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Immunology Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Describe 6 physical and chemical barriers against pathogens.

A
  1. Skin: Blocks pathogen entry, own micro-biome.
  2. Tears, mucus, and saliva: openings are entry pints for pathogens, protected by secretions containing anti-microbial peptides (defensins) or lysozymes to digest bacterial cell walls, also transport pathogens out the body or into stomach.
  3. Cilia: line windpipe to move mucus and trapped particles away from lungs (bacteria or microparticles).
  4. Stomach acid: HCl secreted by parietal cells lowering pH, activates proteases like pepsin to kill pathogens.
  5. Urine flow: regularly flushes out pathogens from bladder and urethra.
  6. Bacterial flora: Occupy niches so aggressive pathogens cannot, act as competition to aggressive pathogens.
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2
Q

Describe a genetic mutation for mucus causing increased infection of the lungs.

A

Cystic Fibrosis, mutation in chloride ion channel resulting in thickened mucus so cilia can no longer move pathogens away from lungs.

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3
Q

How can over-use of antibiotics lead to infection after stopping taking them?

A

Antibiotics will disrupt our body’s natural microbiome, leaving areas for colonization by aggressive pathogens (opportunistic pathogens like C. difficile)

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4
Q

How does the innate immune system distinguish between self and non-self-cells?

A

Toll-like Receptors (TLRs) highly expressed by macrophages, dendritic cells and neutrophils detect pathogen-associated molecular patterns (PAMPs), binding of specific PAMPs to specific TLRs triggers downstream cascade for transcription of pro-inflammatory genes and interferon-inducible genes.

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5
Q

What is a common example of a pathogen-associated molecular pattern (PLC) of Gram-negative bacteria?

A

Lipopolysaccharides (LPS) are components of the Gram-negative bacterial cell wall (endotoxin causing inflammation)

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6
Q

What is a variant of the amino acid methionine used commonly in bacteria but not humans, why is this useful for the immune system?

A

Formylated-methionine, as is not found in human cells can act as a PAMP for pathogen recognition.

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7
Q

What do damaged cells produce and what is the effect of this?

A

Damage-associated molecular patterns (DAMPs) which trigger the cell to be killed by apoptosis

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8
Q

What tissue produce blood cells?

A

Bone marrow

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9
Q

What type of stem cell differentiates into every lymphoid or myeloid cell?

A

Multipotential hematopoietic stem cells

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10
Q

What is the broad type of white cell used for a) Innate b) Adaptive immune systems?

A

a) Myeloid white blood cells provide innate protection.

b) Lymphoid cells generate adaptive immunity.

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11
Q

What are Leukocytes and what are the 2 types?

A

White blood cells, includes both myeloid and lymphoid cells.

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12
Q

How does the innate immune system get triggered?

A

Myeloid cells: macrophages, dendritic cells, neutrophils express TLRs that are activated when they recognise PAMPs and secrete molecular ligands that attract additional cells of the innate immune system.

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13
Q

What 2 responses does activation of Myeloid cells trigger (innate immune response)?

A

1) Inflammation:
>Dilated blood vessels become permeable and endothelial cells become sticky catching white blood cells and facilitating their access.
>Further pro-inflammatory cytokines are released (prostaglandins, histamines, cytokines).
>Localised fever inhibits pathogen proliferation and speeds chemical reactions used by antimicrobial peptides.

2) Recruitment of specialist phagocytic cells: Neutrophils, macrophages and eosinophils.

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14
Q

Why is systemically spread inflammation dangerous?

A

Loss of plasma volume, crash of blood pressure, clotting, cytokine storm.

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15
Q

Describe the 4 types of phagocytic cells.

A

1) neutrophils: 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)

2) macrophages: long lived professional phagocytes in specific tissues, abundant in areas likely to be exposed to pathogens (eg. airways, guts)

3) Eosinophils: are specialists in attacking objects too large to engulf

4) Dendritic cells: Express large variety of TLRs phagocytose pathogens.

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16
Q

What are two phagocytic cells produced from monocyte differentiation?

