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Molecular cellular biology > Immunology > Flashcards

Immunology Flashcards

1
Q

what is immunity?

A

immunity is the state of being insusceptible or resistant to a noxious agent or process, especially a pathogen of infectious disease

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2
Q

what types of organisms or bodies may pathogens be?

A
  • Bacteria
  • Fungi
  • Parasites
  • Foreign bodies
  • Foreign tissues
  • Unwanted cells e.g. necrosis, apoptosis, cancer
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3
Q

what is the body’s first line of defence? give examples:

A

physical and chemical barriers that are always ready and prepared to defend the body from infection:
- skin
- tears, mucus, saliva
- cilia
- stomach acid
- urine flow
- friendly bacteria

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4
Q

how is skin part of the body’s first line of defence?

A
  • biggest organ in our body and can self-renew
  • barrier function – waterproof
  • its own micro-biome: competes with pathogens
  • the lining of the gut is also an epithelium with barrier functions
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5
Q

how are tears, mucus and saliva part of the body’s first line of defence?

A
  • ‘openings’ are potential entry points for pathogens and are protected by secretions
  • many contain anti-microbial peptides (defensives) or enzymes such as lysozyme that digest bacterial cell walls
  • pathogens transported out of the body or into the stomach and killed
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6
Q

how are cilia part of the body’s first line of defence?

A
  • very fine hairs (cilia) lining our windpipe move mucus and trapped particles away from your lungs.
  • Particles can be bacteria or material such as dust or smoke
  • cystic fibrosis is caused by mutation of a chloride ion channel that results in thickened mucus that cilia can no longer move leading to lung infections
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7
Q

how is stomach acid part of the body’s first line of defence?

A

HCl secreted by parietal cells lowers the pH, activating proteases such as pepsin in the stomach and killing pathogens

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8
Q

how is urine flow part of the bod’s first line of defence?

A
  • regularly flushes out pathogens from the bladder and urethra
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9
Q

how are friendly bacteria part of the body’s first line of defence?

A
  • naturally occurring ‘friendly bacteria’ form a microbiome in our guts, skin, mouth, vagina etc acts as competition to reduce the ability of pathogens to colonise and grow
  • BUT, use of antibiotics, anti-bacterial soaps etc can disrupt the microbiome and leave areas for colonisation by pathogens
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10
Q

what is the body’s second line of defence?

A

innate immunity

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11
Q

how can the body distinguish between the pathogen and all the self-cells?

A

by recognising molecules pathogens have that we do not:
- e.g. Lipopolysaccharides (LPS) which are components of the Gram-negative bacterial cell wall or peptides containing formylated-methionine, an amino acid only used by bacteria

these are called pathogen-associated molecular patterns (PAMPs)

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12
Q

how are damaged self-cells recognised by the innate immune system?

A

by identifying damage-associated molecular patterns (DAMPs)

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13
Q

what is the largest family of innate receptors that recognise PAMPs?

A

the largest family of receptors that detect PAMPs are members of the Toll family collectively known as Toll-like Receptors (TLRs)

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14
Q

what are Toll-like receptors (TLRs)?

A
  • 10x TLRs in humans and are highly expressed by macrophages, dendritic cells and neutrophils to recognise PAMPs
  • TLRs are a molecular signalling cascade that signal through downstream effectors such as the Jun/Fos transcription factors and NFkB and ultimately change gene expression
  • Upregulate proinflammatory gene pathways
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15
Q

what leukocytes in our blood provide innate protection?

A

myeloid cells

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16
Q

what leukocytes in our blood provide adaptive protection?

A

lymphoid cells

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17
Q

what do haematopoietic stem cells (HSCs) in the bone marrow differentiate to?

A
  • 100,000-200,000 haematopoietic stem cells at birth, 40-50 HSCs in 80 year olds
  • Differentiate to either common myeloid progenitor or common lymphoid progenitor for white blood cells
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18
Q

what are myeloid cells?

A

Leukocytes of the innate system
- myeloid cells such as macrophages and dendritic cells (both derived from monocytes) and neutrophils express TLRs (as well as other receptors that detect pathogen profiles)
- cells that are activated because they recognise a pathogen-associated molecular patterns (PAMPs) secrete molecular ligands that attract additional cells of the innate immune system

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19
Q

what 2 things does activation of myeloid cells trigger?

