Immunology Flashcards
1
Q
What is vaccination?
A
Deliberate administration of antigens to produce immunological memory
2
Q
When are long lived T and B cells generated?
A
Adaptive immune response
3
Q
Where do long lived plasma cells reside?
A
Bone marrow
4
Q
In immunological memory, how does IgG clear infection before symptoms occur?
A
Direct neutralisation of bacteria
Rapid mobilisation of phagocytes and complement
IgA blocks bacterial binding to mucous membranes
5
Q
What are naïve B and T cells?
A
Mature but not yet activated (induce a strong response in 14-21 days)
6
Q
What can naïve B and T cells become?
A
Effector or memory cells
7
Q
What have memory B cells already undergone?
A
Ig class switching and hypermutation
8
Q
What is immunisation?
A
The process through which an individual develops immunological memory to a disease
9
Q
What is active immunisation?
A
Protection by the persons own immune system- usually permanent
10
Q
What is passive immunisation?
A
Protection transferred by another person or animal- temporary
11
Q
What are the two types of active vaccination?
A
Live attenuated vaccines or inactive vaccines e.g. killed, subunit or toxoid
12
Q
What are some features of inactivated vaccines?
A
Do not multiply, not as effective, antibody based (not T cell), will diminish with time, multiple doses
13
Q
What can under-inactivation cause?
A
Pathogens or toxins within the body
14
Q
What can over-activation cause?
A
Ruins conformation of the antigen so there can be no antibody binding
15
Q
What are some features of a live attenuated vaccine?
A
Similar to natural infection, organism must replicate, needs 1 dose
16
Q
What is the advantage of inactivated vaccines over live attenuated ones?
A
Generally safer and easier to store
17
Q
What is the most common example of natural passive immunisation?
A
Through transfer of maternal antibodies in placenta and maternal antibodies through breast milk
18
Q
What antibody is transferred across the placenta?
A
IgG
19
Q
What are examples of therapeutic passive immunisation?
A
Human immunoglobulin or monoclonal antibodies
20
Q
What makes some organisms difficult to create vaccinations for?
A
Chronic/latent disease or rapidly evolving infections
21
Q
What are some new approach vaccinations?
A
Mucosal vaccines, intranasal vaccine and preventative vaccines against cancer causing viruses
22
Q
What is primary immunodeficiency?
A
Inherited abnormalities associated with a failure of development of components of the immune system
23
Q
What are the hallmarks of immunodeficiency?
A
Serious, persistent, unusual, recurrent infections
24
Q
What is classed as recurrent infection?
A
2 major or 1 major and recurrent minor infections in one year
25
What are typical features of immunodeficiency in general?
Weight loss, failure to thrive, severe skin rash, chronic diarrhoea, mouth ulcers, autoimmune disease, family history
26
What is more common, primary or secondary immunodeficiency?
Secondary
27
What are causes of secondary immunodeficiency?
Physiological, infections, treatment, malignancy, nutritional disorders
28
What do defects of phagocyte production usually cause?
Failure to produce neutrophils or a failure of their maturation
29
What is Kostmann Syndrome?
Rare autosomal recessive disorder of severe chronic neutropenia
30
What are signs of Kostmann Syndrome?
Infections after birth, fever, irritability, ulcers, failure to thrive
31
What is the supportive treatment for Kostmann Syndrome?
Prophylactic antibiotics and antifungals
32
What is the definitive treatment for Kostmann Syndrome?
Stem cell transplant, granulocyte colony stimulating factor
33
What is leukocyte adhesion deficiency?
Genetic defect in leukocyte integrins to cause a failure of neutrophil adhesion and migration
34
What does leukocyte adhesion deficiency show?
Leukocytosis (high WCC) and localised bacterial infections
35
What are opsonins?
Binding enhancers for phagocytosis
36
What do opsonin defects cause?
Defective phagocytosis but not significant disease
37
In general, how are phagocyte deficiencies treated?
Oral/IV antibiotics, surgical drainage of abscess, bone marrow transplant
38
What is chronic granulomatous disease?