A

Macrophages and Dendritic cells.

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17
Q

How do dendritic cell link the innate and adaptive immune systems In 5 steps?

A
  1. Express large variety of TLRs
  2. Phagocytose pathogens
  3. Cleaves and processes pathogen peptides
  4. Binds processed peptide to MHC proteins and are transported to surface
  5. Travel to lymph nodes allowing activation of T cells via MHC presenting processed peptide (links innate and adaptive immunity).
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18
Q

What is GDHD?

A

During stem cell transplant, when host and donor do not match so immune system attacks transplanted stem cells.

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19
Q

Describe the process of Lymphocyte development?

A
  1. Lymphocytes develop in primary lymphoid organs where many multipotent haemopoietic stems cells are found (can differentiate into B cells and T cell). >B cells develop in the bone marrow >T cells develop in the Thymus.
  2. Naïve lymphocytes migrate to secondary lymph organs (e.g. tonsils) where they are exposed to foreign antigens, maturing the lymphocytes to have specific antigen recognising receptors.
  3. Lymph nodes drain into the blood stream.
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20
Q

What is the role of natural killer cells?

A

For early defence against foreign cells and autologous cells (e.g. microbial infection or tumour transformation)

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21
Q

What are antibodies created by and secreted by?

A

produced by B-lymphocytes and ultimately secreted by plasma cells.

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22
Q

What are the 3 subtypes of T cells and their function?

A

i. Cytotoxic T-cells: directly kill infected host cells.

ii. Helper T-cells: activate macrophages, dendritic cells, B cells, and cytotoxic T cells by secreting a variety of cytokines and displaying a variety of co-stimulatory proteins on their surface.
> Many T helper cell subtypes.

iii. Regulatory T-cells: use similar strategies to inhibit the function of helper T cells, cytotoxic T cells and dendritic cells.
>Inhibit immune response when finished with infection.

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23
Q

How does adaptive immunity work in 3 steps (an overview)?

A
  1. Body generates random library of lymphocytes due to exon swapping.
  2. When a processed antigen is presented, e.g. by a dendritic cell to a T helper cell, B and T cells with binding affinity to the antigen become activated.
  3. Leads to proliferation and clonal expansion of B and T cells
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24
Q

Why does a bigger pool of immune cells build after recurring encounters with a an antigen?

A

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

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25
Q

What is the effect of immune responses being independent between different antigens?

A

The body can respond to multiple antigens at once, so we can combine multiple antigens into one vaccine.

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26
Q

At birth what happens to allow the adaptive immune system to recognise what is self despite not having TLRs?

A

> At birth, the immune system choses that everything inside is self and then everything new is foreign.

> cells transplanted into a new-born host will survive and be ‘accepted’ as self. Future transplants from the same source will be treated as self and survive

27
Q

Describe an experiment which shows a) host can mount attack against self-antigens b) immune system can forget what is has previously learned

A

a) 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

b) remove ‘self’ protein from adult animal reintroduce after several weeks / months host now mounts immune response to removed protein

28
Q

What % of blood plasma do antibodies make up?

A

20%

29
Q

What causes B cells to secrete antibodies?

A

Binding between antigen and antibody receptor on B cell causes diving and differentiation into plasma cells to secrete antibodies.

30
Q

What is the most common antibody found in the immune system?

A

IgG (Primary Response)

31
Q

What are both light and heavy chains of antibodies made up of?

A

light & heavy chains are made up of repeating 110aa domains (Immunoglobulin domains) each of which contains an internal di-sulphide bond

32
Q

Describe the structure of antibody variable regions.

A

Antigen binding region consists of two variable domains (one light and one heavy), each light and heavy variable domain contains three hyper variable regions making the shape for antigen binding.

33
Q

Describe the 3D structure of the hypervariable regions of antibodies, and how changing amino acids has an effect.

A

> 3D structure of hyper variable regions shows loops that join onto the immunoglobin domain sheets

> By changing amino acids present in this loops, leads to 3D structures with different grooves for different antigen binding.

34
Q

What are the heavy chains of the Ig domains encoded for by?