A
  1. inflammation - dilation of local blood vessels, pain, redness, heat, swelling
  2. recruitment of specialist phagocytic cells
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20
Q

what is triggered during innate inflammation?

A
  • dilated vessels become permeable and endothelial cells become sticky so ‘catching’ white blood cells and facilitating their access.
  • further pro-inflammatory cytokines are released including prostaglandins, histamines and cytokine from mast cells
  • fever inhibits pathogen proliferation and speeds chemical reactions used by antimicrobial peptides, complement cascade etc
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21
Q

how may innate inflammation responses become dangerous?

A
  • responses appropriate locally can be dangerous systemically (e.g. in response to sepsis)
  • This is a shock: loss of plasma volume, crash of blood pressure, clotting, cytokine storm
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22
Q

what types of phagocytic cells are recruited during the innate response?

A
  • neutrophils
  • macrophages
  • eosinophils
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23
Q

what are neutrophils?

A

short-lived phagocytic abundant in blood but not tissues, respond and migrate to sites of infection (neutrophils make up most ‘puss’ within wounds, spots etc)

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24
Q

what are macrophages?

A

long-lived professional phagocytes abundant in areas likely to be exposed to pathogens (e. g. airways, guts)

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25
Q

what are eosinophils?

A

are specialists in attacking objects too large to engulf

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26
Q

what cells can link the innate and adaptive immune systems?

A

dendritic cells

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27
Q

what are dendritic cells?

A

specialist phagocytic cells derived from monocytes
- express a large variety of recognition receptors (TLRs etc)
- dendritic cells are central to activating the adaptive response

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28
Q

how do dendritic cells in the innate system activate the adaptive system?

A
  • dendritic cells phagocytose pathogens, and cleave them into peptides which are bound to MHC proteins (Major Histocompatibility Complex)
  • dendritic cells display the MHC-peptides on their surface for T cell recognition
  • DCs migrate to lymphoid tissues (e.g. lymph nodes), activate and stimulate T-cells of the adaptive immune system
  • T cells develop TCRs which are highly specific for that pathogen peptide/antigen
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29
Q

what is adaptive immunity?

A
  • can generate highly specific responses to specific pathogens
  • can identify, target and destroy vast range of pathogens / toxins
  • but it’s important to direct AI against foreign targets and NOT host ‘self’ molecules/proteins
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30
Q

what happens if our self-cells are recognised as foreign?

A

accidental targeting of ‘self’ as ‘foreign’ can be lethal

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31
Q

how does the immune system avoid attacking harmless molecules that enter our body?

A
  • harmless molecules enter our bodies and do not warrant a response
  • innate immunity plays key role in recognising targets to attack
  • inappropriately targeting harmless molecules can also cause trouble
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32
Q

what are lymphoid cells?

A

Lymphoid cells (aka Lymphocytes) generate adaptive immune responses
- Lymphocytes develop within the thymus and bone marrow (primary lymphoid organs)
- they then migrate to secondary lymphoid organs where they are exposed to foreign antigens (the skin and respiratory system are also secondary sites)
- Lymph ultimately drains into the bloodstream and cells circulate

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33
Q

what are the 3 main types of lymphoid cells?

A
  1. B cells
  2. T cells
  3. natural killer cells
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34
Q

where do B cells develop?

A

bone marrow

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35
Q

where do T cells develop and where are they matured ?

A

Bone marrow

Thymus

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36
Q

what are natural killer cells?

A
  • participate in early defence against foreign cells and autologous cells undergoing various forms of stress, such as microbial infection or tumour transformation
  • Lymphoid cells BUT considered part of the innate immune response
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37
Q

what are antibodies?

A
  • antibodies (aka Immunoglobulins or Ig) are essential for adult survival and make up around 20% of the protein in blood plasma
  • secreted soluble immunoglobulins of various types that bind to antigens
  • produced by B-lymphocytes and ultimately secreted by plasma cells
  • initially antibody receptors, and when plasma cells are differentiated they become soluble antibody
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38
Q

what is cell-mediated immunity?