Failure of oxidative killing mechanisms. It is x-linked deficiency of NADPH oxidase
39
What does CGD result in?
Excessive inflammation and granuloma formation, recurrent deep bacterial and fungal infections, failure to thrive, lymphadenopathy, hepatosplenomegaly
40
What is the prophylactic treatment for CGD?
Prophylactic antibiotics and antifungals
41
What is the definitive treatment for CGD?
Stem cell transplant, gene therapy
42
What are organisms which can hide from the immune system in cells?
Salmonella, chlamydia, rickettsia
43
Where is it common for organisms to hide in the body?
Macrophages
44
What is reticular dysgenesis?
Failure to produce neutrophils, lymphocytes, monocytes/macrophages, platelets
45
How is reticular dysgenesis treated?
Only by stem cell transplant
46
What is SCID?
Failure to produce lymphocytes in the thymus
47
When are signs of SCID?
Unwell by 3 months, persistent diarrhoea, failure to thrive, infections of all types, family history
48
What is the commonest form of SCID?
X-linked mutation in the IL2 receptor which results in the inability to produce cytokines
49
What is the clinical presentation of SCID?
Low/absent T cells, normal/increased B cells, poorly developed lymphoid tissues
50
How is SCID treated?
Prophylactic antibiotics, stem cell transplant, gene therapy
51
What is DiGeorge syndrome?
Defect of the 3rd/4th pharyngeal pouch so there is failure of thymus development which results in T cell immunodeficiency
52
What are physical signs of DiGeorge syndrome?
Low set ears, high forehead, cleft palate, small mouth
53
What are clinical signs of DiGeorge syndrome?
Hypocalcaemia, T cell lymphopenia, congenital heart disease, recurrent bacterial and viral infections, frequent fungal infection
54
What is the treatment for DiGeorge syndrome?
Prophylactic antibodies and treatment of infection and immunoglobulin replacement
55
What is the good thing about DiGeorge syndrome?
T cell function improves with age
56
What do antibody deficiencies present as?
Recurrent bacterial infections
57
What is Bruton's X-linked Hypergammaglobulinaemia?
Failure to produce mature B cells
58
What is selective IgA deficiency?
A genetic component which only affects about 1/3rd of sufferers
59
What is CVID?
Lots of different diseases, low IgG/IgA/IgE
60
How does CVID present?
Recurrent bacterial infections associated with autoimmune disorder
61
What type of hypersensitivity reactions are allergic responses?
Type 1
62
What is an allergic response?
IgE mediated antibody response to an external antigen
63
What antibodies do non-atopic episodes involve?
IgG and IgA
64
Allergen specific T cells are activated by allergen derived peptides in allergic reactions. What does this cause?
Differentiation of CD4+ T cells into effector Th2 cells which produce cytokines
65
Which interleukins does Th2 produce to synthesise IgE by B cells?
IL4, 13 and 5
66
What does the production of IgE during allergic responses result in?
Eosinophil and mast cell recruitment to the site of allergen
67
Abnormal response to allergens is the normal response to what?
Helminth infection
68
Mast cells release preformed substances. What are these?
Histamine, heparin and tryptase
69
Mast cells synthesise molecules on demand. What are these?
Leukotrienes, prostaglandins and cytokines
70
What do mast cells express receptors for?
The Fc region of the IgE antibody
71
When do clinical features of allergic responses occur?
Within minutes
72
What are clinical features of allergic responses?
Urticaria, angioedema, asthma, allergic rhinitis, conjunctivitis and anaphylaxis
73
In extrinsic asthma, what does the release of histamine and other inflammatory mediators result in?
Muscle spasm (bronchodilation and wheeze), mucosal inflammation and inflammatory cell infiltrate (secretions)
74
What do non-allergic responses occur as a result of?
Spontaneous mast cell degranulation
75
What can non-allergic responses occur as a result of?
Drugs, thyroid disease, idiopathic, physical urticaria
76
What is the management of type 1 hypersensitivity reactions?
Allergen avoidance, block/prevent mast cell activation, anti-inflammatory agents, management of anaphylaxis, immunotherapy
77
What drugs block mast cell activation?
