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Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What are the effects of a type 1 (immediate) hypersensitivity reaction?

A

Mast cell degranulation which can lead to anaphylactic shock - bronchoconstriction, vasodilation leading to hypotension, headaches, vomiting and diarrhoea, angiooedema, flushing, itching, tachycardia.

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2
Q

What causes a type 1 hypersensitivity reaction?

A

When IgE antibodies on Mast cells are cross-linked.

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3
Q

What is the trio of Lewis?

A

Redness, flair, wheal.

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4
Q

What is the basis of the HIV test?

A

Immunoassay, where labelled antibodies bind.

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5
Q

Which cells are targeted by the HIV virus?

A

CD4+ cells.

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6
Q

Name some of examples of common allergens.

A

Pollen, animal dander, latex, food, drugs, mold (fungi), dust mites, insect venom.

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7
Q

What is the compound that phospholipids are converted into that can then either form thromboxane and prostaglandins (by cyclooxygenase) or lipoxins (by lipoxygenase)?

A

Arachidonic acid.

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8
Q

What is released on Mast cell degranulation?

A

Histamine, leukotrienes, kinins, prostaglandins, cytokines.

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9
Q

Which antibody causes Type 2 (cytotoxic) hypersensitivity?

A

IgG

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10
Q

What causes Type 2 hypersensitivity responses?

A

IgG targets antigens on the surface of blood or tissue cells which causes activation of complement (classical pathway) as well as chemotaxis of phagocytes to kill the cells.

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11
Q

What causes a Type 3 hypersensitivity reaction?

A

The person has been sensitised to the antigen so has the IgG antibodies. If equal ratios of antigen and antibody are present, IgG forms an immune complex with the antigen that is small enough to escape phagocytosis. The immune complex can be deposited in filtration organs like glomeruli, and also the basement membrane of the endothelium of capillaries and skin and joint spaces and the alveoli/capillary interface, and activate complement and Mast cells and cause prolonged inflammation.

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12
Q

What is an immune complex?

A

The precipitate of the soluble antigen when it is bound by antibodies.

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13
Q

What causes Type 4 (delayed) hypersensitivity?

A

Occurs 12-72 hours after second exposure to antigen. On first exposure, antigen-presenting cells migrate to lymph nodes and cause clonal expansion of helper T cells. On second exposure the helper T cells become activated by antigen presenting cells and release cytokines to activate macrophages (Interferon gamma) and tumour necrosis factor. The inflammatory response produces skin lesions

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14
Q

What is a hapten?

A

Small molecule that binds to carrier protein, causing antibodies to bind to target self peptides, and MHC activates CD8+ cells.

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15
Q

What are some examples of conditions caused by Type 4 hypersensitivity?

A

Contact dermatitis
Type 1 diabetes
Transplant rejection

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16
Q

What is one of the most clinically significant types of Type 4 hypersensitivity?

A

Granulatomous inflammation - macrophages pack tightly around the antigen to form a granuloma

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17
Q

What is the difference between primary immunodeficiency and secondary immunodeficiency?

A

Primary has a genetic basis, secondary has no genetic basis.

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18
Q

What is the “respiratory burst” used to kill bacteria?

A

Phagocyte NADPH oxidase forms dangerous free radicals (e.g superoxide [02]-, HOCl-, peroxide) in the phagolysosome to kill bacteria.

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19
Q

What is an example of primary immunodeficiency?

A

Chronic granulatomous disease - a mutation in the phagocytes oxidase system means they can’t generate the respiratory burst to kill bacteria, so the innate immune system can’t clear bacteria and there is a type 4 hypersensitivity reaction as the acquired immune system tries to clear it and forms granulomas.
Symptoms = lymphodenopathy, infections, impetigo, recurrent pneumonia, skin and rectal abscesses.

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20
Q

What is an example of secondary immunodeficiency?

A

HIV/AIDS - infection with a retrovirus which decreases the CD4+ cell count. AIDS is stage 3 of the HIV infection, and many patients die of a reactivation of a cytomegalovirus or toxoplasmosis infection.

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21
Q

What is an example of immunodeficiency leading to cancer?

A

The B and T cells don’t recognise and kill tumour cells sufficiently.

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22
Q

What is an example of too much immunity leading to cancer?

A

Overproduction of abnormal white cells in leukaemia leads to underproduction of red blood cells, platelets and normal white blood cells.

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23
Q

What are the two types of too much immunity?

A

Autoinflammation - innate immune response against own cells

Autoimmunity - autoimmune response against own cells, failure to recognise self MHC1

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24
Q

What are some examples of autoinflammatory diseases?

A

Familial Mediterranean Fever
Neonatal Onset Multisystem Inflammatory Disease (NOMID) - overproduction of IL-1
Tumour Necrosis Factor Receptor Associated Periodic Syndrome (TRAPS)
Deficiency of IL-1 Receptor Antagonist (DIRA)
Behecet’s disease
[all the autoinflammatory diseases are related to phagocytes, cytokines, communication between cells of the inflammatory response]

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25
Q

What type of cells are responsible for autoimmune diseases?