A
  • adaptive immunity carried out by T cells which trigger cellular level responses
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39
Q

what are the 3 subtypes of T cells?

A
  1. cytotoxic T cells
  2. helper T cells
  3. regulatory T cells
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40
Q

what are cytotoxic T cells?

A
  • directly kill infected host cells by inducing apoptosis
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41
Q

what are helper T cells?

A

they activate macrophages, dendritic cells, B cells and cytotoxic T cells by secreting cytokines and displaying co-stimulatory proteins on their surface

42
Q

what are regulatory T cells?

A

use cytokines to inhibit the function of helper T cells, cytotoxic T cells and dendritic cells
- tunes the immune system so that it is not excessively active

43
Q

how is adaptive immunity activated?

A
  • the body randomly generates a ‘library’ of lymphocytes most of which remain dormant
  • when an antigen is presented (e.g. by dendritic cells or T-helper cells) those that have some binding affinity to the antigen of interest become ‘activated’
  • binding of antigen to activated cells leads to their proliferation and clonal expansion
  • expansion triggers differentiation into effector cells
  • an expansion round occurs every time an antigen is encountered
  • subsequent encounters stimulate the memory cells made previously so building a bigger pool of cells able to bind
  • the body can now respond to multiple antigens at once, specifically
44
Q

what is immune tolerance?

A
  • adaptive immune system needs to identify and respond to an almost infinite range of unknown antigens but simultaneously ignore a huge range of very similar ‘self’ antigens
  • adaptive immune system can ‘learn’ not to respond to self-antigens.
  • Cells/organs transplanted between adults will be rapidly destroyed by the hosts T-cell response
  • cells transplanted into a newborn host will survive and be ‘accepted’ as self as the immune system is still naive.
  • Future transplants from the same source will be treated as self and survive
45
Q

how can immune tolerance be studied experimentally?

A
  1. knock out a gene encoding a ‘self’ protein
    - allow animal to grow, then reintroduce KOed self-protein
    - host now mounts immune response as it hasn’t ‘learnt’ this is self
    - this shows host CAN mount attack against self-antigens
  2. remove ‘self’ protein from adult animal
    - reintroduce after several weeks / months
    - host now mounts immune response to removed protein
    - the system can ‘forget’ what it has previously learnt
46
Q

what are the 5 classes of antibody?

A
  1. IgG
  2. IgM
  3. IgA
  4. IgD
  5. IgE

each have different heavy chains, dinge and tail structures, so have unique characteristics and functions

47
Q

what is the most common antibody in the body?

A

IgG

48
Q

what is the structure of IgG?

A
  • made up of two copies of two proteins (4 in total) linked by covalent di-sulphide bonds
  • 2x Heavy chains (around 440aa) and 2x Light chains (around 220aa)
  • Antigen-binding site at N-terminus of heavy and light chains
  • each chain consists of variable and constant domains
  • both light & heavy chains are made up of repeating 110aa domains as Immunoglobulin domains, each containing an internal di-sulphide bond. Likely to be the result of gene duplications during evolution
  • antigen-binding region consists of two variable domains made up of a single modified Ig domain and containing three hyper variable regions
49
Q

what is the role of the constant domain of IgG?

A

constant domains interact with other parts of the immune system (e.g. Innate immune & complement systems)

50
Q

what is the role of the variable domain of IgG?

A
  • variable domains make up the antigen-binding sites
  • antigen-binding region consists of two variable domains made up of a single modified Ig domain and containing three hypervariable regions
51
Q

how do the structures of hypervariable domains of antibodies vary and why?

A

3D structure of the hyper variable domains vary following in vivo evolution:
- selects the best structure to best interact with the antigen
- variable domain has barrel structure formed by beta-sheets, that makes it specific to antigen
- by mutating amino acids in the loops produces 3D pockets/grooves which antigens can bind to
- somatic hypermutation

52
Q

how is the constant domain of an antibody encoded for?

A
  • the Ig domains that make up the constant part of the heavy chain are each encoded by a single exon
53
Q

what is the primary antibody repertoire?

A

a naive, unchallenged human immune system can generate around 1x10^12 different antibody molecules

54
Q

how many antibodies are generated in the primary antibody repertoire?

