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Phase 2A Medicine > General Immunology > Flashcards

General Immunology Flashcards

1
Q

Give examples of non-specific defences.

A

Mechanical barriers such as skin and mucociliary lining of resp tract
Secretory factors like lysozyme or stomach acid.
Ciliary motion in resp tract
complement proteins
colonisation by commensal bacteria

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2
Q

How is the innate immune system activated?

A

By pattern recognition receptors and damage recognition receptors on dendritic cells recognising PAMPs and DAMPs on microbes.

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3
Q

What are the key components of innate immunity?

A
  1. Toll-like receptors- found on macrophages, dendritic cells and neutrophils. Induce signal transduction, sequential cellular events and pro-inflammatory cytokines on binding to their ligands.
  2. Cellular factors- neutrophils, macrophages, eosinophils, basophils, NK cells.
  3. Complement- plasma proteins involved in antibody-mediated immune reactions.
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4
Q

What are the four essential features of the immune system?

A

specificity
diversity
memory
recruitment of other defence mechanisms

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5
Q

What are antigens?

A

Antigens are substances able to provoke an immune response and react with the products of that response.

They are substances that can be recognised by the immunoglobulin receptor of B cells or the T-cell receptor when complexed with MHC.

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6
Q

What are antibodies?

A

Antibodies are immunoglobulin molecules produced in plasma cells in response to antigens and they can bind only with the antigen that induced their formation. Antigen-binding properties reside in the Fab fragments, while effector functions lie in the proteins and oligosaccharides of the FC fragments.

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7
Q

What MHC classes do T cells recognise?

A 
Helper T cells recognise antigenic peptides in association with MHC class II molecules and use CD4 molecules to increase binding and signalling.
Cytotoxic T cells recognise MHC class I and use CD8 to increase binding and signalling.
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8
Q

What are cytokines?

A

Cytokines are soluble mediators that act as stimulatory or inhibitory signals between cells.
Cytokines that are between cells of the immune system are called interleukins.
Those that induce chemotaxis of leucocytes are called chemokines.

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9
Q

What are thymus-dependent and thymus-independent antigens?

A

T-dependent antigens require T cell participation to provoke the production of antibodies. Examples: most proteins.

T-independent antibodies require no T cell cooperation for antibody production. They directly stimulate specific B lymphocytes by cross-linking antigen receptors on the B cell surface but provoke poor immunological memory. Examples: bacterial cell wall polysaccharides.

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10
Q

What extrinsic properties of the antigen influence the quality of the immune response?

A
  1. nature of molecule
  2. dose
  3. route of entry
  4. addition of substances with synergistic effects adjuvants)
  5. genetic background of recipient
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11
Q

What are adjuvants?

A

Substances that improve a host’s immune response to a separate antigen. Used in immunisation programmes in childhood.

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12
Q

What is a superantigen?

A

Superantigen is the term given to foreign proteins that simultaneously activate large numbers of T lymphocytes carrying a particular T-cell receptor V-beta gene, regardless of the specificity of the TCR.

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13
Q

What is affinity?

A

It is a measure of the binding strength between an epitope and an antibody binding site. The higher the better.

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14
Q

What are the different classes of immunoglobulins?

A 
IgM
IgA
IgD
IgG
IgE
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15
Q

Describe IgM.

A

Characteristic of primary immune response
Involved in opsonisation, agglutination and complement activation
Intravascular neutralisation of organisms (especially viruses)

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16
Q

Describe IgA.

A

Important in defence of mucosal surfaces
Secreted by plasma cells in respiratory and intestinal mucosa
found in tears, saliva and breast milk

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17
Q

Describe IgD.

A

Found of the surface of B lymphocytes

Acts as B cell antigen receptor

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18
Q

Describe IgG.

A

Most abundant in plasma and ECF.
Only Ig that crosses placenta to provide immune protection to neonate.
Can neutralise pathogens.
Involved in opsonisation and complement activation.

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19
Q

Describe IgE.

A

Produced by plasma cells but taken up by specific receptors on mast cells and basophils.
Mediates anaphylactic hypersensitivity

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20
Q

What are the common features shared by all cytokines?