A

Autoreactive B and T cells (supposed to be destroyed in negative selection)
Autoimmunity occurs due to clonal selection of these auto reactive B and T cells.

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26
Q

What are 6 examples of types of drugs that can be used to treat auto inflammation and autoimmunity?

A

1) Anti IL-1 drugs
2) Anti TNF drugs
3) Steroids - interfere with the signalling pathways for lymphocytic activation
4) Antagonists of B and T cell receptors
5) Actively inducing tolerance (turning off the auto reactive T cells)
6) Cytotoxic anti-B cell antibodies (kill the immune cells causing the disease)

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27
Q

What are the five cardinal signs of inflammation?

A 
Pain
Heat
Redness
Oedema
Loss of function
28
Q

What are the two types of inflammatory mediators that are produced by the liver and preformed in the circulation?

A

Clotting factors

Complement proteins

29
Q

What are the three types of inflammatory mediators which are preformed in granules in the cell for constitutive secretion?

A

Histamine
Serotonin
Lysosomal enzymes

30
Q

What are the three types of inflammatory mediators newly synthesised by the cell during an inflammatory response, and which are produced fastest?

A

Leukotrienes
Prostaglandins
Cytokines
[Prostaglandins and leukotrienes are produced faster because they are lipids so don’t require gene transcription, cytokines are produced slower because they are proteins so require gene transcription]

31
Q

What are the receptors on the plasma membrane of Mast cells which bind IgE for Type 1 hypersensitivity reactions?

A

FcE receptors

Fragment crystallisable epsilon receptors

32
Q

What are 4 effects of histamine released by Mast cell degranulation in Type 1 hypersensitivity?

A

Increased capillary permeability
Vasodilation
Contraction of (non-vascular) smooth muscle causing bronchodilation
Increased mucus secretion

33
Q

What are two effects of prostaglandins released in Type 1 hypersensitivity?

A

Increased mucus secretion in the airways, bronchoconstriction.

34
Q

What are two effects of leukotrienes released in Type 1 hypersensitivity?

A

Bronchial spasms, chemotaxis to recruit neutrophils.

35
Q

What stimulates class switching of the B cells to produce IgE during Type 1 hypersensitivity reaction?

A

Cytokines

36
Q

What effects does Mast cell degranulation have on the gastrointestinal tract?

A

Increased fluid secretion and peristalsis which leads to diarrhoea and vomiting (common in food allergies).

37
Q

What are the 5 effects of Mast cell degranulation?

A 
Diarrhoea and vomiting
Rhinorrhea and watery eyes
Bronchoconstriction
Hypotension
Angiooedema
38
Q

What are the substances secreted by Mast cells immediately on degranulation?

A 
Substances that were preformed in granules and released by constitutive secretion:
Histamine
Serotonin
Proteases
Tumour Necrosis Factor
Heparin
39
Q

What are the substances secreted by Mast cells a few minutes after degranulation?

A

Leukotrienes
Prostaglandins
Thromboxan A2
(membrane derived lipid mediators)

40
Q

What are the substances secreted by Mast cells hours after degranulation?

A

Cytokines (IL-4, IL-13) which cause class switching from IgG to IgE so more IgE is formed and the response is more severe next time (more Mast cells are activated).

41
Q

What are the four effects Mast cell degranulation can have on the eye (due to vasodilation and increased capillary permeability)?

A

Erythema
Conjunctivitis
Eyelid swelling
Lower eyelid venus stasis

42
Q

What are the three common reactions to allergies?

A

Rhinorrhea
Itching (urticaria)
Nasopharynx congestion

43
Q

What are the effects of Mast cell degranulation in the lungs, in restrictive diseases such as asthma?

A

Remodeling the airway wall so it is inflamed and thickened.
Narrowing the airway even more during an asthma attack by bronchoconstriction and vasodilation.
Recruiting phagocytes into the airway.
Hypoplasia of the smooth muscle cells leading to fibrosis.

44
Q

Why does the influx of inflammatory cells into the airway lead to fibrosis?

A

Activated macrophages secrete TNF alpha which leads to a loss of epithelial cells (so gas exchange is decreased) and also hypoplasia of the smooth muscle cells leading to additional collagen secretion and fibrosis.

45
Q

How is asthma treated?

A

Bronchodilators (B2 agonists) e.g salbutamol and salmeterol.
Steroids to reduce the inflammation in the lung.
Monoclonal antibodies to block IgE and IL-5 and IL-13 (second generation treatments).

46
Q

What causes hives/urticaria?

A

Degranulation of skin-resident Mast cells

47
Q

What two things can be used to treat anaphylactic shock?

A

Adrenaline, to vasocontrict.

H1 receptor antagonists.