A

1x10^12

55
Q

how many antibodies can a mature immune system generate?

A

a mature immune system can make antibodies able to bind to essentially any antigen (essentially infinite flexibility)

56
Q

how is the variable domain of an antibody encoded for?

A
  • in the germline a k-light chain gene variable domain contains 40x V domains, 5x J domains and a single C domain
  • and a heavy chain gene variable domain contains 40x V domains, 25x D domains, 6x J domains and 5x C domains
  • In developing B-cells these are recombined in a process known as VJ or V(D)J recombination
57
Q

what domains does the variable k-light chain gene contain?

A

k-light chain gene variable domain contains 40x V domains, 5x J domains and a single C domain

58
Q

what domains does the variable heavy chain gene contain?

A

heavy chain gene variable domain contains 40x V domains, 25x D domains, 6x J domains and 5x C domains

59
Q

what process generates the primary antibody repertoire?

A

V(D)J recombination

60
Q

how is the primary antibody repertoire generated in development?

A

developing B cells join together separate gene segments in DNA in order to create the genes that encode the primary repertoire of low-affinity antibodies:

  1. during the development of a B cell a coding sequence joining a V to a J segment is assembled by removing the intervening DNA (in this case joining V3 to J3)
  2. transcription starts immediately upstream of the fused V segment (in this case V3) which lies immediately upstream of a J region (J3 in this case).
  3. Extra downstream J segments (J4 & J5) are transcribed but edited out of the mRNA transcript via splicing
  4. An mRNA is translated containing V3, J3 and C
61
Q

what is the process of V(D)J recombination?

A

The process of V(D)J recombination joins separate antibody gene segments together to form a functional VL- or VH-region coding sequence
- DNA splicing is driven by the V(D)J recombinase enzyme (encoded by RAG1 & RAG2 genes)
- Has recombinase and ligase (joining) activity

62
Q

what does V(D)J recombination generate?

A

fully formed primary antibody repertoire

63
Q

what is junctional diversification?

A

during joining of gene segments a variable number of nucleotides are often lost or inserted from the ends of the recombining gene segments.
- This is called junctional diversification.
- in many cases, this will shift the reading frame to produce a non-functional gene.
- These developing B cells never make a functional antibody molecule and die in the bone marrow.
- 2/3s of B cells cannot make a functional antibody
- B cell survival depends on its ability to make antibody, so if it can’t it is apoptosed

64
Q

what is allelic exclusion?

A
  • Developing B & T-cells are diploid (one maternal & one paternal copy) but chose just one allele to recombine (this is known as allelic exclusion)
  • Further increases antibody diversity
65
Q

what does a mutation in recombinase enzyme genes RAG1 and RAG2 result in?

A

RAG1 or RAG2 mutants have a severe combined immunodeficiency phenotype (SCID).

66
Q

how is the primary antibody repertoire encoded for, when the entire genome only encodes 25,000 genes?

A
  1. The process of V(D)J recombination
  2. the gain or loss of nucleotides during recombination – junctional diversification
  3. choice of one allele – allelic exclusion

these processes enable the random combination of domains of genes to generate a diverse array of antibodies in development

67
Q

how is the primary antibody repertoire of 1x10^12 increased to infinite antibodies?

A

by antigen-driven somatic hypermutation

68
Q

what is affinity maturation?

A

over time after initial immunisation there is a progressive increase in affinity of the antibodies to the antigen

69
Q

what happens to B cells genes during affinity maturation and antigen stimulation?

A
  • Accumulation of point mutations in both heavy and light chain V-region coding sequences of the B cells that are being amplified
  • This happens AFTER recombination has assembled the gene segments
  • After B cells have been stimulated by antigen and helper T cells in a peripheral lymphoid organ, some of the activated B cells proliferate rapidly in the lymphoid follicles and form structures called germinal centres.
70
Q

what is somatic hypermutation?

A

B cells mutate at the rate of about one mutation per V-region coding sequence per cell generation
- Every time the cell divides, each V-region mutates
- Approximately 1 million times faster than ‘background’ mutation rate
- this is termed somatic hypermutation

71
Q

what enzyme drives somatic hypermutation?