A
  1. short half-lives
  2. rapid degradation
  3. local action within the microenvironment of cells
  4. act on cells to promote further activation and differentiation
  5. may affect multiple organs in the body
  6. exhibit overlapping functions
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21
Q

What are the four main properties of the adaptive immune system?

A

Diversity
Self-tolerance
Effector functions
Development of immunological memory

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22
Q

What is immune tolerance?

A

A state of unresponsiveness of the immune system to substances or tissues that have the capacity to elicit an immune response.

Tolerance can be to self, in pregnancy, in allografts, to pathogens in chronic infections, to cancers.

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23
Q

What are the two types of immune tolerance?

A

Central tolerance- established early in life in bone marrow and thymus. Allows immune system to distinguish self from non-self. Cells that react with self-antigens undergo apoptosis.

Peripheral tolerance- mainly occurs in lymph nodes. Autoreactive clones escaping central tolerance are suppressed by T helper regulatory cells.

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24
Q

During inflammation, what are the three stages of leucocyte emigration that are mediated by cell adhesion molecules?

A
  1. Rolling of leucocytes along activated vascular endothelium is selectin-dependent.
  2. Tight adhesion of leucocytes is integrin-dependent.
  3. Transendothelial migration occurs under the influence of chemokines.
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25
Q

What is the complement system?

A

Complement is a complex series of interacting plasma proteins which form a major effector system for antibody-mediated immune responses.

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26
Q

What is the purpose of the complement pathway?

A

To remove or destroy antigens either by direct lysis or opsonisation.

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27
Q

What are the three ways by which the complement pathway can be activated?

A
  1. antibody (classical)
  2. bacterial cell wall (alternative)
  3. mannose-binding lectin (lectin)

All three cause the cleavage of C3 by C3 convertases.

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28
Q

What are the three ways by which the complement pathway can be controlled?

A
  1. activated complement components are unstable and decay rapidly if the next protein in the pathway is not immediately available.
  2. specific inhibitors- C1 esterase inhibitor, Factors I and H.
  3. Cell membrane proteins like CD46 and CD55 break down activated components.
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29
Q

What is primary immunodeficiency?

A

Due to intrinsic defect in the immune system

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30
Q

What is secondary immunodeficiency?

A

Due to underlying condition

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31
Q

What are the two types of primary antibody deficiencies?

A
  1. panhypogammaglobulinaemia - involves all Ig classes

2. selective deficiency- involves only class/subclass of Ig

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32
Q

What is chronic granulomatous disease?

A

It is a group of disorders resulting from a failure to produce increased concentration of toxic oxygen free radicals during the respiratory burst that accompanies activation of phagocytes. It is due to a failure to produce NADPH oxidase.

33
Q

What is hypersensitivity?

A

Damaging immunological reactions to extrinsic antigens.

34
Q

What are the 4 types of hypersensitivity reactions?

A
  1. Immediate (allergy)
  2. Antibody to cell-bound antigen
  3. Immune complex
  4. Delayed-type
35
Q

Describe immediate HS.

A

Due to activation of IgE antibody on mast cells or basophils by an antigen. Antigens binds to adjacent IgE antibodies causing a bridging effect between Fc receptors. This triggers the mast cell to release mediators (from preformed granules) like histamine, chemokines and heparin. Hence, these have immediate clinical effects.

36
Q

Give examples of immediate HS.

A

Allergic rhinitis
Atopic eczema
Asthma

37
Q

What is atopy?

A

Atopy defines an inherited tendency for overproduction of IgE antibodies to common environmental antigens.

38
Q

How can immediate HS lead to anaphylaxis?

A

If the antigen enters systemic circulation it can lead to generalised degranulation of IgE-sensitised mast cells and basophils. This would result in hypotension, bronchoconstriction and collapse. Bee and wasp venom.

39
Q

Describe the type II HS reaction.

A

IgG or IgM antibody to cell-bound antigen causes cell destruction by activating complement or promoting phagocytosis.

40
Q

Describe the type III HS reaction.

A

It results from the deposition or formation of IgG-containing immune responses in tissues, particularly the skin, joints and kidneys.

41
Q

How is the type IV HS reaction mediated?

A

It is mediated by IL-2, interferon-gamma and other cytokines released by T lymphocytes.