48
Q

What are the two features of anaphylactic shock in particular that could be fatal?

A

Hypotension

Dyspnoea

49
Q

What is eczema (atopic dermatitis) an example of and what is it?

A

Type 1 hypersensitivity.
Occurs when there is a loss of keratinised squamous epithelium, so there skin is no longer an effective functional barrier. The allergen is allowed through the barrier and exacerbates the eczema, itching breaks the barrier down further. The skin thickens. The damaged keratinocytes produce TSLP which increases itching.

50
Q

What are two treatments used for eczema/atopic dermatitis?

A

Steroids to stop immune response

Emolients to keep skin barrier in tact

51
Q

What is contact hypersensitivity?

A

Occurs when chemical act as haptens, and the first contact sensitises someone and creates memory T cells, the second exposure elicits a dermatitis response.

52
Q

What is the process meant to destroy autoreactive T and B cells?

A

Negative selection.

53
Q

What are some examples of Type 2 hypersensitivity reactions?

A

Incompatible blood transfusion
Haemolytic disease of the newborn (caused by Rhesus incompatibility)
Allergy to penicillin (caused by drug molecule binding to the outside of red blood cells and being recognised as foreign antigen by antibodies)
Myasthenia gravis

54
Q

Why does Haemolytic Disease of the Newborn occur?

A

If the mum is rhesus -ve and the foetus is rhesus +, then with the first delivery, some Rh+ red blood cells may cross the placenta and the mum will form antibodies against them.
With the second pregnancy, if the foetus is Rh+ again the mum’s IgG anti-Rh antibodies will cross the placenta and cause agglutination and haemolysis in the foetus.
HDN is treated by giving the mother passive immunisation with anti Rh antibodies at the first delivery so her body does not make its own.

55
Q

What are some examples of Type 2 hypersensitivity caused by bacteria producing antigens very similar to self-peptides?

A

Rheumatic fever - strep throat bacteria produce antigens similar to proteins expressed on heart muscle, the antibodies produced to target strep then cause inflammation in the heart
Guillain-Barre syndrome - Campylobacter jejuni have similar sugar antigen as is expressed on nerve fibres, the myelin sheath is attacked by autoantibodies leading to the demyelination of nerve fibres

56
Q

What are two examples of conditions caused by autoantibodies targeting thyroid proteins (Type 2 hypersensitivity)?

A

1) Grave’s disease - autoantibodies bind to thyroid gland and stimulate thyroid hormone production, causing hyperthyroidism
2) Hashimoto’s thyroiditis - antibodies cause thyroid cell destruction leading to hypothyroidism, and also cause myxoedema (weight gain, mental dullness, sensitivity to cold)

57
Q

What is an Type 3 hypersensitivity reaction caused by IgA being trapped in the skin?

A

Serum sickness

58
Q

How is glomerulonephritis caused by Type 3 hypersensitivity?

A

Immune complexes lodge into the glomeruli of the kidney, and the inflammation destroys the basement membrane, leading to a loss of kidney function.

59
Q

Name some multisystem autoimmune diseases that are examples of Type 3 hypersensitivity.

A

Systemic lupus erythematosus (SLE)

Rheumatoid arthritis

60
Q

What are the causes and symptoms of systemic lupus erythematosus?

A

Autoantibodies are produced which target DNA, nucleic proteins, blood cells and tissues, causing the cells to die. The antigens left behind by the dead cells form immune complexes with the autoantibodies that deposit in the joints, skin, kidneys, blood vessels, CNS.
This causes a photosensitive butterfly rash on face, arthritis, kidney damage.

61
Q

What is used to treat systemic lupus erythematosus?

A

Monoclonal antibody that targets auto reactive B cells to dampen down ability to chronically secrete autoantibodies.

62
Q

What are some causes of rheumatoid arthritis?

A

Autoantibodies (IgM), phagocytes etc. inducing inflammation which damages the joint.
Can be caused by cyclic citrinullated proteins (CCP) from the gums which induce antibody and T cell responses. There is high CCP in smokers.

63
Q

Why do patients have such different responses to treatment for rheumatoid arthritis?

A

The molecular pathology on a cellular level can be very different in each case.

64
Q

What causes multiple sclerosis and what is it an example of?

A

Type 4 hypersensitivity - CD8+ cells and microglial cells (macrophages in CNS) attack the myelin sheath, resulting in the demyelination of neurones.
This causes weakness, tremors, blurred vision, paralysis.

65
Q

What is MS treated with?

A

Finglimod - blocks T cells leaving lymph nodes, so activated T cells are trapped in the lymph node and can’t migrate back to the CNS to attack the myelin sheath.

66
Q

What causes Type 1 diabetes and what is it an example of?

A

Type 4 hypersensitivity - CD8+ cells attack beta cells in the islets of Langerhans in the pancreas so there is insufficient insulin secretion.

Immunology (5 decks)

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