A

activation-induced deaminase (AID), which is expressed in the germinal centres of B cells

72
Q

what stimulates B cell clonal expansion

A

Developing B cells present their antibodies on their surface and binding of antigen stimulates their proliferation

73
Q

how is B cell survival determined in somatic hypermutation?

A
  • most somatic mutations will have no effect or will make the antibody worse. This will stop antigen binding, remove stimulus, and these B cells will apoptose
  • B cells containing mutations that increase affinity of the antibody to the antigen will increase the stimulus.
  • These clones will survive and proliferate (especially as antigen levels get very low)
  • in vivo evolution that selects cells with beneficial mutations
74
Q

why are V(D)J recombination and somatic hypermutation dangerous?

A

Normally cells experiencing double-stranded breaks (e.g. during V(D)J recombination) and high levels of DNA damage [eg somatic hypermutation] will apoptose via the p53 pathway that acts as a ‘watch keeper’ to kill cells with potentially oncogenic mutations
- may generate oncogenic mutations

75
Q

how is the p53 pathway inhibited in V(D)J recombination and somatic hypermutation?

A
  • BCL-6 is a transcriptional repressor expressed in germinal centres of B cells
  • BCL-6 binds to sites in the p53 promoter switching off expression
  • leaves GC without ‘watch keeper’ oversight.
  • high risk (may cause oncogenic mutation)/ high reward (specific antibody with high affinity produced)
76
Q

B cells and antbody summary:

A
  • VJ and V(D)J recombination shuffles the light & heavy chain genes in the region encoding the variable domains
  • nucleotide lost /gain in recombining gene segments creates junctional diversification
  • initial ‘primary repertoire’ library of 1x1012 B-cells
  • affinity maturation via ‘in vivo evolution’ based on binding of antigens
  • this selects amongst variations induced by somatic hypermutation
77
Q

how are T cells activated?

A

T cells are activated by partly degraded antigens displayed on the surface of antigen-presenting cells
- MHC proteins on antigen-presenting cells bind to the peptide fragments and carry them to the cell surface where T cells can recognise them via their TCRs

78
Q

how can antigen-presenting dendritic cells activate T cells?

A

activating DCs present three proteins: MHC with a foreign antigen, stimulating ligands and cell-cell adhesion molecules

79
Q

how can antigen-presenting dendritic cells tolerise T cells?

A

tolerising DCs present self-antigens on their MHCs but do NOT include the co-stimulatory activator protein
- T cells will be exposed to the antigen but will not trigger adaptive immunity processes

80
Q

how do T cells recognise APCs?

A

T cells bind to MHCs on APCs via their T-cell Receptors (TCRs)

81
Q

what is the structure of TCRs?

A

TCRs are immunoglobulins and contain variable domains and hypervariable loops much like antibodies

82
Q

how are TCRs diverse?

A

TCR diversity generated by V(D)J-like recombination & junctional diversification in the thymus to give diversity of 1x108 (this decreases with age by 2-5 fold)

83
Q

give 3 examples of pathogens which can evade/harness the immune system:

A
  1. Candida albicans
  2. Staphylococcus aureus
  3. HIV
84
Q

how does Candida albicans evade the immune system?

A

Candida albicans: a yeast that usually lives on skin, mouth gut, vagina without issues, but can become pathogenic.
- Grows as several forms including ‘normal’ yeast cells and pseudohyphal filamentous forms
- Phagocytosis by macrophages can induce switch to hyphae form
- in hyphae form they can break out of the phagocyte

85
Q

how does Staphylococcus aureus evade the immune system?

A

Staphylococcus aureus: a Gram-positive spherically bacterium, frequently found in the upper respiratory tract and on the skin.
- produces Protein A (A for aureus) - a 42 kDa cell [wall] surface protein that binds to the constant domain of IgGs.
- Bacteria are covered with ‘self’ proteins and no longer recognised by innate immune system

86
Q

how does HIV evade the immune system?

A

Human Immunodeficiency Virus (HIV) : an RNA lentivirus that specifically infects T-helper cells, dendritic cells and macrophages expressing the CD4 receptor.
- infected immune cells no longer function AND trigger immune responses that trigger T-cells to target cells absolutely required for adaptive immune system function
- resulting immune deficiency leads to infections (e.g. Candida and Aspergillus) and cancers rarely seen in those with intact immune systems

87
Q

what is Kaposi’s sarcoma?

