused neutrophils, basophils etc to adhere to blood vessel surface)

Cytokines (IL-2, 3, 4, 5, 6, TGFβ and GM-CSF) - Multiple immunological effects

25
How do these mediators trigger a cycle
Chemotaxis – more monocytes, mast cells, eisonophils causing more inflammation and cytokine production Inflammatory response Vasodilation, oedema (fluid), microthrombi (small clots) = more tissue damage so more inflammation Spasmogens Brocheospasm, oedema, mucous secretion = airway narrowing
26
What are cutaneous reactions
Can be used to determine relative sensitvity - skin prick or skin patch test
27
How does IgE function
Most humans only mount significant IgE responses to parasitic infections Serum IgE levels remain high post-exposure to ensure the parasite is gone
28
How does IgE function differently during allergy
Atopic people (prone to allergy) - hereditary predisposition to develop immediate HSR's to common innocuous environmental antigens (allergens) Tend to have increased serum IgE and increased frequency of peripheral eosinophils
29
What is atopy
Umbrella term covering asthma, hay fever, food allergy, utricaria etc Atopic people show immediate wheal and flare skin reactions Worst case scenario is anaphylaxis
30
What are the genetic factors linked to atopy
5q (encodes; IL-3, IL-4, IL-5, IL-9, IL-13 & GM-CSF) - 11q (encodes the β-chain for the high affinity IgE-receptor) - Over 100 genes associated with asthma
31
How are type II reactions mediated
Type-II HSR's are also antibody mediated – IgM and IgG are involved instead of IgE
32
How does antibody mediated cell destruction work
1. IgM or IgG binds cell / tissue bearing appropriate antigen 2. Ig’s in turn will activate complement of a variety of effector cells (those which express Fcγ-Receptors for example – causes cellular damage 3. Antibody-dependent cellular cytotoxicity (ADCC) is an important effect cell function 4. Activation of complement creates membrane attack complex in Ig labelled cells / tissues
33
How can antibody dependent cell cytotoxicity (ADCC) differ
can be phagocytic or non-phagocytic (e.g. NK cell or neutrophil…)
34
What are the causes of type II reactions
Not autoimmune reactions and tend to occur as a result of modern medicine Like blood transfusions ABO mismatch and host (IgM and IgG) reac.t with antigen on donor cells
35
What are the clinical manifestations of type II reactions
Clinical manifestations - Massive intravascular haemolysis of transfused red blood cells (Ig and complement mediated) - Immediate reaction due to ABO incompatibility - Shock (low blood pressure, high heart rate), may occur only after a few ml’s of blood; urticaria, fever, kidney pain (due to shock), haemoglobinurea, vomiting, fitting and blood clotting
36
Why do delayed type II reactions occur
Delayed type of reactions occur when donors have received ABO matched blood – one of the minor antigens are mismatched (minor histocompatibility) Can occur 2-6 days post transfusion Mismatch induces clone proliferation of IgG polarised B cells
37
What are other examples of type II reactions
1. Haemolytic disease of the new born (where mother Rh -ve and foetus is Rh +ve); problem during second pregnancy of Rh +ve foetus (IgG can cross the placenta) 2. Drug reactions; i.e. certain antibiotics (penicillin, cephalosporin & streptomycin) can adsorb onto proteins on erythrocyte forming an immunogenic complex – haemolysis and anaemia until drug is withdrawn
38
How are type III reactions mediated
Are immune complex mediated Antigen + antibody – they are usually cleared during phagocytosis
39
Why do immune complexes trigger type III reactions
Very high levels of these complexes can develop hypersensitivity Immune complexes occur in serum at a magnitude beyond which cannot be cleared by phagocytosis Complexes accumulate in the body (kidneys and lungs are particularly effected) - affect glomerulus filtration
40
How does the complement system effect type III reactions
Activation of complement and recruitment of macrophages (secrete TNFα & IL-1) in the areas causes destruction of the tissue / organ C3a and C5a generated = anaphylatoxins
41
How does C5a effect neutrophils
Neutrophils are attracted to the area by the action of C5a but cannot phagocytose (due to self-tolerance) and so release contents from cell – local mast cells degranulation in response to C5a
42
What are Basophils and platelets attracted to
FcγR’s
43
What happens after roughly 1 week
Ag : Ab complex forms, precipitates out (serum sickness) Persistent exposure to antigen makes it difficult to resolve TYPE-III HSR’s
44
What are the causes of type III reactions
Certain persistant infections can generate immune complexes; viral hepatitis (B) and leprosy Autoimmune disease – complications caused due to immune complexes formed toward "self-antigen" Inhaled antigen, repeat exposure to mould (aspergilla) – lead to immune complex formation - Farmer’s lung (crop mould) - Pigeon fancier’s lung (avian antigen)
45
How are type IV reactions mediated
Are delayed (T cell mediated) Does not involve antibodies
46
Examples of type IV reactions are
Contact dermatitis – 48-72 hours post exposure Tuberculin (basis of BCG test) - 48-72 hours post exposure Granulomatous – 21-28 days
47
How does hapten trigger type IV reactions
Hapten is too small to activate BCR and produce an immune response on its own – it is technically not an antigen Haptens come from soap powder or poison ivy Absorbed through the skin and form complexes with body proteins (within tissue macrophages)
48
What are the 2 stages hapten triggers to induce type IV reactions
Sensitisation – hapten / protein carrier complex is presented to T cells by Langerhan cells (tissue macrophages) Elicitation - T cells recirculate to contact zone and migrate to area (adhesion molecules and cytokines) and partake in an immune response in dermal region
49
What is granulomatous
a type of tissue inflammation characterized by the formation of granulomas, which are collections of immune cells that clump together
50
What does granulomatous persistence of macrophages do
They contain intracellular antigen (could be bacteria; leprosy, TB) cannot breakdown (could occur through persistence of immune complexes as seen in TYPE-III) Macrophages and epithelial cells fuse (giant cell; multinucleated) Granuloma forms (i.e. in lungs) where activated macrophages in middle are surrounded by T cells - Appears as shadow on x-ray

Clinical immunology (11 decks)

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