42
Q

What is autoimmunity?

A

It is an immune response against a self-antigen.

43
Q

What is autoimmune disease?

A

It is tissue damage or disturbed function resulting from an autoimmune response.

44
Q

What are the types of immunological tolerance?

A
  1. Thymic

2. Peripheral- immunological ignorance, anergy, regulation and suppression, B-cell tolerance.

45
Q

Describe immunological ignorance.

A

The antigen is isolated in an avascular organ such as the vitrous humour of the eye. There is a limited distribution of MHC class II molecules so it does not induce T cell activation.

46
Q

Describe anergy.

A

Naïve CD4+ T cells need two signals to activate an immune response- antigen-specific signal through T cell receptor and non-specific co-stimulatory signal. If there is no co-stimulatory signal, then stimulation through T cell receptor alone leads to apoptosis or a state of long-standing unresponsiveness called anergy. (absence of normal immune response to antigen)

47
Q

What is molecular mimicry?

A

When structural similarity between self-proteins and microbial antigens trigger an immune response by causing a breakdown of tolerance.

48
Q

What is epitope spreading?

A

Once tolerance has broken down, the resulting inflammatory process may allow presentation of further peptides causing a broadened immune response and acceleration of local tissue damage.

49
Q

What are the causes of autoimmunity?

A 
Genes
Hormones
Infections
Drugs
UV radiation
50
Q

What are the main features of innate immunity?

A

Rapid response
non-specific to pathogen
no immunological memory
does not confer long-lasting immunity to host

51
Q

What are the four main components of innate immunity?

A
  1. Natural barriers - skin, mucous membranes
  2. Cellular defences - neutrophils, macrophages, natural killer cells, NK-T cells, mast cells
  3. Soluble mediators - kinnins, cytokines, complement, interferon
  4. Pattern-recognition molecules - toll-like receptors
52
Q

What are epitopes?

A

Epitopes are the immunologically active regions of an antigen that bind to specific membrane receptors on lymphocytes or to secreted antibodies. B and T cells recognise different epitopes on the same antigenic molecule. B cells recognise soluble antigen (exogenous). Epitopes recognised by T cells are often internal peptides that are exposed by processing with APCs (endogenous).

53
Q

What are the end results of B-cell and T-cell responses?

A

B-cell response: formation of humoral antibodies hence humoral immunity (protection against extracellular infection).

T-cell response: formation of cellular immunity hence cellular immunity (protection against intracellular organisms like viruses and some bacteria).

54
Q

Differences in structure of which part of an immunoglobulin allows separation of the five Ig classes?

A

Heavy chains

55
Q

What two forms do the lights chains in an immunoglobulin exist?

A

Kappa and Lambda.

In any one molecule, both chains are of the same type.

56
Q

Describe the Fc part of an immunoglobulin molecule.

A

Fc stands for fragment crystalline. It is the constant part of the molecule and does not participate in antigen binding. Secondary effects after antigen binding has occurred include complement activation, chemotaxis and opsonisation.

57
Q

What are the various antibody mediated effector functions in humoral immunity?

A
  1. Opsonisation - Fc receptors on neutrophils and macrophages can bind to Fc of Ig molecules leading to phagocytosis of ag-ab complex.
  2. Complement activation - by IgG and IgM subclasses.
  3. ADCC (antibody-dependent cellular cytotoxicity) - antibodies bound to target cells (virus-infected) link with Fc receptors on NK cells leading them to recognise and kill the target cell.
  4. Transcytosis (crossing of epithelium) - delivery of antibody to mucosal surfaces and breast milk.
  5. Activation of mast cells, eosinophils, basophils by IgE.
58
Q

Which complement pathways form a part of the innate immune system?

A

The Mannose-binding lectin (MBL) and alternative pathways do not require antibody activation and are therefore a component of the innate immune system.

59
Q

How do antibodies protect against infection?

A 
• Specific binding/ multivalency (Fab) 
o Neutralize (toxins) (IgG, IgA)
o Immobilise motile microbes (IgM) 
o Prevent bind to and infection of host cells 
o Form complexes 
• Enhance innate mechanism 
o Activate complement (IgG, IgM) 
o Bind Fc receptors (enhance phagocytosis, mast cells release inflammatory mechanisms and enhance killing of infected cells by natural killer cells
60
Q

How do T cells recognise antigens?