A

Encoded by a single exon.

35
Q

How are an unlimited supply of different variable regions of antibodies generated?

A

By VJ (also called V(D)J) recombination

36
Q

How many different antibodies does a naïve unchallenged human immune system have at birth?

A

1*10^12

37
Q

What does a) Light chain variable domain b) Heavy chain variable domain contain in its DNA?

A

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

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

38
Q

Describe VJ (or V(D)J) recombination, and the role of a) DNA cutting b) mRNA splicing

A

> Variable regions are composed of three gene segments: V (variable), D (diversity), and J (joining).

a) By cutting DNA between these segments, they can fuse together and therefore be transcribed together.

b) The mRNA created will start with a V region, contain multiple J regions (in the middle) and end with a C region. RNA splicing will remove any J sequence found after the first J (just takes the first J).

39
Q

What is the role of RAG1 and RAG2 genes in the immune system?

A

DNA splicing is driven by the V(D)J recombinase enzyme (encoded by RAG1 & RAG2 genes)

40
Q

What is junctional diversification and what is the effect of this?

A

> During joining of gene segments (V(D)J recombination) a variable number of nucleotides are often lost or inserted from the ends of the recombining gene segments (B cells don’t have telomeres at ends of genes). 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.

41
Q

As well as V(D)J recombination, how do B and T cells further increase variation of antibodies?

A

Developing B and T cells are diploid, but each B cell randomly chooses a paternal or maternal copy to inherit, further increasing variation in antibodies.

42
Q

What is affinity maturation of B cells?

A

Only the B cells with the highest affinity can bind to antigen after the immune system starts degrading pathogen, so natural selection occurs; the antibodies with higher affinity are positively selected

43
Q

How does affinity maturation of B cells occur?

A

> By somatic mutation ( leads to affinity maturation due to rapid mutations producing different antibodies with varying affinities for antigen):

  1. B cells with affinity to an antigen bind and with stimulation by T helper cells, proliferate.
  2. During proliferation, there is an accumulation of point mutations in the V-regions in both light and heavy chains.
  3. B cells mutate every time they divide in their V regions
  4. B cells that produce high-affinity antibodies are preferentially selected for survival and further proliferation, while those that produce low-affinity or non-functional antibodies are eliminated through apoptosis. (causing affinity maturation/ in vivo evolution)
44
Q

What are Germinal Centres and why are they important?

A

> After B cells have been stimulated by antigen and helper T cells in a secondary lymphoid organ, some of the activated B cells proliferate rapidly in the lymphoid follicles and form structures called germinal centres.

> Somatic hypermutation is driven by activation-induced deaminase (AID) expressed at germinal centres.

45
Q

Where does somatic hypermutation of B cells occur?

A

In secondary lymph tissues (where germinal centres are).

46
Q

What is the p53 pathway and why must it be inhibited during B cell development.

A

> Normally cells experiencing double stranded breaks [e.g. during V(D)J recombination] and high levels of DNA damage [e.g. somatic hyper mutation] will apoptosis via the p53 pathway.

> So the p53 pathway would inhibit the mutations required for antibody variability if not inhibited during B cell development.

47
Q

How is the p53 pathway inhibited during B cell development?

A

BCL-6 is a transcriptional repressor expressed in germinal centres, that switches off expression of p53

48
Q

What are the 2 ways dendritic cells can activate T cells and what is the function of both?

A
  1. Activate: If dendritic cell presents degraded antigen as well as co-stimulatory protein, stimulates T cell to kill pathogens with this antigen.
  2. Tolerate: If just self-antigen and not the co-stimulatory protein, causes T cells to note the antigen but not kill it, to train T cells not to attack self-proteins.
49
Q

What do T cells bind to MHC proteins presenting antigen using?

A

T-cell receptors (TCR’s)

50
Q

What is the structure of a T-cell Receptor (TCR) and how are they made?

A

> TCRs are immunoglobulins and contain variable domains and hyper variable loops much like antibodies

> TCR diversity generated by V(D)J-like recombination & junctional diversification in the thymus to give diversity (is less than antibody diversity however).