Sodium cromoglicate
78
What drugs prevent mast cell activation?
Antihistamines, leukotriene receptor antagonists
79
What are anti-inflammatory agents?
Corticosteroids
80
What is given to manage anaphylaxis?
Adrenaline
81
What do type II hypersensitivity reactions involve?
Direct cell killing
82
What are type II hypersensitivity reactions triggered by?
Antibody binding to an antigen on the cell surface or extracellular matrix
83
What is the result of type II hypersensitivity reactions?
Cell lysis or inflammatory reactions at the site of antibody deposition
84
When the antibody binds to a cell surface antigen, what does this result in?
Activation of complement for cell lysis and opsonisation
85
What antibodies are involved in type II hypersensitivity reactions and why?
IgG and IgM as they activate complement
86
Complement activation results in the activation of C3. What does this cause?
Chemotaxis, solubilisation of immune complexes, direct killing of bacteria and opsonisation
87
What type of bacteria does complement generally kill and how?
Directly encapsulated bacteria through the membrane attack complex
88
What complement proteins are involved in type II hypersensitivity reactions?
C3a and C5a
89
How does direct cell killing take place in type II hypersensitivity reactions?
Through B cells producing antibodies directed against the cell membrane protein
90
What other immune system components are involved in type II hypersensitivity reactions?
Eosinophils and natural killer cells
91
What are clinical examples of type II hypersensitivity reactions?
Blood cells (transfusion reactions), Goodpasture's syndrome, myasthenia gravis, binding of antibodies to TSH receptor
92
How are type II hypersensitivity reactions managed?
Removal of the pathogenic antibody (blood removed by cell separator) or immunosuppression
93
What are type III hypersensitivity reactions?
Immune complex mediated
94
What is the key feature of type III hypersensitivity reactions?
Antibodies binding to soluble antigens
95
What triggers type III reactions and what happens to these?
Excess antigens- antibody binds to them to form small immune complexes
96
Where are the immune complexes of type III reactions found?
Trapped in blood vessels, joints and glomeruli
97
What is activated in type III reactions?
Complement
98
What is the result of type III reactions?
Antibody mediated phagocytosis and infiltration and activation of neutrophils and macrophages to result in tissue damage
99
A clinical example of type III reactions is farmer's lung. What happens here?
Inhaled fungal particles are deposited which stimulates antibody binding
100
What does immune complexes in the walls of the alveoli and bronchioles result in?
Leukocyte accumulation and activation
101
What are symptoms of leukocyte accumulation in the lungs?
Wheezing and malaise 4-8 hours after antigen exposure. Can also be dyspnoea, pyrexia and a dry cough
102
What are other examples of type III hypersensitivity reactions?
Acute hypersensitivity pneumonitis, systemic lupus erythematosus
103
What is the difference between types II and III reactions?
Type II is localised and type III is systemic
104
How do you test for type III reactions?
Test for specific IgG antibodies
105
How do you manage type III reactions?
Allergen avoidance, steroids, immunosuppression
106
What are type IV reactions?
Delayed hypersensitivity
107
What are autoimmune examples of type IV reactions?
Type 1 diabetes, psoriasis, rheumatoid arthritis
108
What are non-autoimmune examples of type IV reactions?
Nickel hypersensitivity, TB, leprosy, sarcoidosis, cellular rejection of organ transplant
109
What differentiates type IV reactions?
T cell mediated
110
In type IV hypersensitivity reactions, what is generated on initial sensation to an antigen?
Effector Th1 cells
111
What happens on subsequent exposure to antigens in type IV reactions?
Activation of Th1 cells, recruitment of macrophages, lymphocytes and neutrophils to cause persistent inflammation
112
What do Th1 cells activate in type IV reactions?
Interferon gamma cytokines
113
What is poison ivy an example of?
Type IV reaction
114
What is sarcoidosis?
Multi-system granulomatous disease
115
What type of immune response is involved in sarcoidosis?
Non specific response involving T cells and macrophages
116
What does sarcoidosis result in?
Persistent production of activated cytokines