A
  • B cells recognise soluble free native antigens
  • T cells recognise cell associated processed antigen
  • Cytotoxic T cell recognises peptide bound to MHC1
  • Virus infected cell – viral proteins broken down in cytosol
  • Peptides transported to ER and bind to MHC1 on cell surface
  • Activated cytotoxic T cells kill the infected cell by inducing apoptosis
  • Helper T cell recognises peptide bound to MHC2
  • Macrophage/dendritic cell/B cell internalises and breaks down foreign material
  • Peptides bind to MHC2 in endosomes on cell surface
  • Activated T helper cells help B cells make antibody and produce cytokines that activate/regulate other leukocytes
61
Q

What is passive immunisation?

A

Administering pre-formed antibodies targeted against a specific pathogen. It provides prevention before exposure and attenuation after exposure.

62
Q

What are the advantages of passive immunisation?

A

immediate protection

effective in immunocompromised patients

63
Q

What are the disadvantages of passive immunisation?

A

short-lived effects
possible transfer of pathogens
serum sickness in transfer of animal sera
risk associated with blood products

64
Q

What are the different kinds of post-exposure prophylaxis with immunoglobulins?

A
  1. Human Normal Ig/pooled Ig

2. Human Specific Ig

65
Q

Give examples if human normal Ig immunisations.

A 
Hep A (if longer than one week since onset of jaundice)
Measles (if exposed child has heart or lung disease)
66
Q

Give examples of human specific Ig immunisations and when they are administered.

A

Hep B- sexual partners, inoculation injuries, infants born to infected mothers

Tetanus- high-risk wounds or when immunisation status is incomplete or unknown

Varicella Zoster (chickenpox)- immunocompromised children or adults, pregnant women

Rabies- after exposure until vaccine becomes effective

67
Q

What is active immunisation?

A

Aka vaccination. Administering live attenuated or non-living forms of pathogens to trigger an immune response which would protect the individual on infection from the actual agent.

68
Q

What are whole killed vaccinations?

A

The bacteria/virus is grown in vitro and inactivated using formaldehyde or beta-propionolactone. Does not cause infection but antigens induce immune response.

69
Q

What are toxoids?

A

Aka component vaccines. They contain only extracted or synthesised components of microorganisms (polysaccharides or proteins).

70
Q

What are live attenuated vaccines?

A

Contain whole cell organisms with reduced virulence which induce T-lymphocyte and humoral responses. This makes them more immunogenic than killed but require careful consideration when used in immunocompromised individuals.

71
Q

What are the problems and limitations with whole cell vaccines?

A

Microorganisms must be grown to a high titre
Whole pathogens often cause excessive reactions
immune response not always close to normal response to infection (no mucosal immunity, no CTL response)
Usually need at least 2 shots

72
Q

Give examples of whole cell bacterial vaccines.

A

Diphtheria - toxoid
Tetanus - toxoid
Cholera - heat-killed

73
Q

Give examples of whole cell viral vaccines.

A

Polio
Influenza
Hep A
Rabies

74
Q

Which disease require post-exposure prophylaxis with Human Normal Immunoglobulins?

A

Hep A
Measles
Mumps
Varicella

75
Q

Which diseases require post-exposure prophylaxis with Human Specific Immunoglobulins?

A

Hep B
Tetanus
Varicella zoster
Rabies

76
Q

Give examples of pathogens that we lack vaccines for?

A

HIV, malaria, herpes simplex virus, rhinoviruses

77
Q

Why do we lack vaccines for certain pathogens?

A
  1. pathogen hard to grow
  2. killed pathogen is not protective
  3. impossible to obtain attenuated and suitably immunogenic strain
  4. too many strains causing disease (influenza)
78
Q

Name 6 new approaches to developing vaccines.

A
  1. recombinant proteins
  2. synthetic peptides
  3. live attenuated vectors
  4. DNA vaccines
  5. Heterogenous prime boost
  6. Conjugate vaccine

Phase 2A Medicine (16 decks)

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