51
Q

How are T-cells linked with older people getting cancer?

A

As T-cell number decreases with age, so recognise less cancerous cells.

52
Q

What are 2 examples of benign pathogens which are opportunistic?

A
  1. Candida albicans : a yeast that usually lives on skin, mouth gut, vagina without issues, but can become pathogenic.
    >Phagocytosis by macrophages can induce switch to hyphae form, Hyphae tubes burst open macrophages.
  2. Staphylococcus aureus : a Gram-positive spherically bacterium, frequently found in the upper respiratory tract and on the skin.
    >Produces protein A, which binds to constant domain of IgGs and presents the variable domains of IgGs, meaning the innate immune system no longer attacks it as sees it as self
53
Q

What is HIV and how does it damage the body?

A

> Human Immunodeficiency Virus (HIV) : an RNA lentivirus that specifically infects T-helper cells, dendritic cells and macrophages expressing the CD4 receptor.

> Binds to CD4 receptor and infects these cells, destroys process of adaptive immunity. Resulting in immunodeficiency.

54
Q

What is an example of a disease which only harms people with HIV?

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

55
Q

Describe the autoimmune diseases 1) Type 1 diabetes 2) Multiple Sclerosis 3) Autoimmune inflammatory diseases

A

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

2) Multiple Sclerosis
>The immune system responds to proteins within the myeline sheath of neutrons within the CNS causing less quick synaptic transmission. Associated with a range of symptoms, progressive loss of myelination can ultimately be fatal

3) Auto immune inflammatory diseases: rheumatoid arthritis, psoriasis, Crohn’s disease, inflammatory bowel disease (IBD)
>defects in the ‘self-tolerance’ process leading to the production of antibodies that trigger inflammatory responses by the innate immune system

56
Q

What can multiple injuries in the same place lead to?

A

chronic inflammatory response

57
Q

Describe an experiment which shows the immune system can recognise tumours as not self.

A

In mice, inject tumour into immunologically compromised host then the tumour is accepted, if injected into mice with working immune system, it s destroyed, showing immune system recognises if tumour is not self.

58
Q

What is the biggest risk factor for cancer and why?

A

Ageing as immune competence decreases with age, so less immune cells to recognise the non-self tumour.

59
Q

What histology evidence backs up the cancer immune surveillance model?

A

That tumour infiltrating lymphocytes (white blood cells) are always found near tumours.

60
Q

What is the cancer immune surveillance model?

A

The cancer immune surveillance model proposes that the immune system plays a critical role in recognizing and eliminating cancer cells in the body.

61
Q

What is a limitation to the cancer immune surveillance model?

A

As many people with healthy immune systems get cancer

62
Q

What are the 3 phases of cancer immunoediting?

A

1) The elimination phase, tumour cells are killed by NK, CD4+ and CD8+ cells
>Could eliminate tumour cells here.

2) A state of equilibrium between immune and tumour cells

3) When the immune system is unable to destroy the tumour cells ‘escape’ leads to clinically detectable tumours

63
Q

What are 7 cancer immunotherapies being studied due to the fact the immune system can identify cancer?

A
  1. checkpoint inhibitors:
    >Checkpoints in cell cycle is similar in immune system
    >If we inhibit the checkpoints.
  2. cytokines: to stimulate the immune cells to attack cancer
    >Give more cytokines
  3. immunomodulators:
    >boosts parts of the immune system
  4. cancer vaccines:
    >vaccines that direct an immune response designed to prevent a specific cancer epitope or cancer causing pathogen (eg. HPV)
  5. monoclonal antibodies (mAbs):
    >directed against cancer specific antigens
  6. oncolytic viruses:
    >viruses that have been modified in a lab to infect and kill certain tumour cells
  7. Chimeric antigen receptor T-cell Therapy (CAR-T):
    >Take T-cells from patient, infect with recombinant virus causing expression of TCR complimentary to the tumour antigen, transfuse these T-cells back into patient so can attach and kill cancer.

Advanced Molecular Biology (9 decks)

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