A

Kaposi’s sarcoma is caused by herpesvirus 8 (HHV-8), a relatively common virus, that only causes cancer in people with a weakened immune system e.g. HIV infection

88
Q

what are examples of autoimmune diseases?

A
  1. type 1 diabetes
  2. multiple sclerosis (MS)
  3. autoimmune inflammatory diseases such as rheumatoid arthritis
89
Q

how is type 1 diabetes an autoimmune disease?

A

In Type 1 diabetes the immune system develops killer T-cells that attack insulin producing beta-cells within the Islets of Langerhans within the pancreas

90
Q

how is MS an autoimmune disease?

A

In Multiple Sclerosis the immune system responds to proteins within the myelin sheath of neurons within the CNS.
- Associated with a range of symptoms, progressive loss of myelination can ultimately be fatal

91
Q

what are examples of autoimmune inflammatory diseases and how are they triggered?

A
  • Autoimmune inflammatory diseases: rheumatoid arthritis, psoriasis, Crohn’s disease, inflammatory bowel disease (IBD), ulcerative colitis
  • defects in the ‘self-tolerance’ process leading to the production of antibodies that trigger inflammatory responses by the innate immune system
92
Q

how are immunity and cancer linked?

A

immune competence decreases with age - “immunosenescence” - implying that decreased immunosurveillance against cancer contributes to increased disease in the elderly (age is the biggest risk factor for cancer)

93
Q

can the immune system recognise and attack tumours?

A

In mouse transplantation models, tumours are rejected in syngeneic (immunologically compatible) hosts, while transplantation of normal tissues are accepted.
- So confirming the existence of tumour-specific antigens which can be recognised as non-self
- Overall, there seems to be compelling evidence that our immune systems identify and kill cancerous [and pre-cancerous] cells

94
Q

how can the immune system detect cancers?

A

tumour-infiltrating lymphocytes (TILs)

95
Q

what are the 3 phases of cancer immunoediting?

A
  1. the elimination phase, tumour cells are killed by NK, CD4+ and CD8+ cells
  2. a state of equilibrium between immune and tumour cells
  3. When the immune system is unable to destroy the tumour, tumour cells ‘escape’ leads to clinically detectable tumours
96
Q

can the adaptive immune system be used to attack cancers?

A

Yes:
- stimulating, or boosting, the immune system so it is more effective at identifying and attacking cancer cells
- approaches to help restore or improve how the immune system works to find and attack cancer cells

97
Q

how is the immune system limited in fighting cancer by itself?

A
  • the immune system doesn’t see the cancer cells as foreign because the cells aren’t different enough from normal cells.
  • the immune system recognizes the cancer cells, but the response might not be strong enough to destroy the cancer.
  • cancer cells themselves can also give off substances that keep the immune system from finding and attacking them.
98
Q

what cancer immunotherapies may be useful in treating cancer?

A
  • checkpoint inhibitors: takes the ‘brakes’ off the immune system
  • cytokines: to stimulate the immune cells to attack cancer
  • immunomodulators: boosts parts of the immune system
  • cancer vaccines: vaccines that direct an immune response designed to prevent a specific cancer epitope or cancer causing pathogen (e.g. HPV)
  • monoclonal antibodies (mAbs): directed against cancer specific antigens
  • oncolytic viruses: viruses that have been modified in a lab to infect and kill certain tumour cells
  • chimeric antigen receptor (CAR) T-cell therapy
99
Q

what is chimeric antigen receptor (CAR) T-cell therapy?

A

this approach takes the patients T cells and infects them (ex vivo) with a recombinant virus that causes the expression of a TCR with an antibody-derived variable (antigen binding) domain specific to a tumour antigen. This generates T-cells able to attach to tumour cells. These are transfused back into the patient so they can find, attach to and kill the cancer

100
Q

what is graft versus host disease (GVHD)?

A

a relatively common side effect of heterologous haematopoietic stem cell / bone marrow transplantation where transplanted T cells will attack and kill the new host

Molecular cellular biology (13 decks)

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