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Advanced molecular & cell L2 > Lecture 26 - Immunity > Flashcards

Lecture 26 - Immunity Flashcards

1
Q

What is immunity?

A

The state of being unsusceptible or resistant to a noxious agent or process, especially a pathogen or infectious disease

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2
Q

What are examples of pathogens?

A
  • bacteria
  • fungi
  • parasites
  • ‘foreign bodies’
  • ‘foreign tissues’
  • ‘unwanted cells’ (necrosis, apoptosis, cancer)
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3
Q

What are examples of the first line of defence?

A
  • Skin (epithelium)
  • Tears, mucus & saliva
  • Cilia
  • Stomach acid
  • Urine flow
  • ‘Friendly bacteria’
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4
Q

What is the first lines of defence?

A

physical and chemical barriers that are always ready and prepared to defend the body

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5
Q

How does skin act as a defence?

A
  • biggest organ in our body
  • barrier function
  • its own micro-biome
  • the lining of the gut is also an epithelium with barrier functions
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6
Q

How does cilia act as a 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 duct or smoke
  • cystic fibrosis is caused by mutation of a chloride ion channel that results in thickened mucus that cilia can no linger move leading to lung infection
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7
Q

How do tears, mucus & saliva act as a defence?

A
  • ‘openings’ are potential entry points for pathogens and are protected by secretions
  • many contain anti-microbial peptides (defensins) or enzymes such as lysozyme that digest bacterial cell walls
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8
Q

How does stomach acid act as a defence?

A
  • HCI secreted by parietal cells lowers the pH, activating proteases such as pepsin in the stomach and killing pathogens
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9
Q

How does urine flow act as a defence?

A

Regularly flushes out pathogens from the bladder and urethra

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10
Q

How does friendly bacteria act as a defence?

A
  • naturally occuring friendly bacteria form a microbiome in our guts, skin, mouth, vagina etc, as competition to reduce the ability of pathogen to colonize and grow.
  • use of antibiotics, anti-bacterial soaps etc, can disrupt the microbiome and leave areas for colonization by pathogens.
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11
Q

How can the body distinguish between the pathogen (that has made it past the first line of defence) and all the ‘self’ cells?

A

Things are different between us and the pathogen - 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.

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12
Q

What are the identification of gram-negative bacterial cell wall (e.g. lipopolysaccharides - LPS) and peptides containing formylated-methionine (an amino acid only used by bacteria) examples of?

A

Pathogen-associated molecular patterns (PAMPs)

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13
Q

What is the name given to the mechanisms used to identify damaged ‘self’ cells - which is similar to PAMPs?

A

DAMPs - damage-associated molecular patterns

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14
Q

What is the largest family of receptors that detect PAMPs?

A
  • members of the ‘Toll’ family, collectively known as ‘Toll-like receptors’ (TLRs). 10x TLRs in humans and are highly expressed by macrophages, dendritic cells and neutrophils.

TLRs (Toll-like receptors) are a molecular signalling cascade that signal through downstream effectors through downstream effectors, such as Jun/Fos transcription factors and ultimately change gene expression

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15
Q

Describe features of our blood?

A

Adults contain approximately 5 litres of blood made up of about 35 trillion cells
- Bone marrow makes around 5 billion new blood cells per day, 2.4 million a second.

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16
Q

What do myeloid white blood cells provide?

A

provide innate protection and lymphoid cells that generate adaptive immunity

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17
Q

What it is encompassed within the term leukocytes (white blood cells)?

A

includes both myeloid & lymphoid cells

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18
Q

What do myeloid cells do?

A

Myeloid cells such as macrophages and dendritic cells (both derived from monocytes) and neutrophils express TLRs (Toll-like receptors) - as well as other receptors that detect pathogen profiles.

19
Q

Why are cells activated?

A

Cells that are activated because they recognise a PAMP (pathogen-associated molecular pattern) secrete molecular ligands that attract additional cells of the innate immune system

20
Q

What does activation of myeloid cells lead to?

A
  • inflammation causing dilation of local blood vessels, pain, redness, heat & swelling
  • dilated blood 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 & cytokines
  • fever inhibit pathogen proliferation and speeds chemical reactions used by antimicrobial peptides, complement cascade etc.
  • response appropriate locally can be dangerous systemically (e.g. in response to sepsis). This is shock - loss of plasma volume crash of blood pressure, clotting & cytokine storm.
21
Q

What are 3 specialist phagocytic cells that can be recruited?

A
  • neutrophils
  • macrophages
  • eosinophils
22
Q

What are neutrophils?

A

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

23
Q

What are macrophages?

A

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

24
Q

What are eosinophils?

A

are specialists in attacking objects to large to engulf

25
Q

What are dendritic cells?

A

Specialist phagocytic cells derived from monocytes
- express a large variety of recognition receptors (e.g. TLR etc.)
- phagocytoses pathogens, cleaves into peptides which are bound to MHC (major histocampatibility complex)
- dendritic cells migrate to lymphoid tissues (e.g. lymph nodes), activate & stimulate lymphocytes of the active immune system

26
Q

What are key points of the adaptive immunity?

A
  • AI can generate highly specific responses to specific pathogens
  • AI can identify, target & destroy vast range of pathogens/toxins
  • BUT it is important to direct AI against foreign targets and NOT host ‘self’ molecules/protein
27
Q

How can accidental targeting of ‘self’ as ‘foreign’ can be bad?

A
  • harmless molecules also enter our bodies and don’t warrant a response
  • innate immunity plays a key role in recognizing targets to attack
  • inappropriately targeting harmless molecules can also cause trouble
28
Q

What do lymphoid cells do?

A

lymphoid cells (aka lymphocytes) generate adaptive immune response

29
Q

Where do lymphocytes develop?

A

Lymphocytes develop within the thymus & bone marrow (primarily 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

30
Q

Where are B-cells made?

A

Bone marrow

31
Q

Where are T-cells made?

A

Thymus

32
Q

What organs are involved in the adaptive immunity?

A
  • adenoid
  • tonsil
  • thymus
  • lymphatic vessels
  • lymph nodes
  • spleen
  • Peyer’s patches in small intestine
  • appendix
  • bone marrow
33
Q

What are features of 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 response
34
Q

What are features of the antibody response?

A
  • secreted soluble immunoglobulins of various types that bind to antigens
  • produced by B-lymphocytes and ultimately secreted by plasma cells
35
Q

What are the 3 types of T-cell responses?

A
  • Cytotoxic T-cells
  • Helper T-cells
  • Regulatory T-cells
36
Q

What do cytotoxic T-cells do?

A

directly kill infected host cells

37
Q

What do helper T-cells do?

A

activate macrophages, dendritic cells, B cells and cytotoxic cells, by secreting a variety of cytokines and displaying a variety of co-stimulatory proteins on their surface

38
Q

What do regulatory T-cells do?

A

Use similar strategies to inhibit the function of helper T-cells, cytotoxic T cells and dendritic cells

39
Q

How does adaptive immunity work?

A
  • at birth, the body contains and randomly generates a library of lymphocytes most of which remain dormant
  • when an antigen is presented (e.g. by dendritic cells of 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
40
Q

When does expansion occur?

A

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 respond to multiple antigens at once
- these are the principals underlying ‘booster’ vaccinations and combined vaccinations (e.g. MMR)

41
Q

Describe the lag and response times to the first & second immunizations

A
  • Lag time after second immunization is shorter
  • Response is shorter
42
Q

What is immune tolerance?

A
  • cells of the innate immune system use pattern recognition receptors such as Toll-like receptors to identify foreign antigens based on ‘known’ factors
  • 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 into a newborn host will survive and be ‘accepted’ as self. Future transplants from the same source will be treated as self & survive.

-e.g. skin graft from a brown mouse survives as the host mouse was injected with bone marrow cells from the brown mouse as a pup

43
Q

What are 2 experiments to show immune tolerance?

A

1) Knock out a gene encoding a ‘self’ protein - allow animal to grow, then reintroduce KOed self-protein. The host now mounts immune response as it hasn’t learnt this is self - shows host CAN mount attack against self-antigens.

2) Remove ‘self’ protein from adult animal - reintroduce after several months/years. The host now mounts immune response to remove proteins - i.e. the system can ‘forget’ what it has previously learnt

Advanced molecular & cell L2 (28 decks)

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