Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

what is required of immune system for optimal effectiveness?

A

a balanced immune system (not over reaction = allergies but not under reaction = cancer)
which means:
- protection from pathogens
- elimination of abnormal host cells (like cancerous cells, when you have weakened immune system e.g. HIV, you’re more vulnerable to cancers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is immune system?

A
  • pre-programmed system to distinguish “self” and “non-self” moelcules
    AND/OR
  • identifying “danger” signals (from acute inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what happens if immune system goes wrong in response to INTERNAL threat and OVER-reacts?

A

Auto-immune problems like type 1 diabetes, rheumatoid arthritis, multiple sclerosis etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what happens if immune system goes wrong in response to INTERNAL threat and UNDER-reacts?

A

cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what happens if immune system goes wrong in response to EXTERNAL threat and OVER-reacts?

A

Allergic reaction like hay fever, eczema, asthma, sinusitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what happens if immune system goes wrong in response to EXTERNAL threat and UNDER-reacts?

A

Infection like viruses, bacteria, funghi, parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do pathogens enter the body?

A
  • digestive system
  • respiratory system
  • urogential system
  • skin damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the routes in the body for pathogens?

A

-circulatory system
-lymphatic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the most important barrier to infection?

A

skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe the physical properties of the skin barrier?

A
  • composed of tightly packed, highly keratonised multi-layered cells
    -constantly undergo renewal & replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the physiological factors of skin (barrier)?

A
  • low pH of 5.5
    -low oxygen tension (lots of pathogenic organisms are aerobic so rely on oxygen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why do sebaceous glands help skin be a barrier to infection?

A
  • secrete hydrophobic oils
    -lysozyme (chemical secretion)
    -ammonia
    -antimicrobial peptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do epithelial cells that line tracts secrete?

A

mucous - continuously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where are mucous membranes found?

A

all body cavities that meet the environment = respiratory, gastrointestinal, urogenital tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is mucous membrane?

A
  • physical barrier to trap invading pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does secretory IgA do?

A

it’s in mucous membrane and prevents bacteria & viruses attaching to and penetrating endothelial cells (by neutralisation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is in mucus that directly kills invading pathogens?

A
  • lysozyme
    -defensins
    -antimicrobial peptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does lactoferrin in mucus do?

A

acts to starve invading bacteria of iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does cilia in mucus do?

A

directly trap pathogens and contribute to removal of mucous, assisted by physical manoeuvres such as sneezing and coughing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is likely to happen if no cilia?

A

susceptible to lung infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is innate immunity?

A
  • a general response to any pathogen (generic protective response).
    -same response every time irrespective of particular species.
  • present from birth, genetically encoded.
    -activate by ability to distinguish between self & non-self
  • no immunological memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is acquired immunity?

A
  • always tailored to specific immune system (tailored to specific e.coli strain)
    -unique response developed individually so it takes time for unique response to be created, so this one takes longer than innate
    -immunological memory so second response quicker
    -self regulating, through regulatory T cells
23
Q

what are commensal bacteria?

A
  • “friendly” bacteria
    -100 trillion bacteria normally reside at epithelial surfaces
  • 500 different microbial species
  • symbiotic relationship with the host
24
Q

constitutive barriers are effective until breached… in what ways can they be breached?

A
  • wounds
    -burns
    -bites
    -catheters
    -protein pump inhibitors
    -anti-microbial wipes (too clean)
25
Q

what are components of acquired immunity?

A

soluble factors
= cytokines & antibodies
Immune cells
= B & T cells

26
Q

what are components of innate immunity?

A

natural & physical barriers

soluble factors
=cytokines, acute phase proteins, inflammatory mediators, complement proteins

immune cells
= macrophages, mast cells, NK cells, neutrophils

27
Q

what is function of macrophages?

A

= phagocytosis (like pacman)
= releases both pro/anti inflammatory mediators
= bacterial killing mechanisms
= antigen presentation
= wound healing/ tissue repair

28
Q

what is function of mast cells?

A

(they eat things that are too big for macrophages and release toxic granules that attack & kill parasites)
- pro-inflammatory
-parasitic killing mechanism
- linked to allergy & asthma

29
Q

what is function of NK cells?

A

natural killer cells
- killing of virally infected cells
- killing of cancer cells

30
Q

how do cells recognise pathogens?

A

pathogens express signature molecules that are not found on/in human cells
= PAMP’s (pathogen associated molecular patterns)
- these are common to many different pathogenic species

31
Q

what are PRR’s?

A

Pattern-recognition receptors = found on cell surface & in cytosol for detection of intra/extracellular pathogens
-> innate immune cells (and some other types) express PRR’s as partner receptor to PAMP’s

32
Q

what are ingested by macrophages?

A

extracellular bacteria & funghi (later ingested by neutrophils)

33
Q

what are the modes of ingestion?

A
  1. pinocytosis
  2. receptor mediated endocytosis
  3. phagocytosis
34
Q

what is pinocytosis?

A

mode of ingestion
= Ingestion of fluid surrounding cells

35
Q

what is receptor-mediated endocytosis?

A

mode of ingestion
=Molecules bound to membrane receptors is internalized.
=An important step in the generation of adaptive immunity.

36
Q

what is phagocytosis?

A

mode of ingestion
=Intact particles (e.g. bacteria) are internalized whole.
These are facilitated by “Opsonisation” (tagging of foreign objects)

37
Q

describe phagocytosis

A
  1. macrophages & neutrophils expressed as a set of PRR’s
  2. receptor binding to PAMP’s signals the formation of a phagocytic cup
  3. cup extends around target and pinches off, forming a phagosome
  4. fusion with lysosomes to form a phagolysosome - killing of pathogens and degredation of contents
  5. Debris (including antigens) is released into extracellular fluid
  6. Pathogen-derived peptides are expressed on special cell surface receptors (MHC-II molecules)
  7. Pro-inflammatory mediators are released (e.g. TNFα)
38
Q

what is opzonization?

A

the coating of pathogens by soluble factors (opsonins) to enhance phagocytosis
(macrophage can recognise & respond twice as effectively)

39
Q

what are example of opsonins?

A

-C3b
-C-reactive protein (CRP)
-IgG/IgM antibiodies

40
Q

how are mast cells activated?

A

by danger signals from tissue damage

41
Q

what do mast cells do in response to danger signals?

A

they degranulate and release pre-formed pro-inflammatory contents of granules (like histamine) & production of new pro-inflammatory substances (leukotrienes & prostaglandins)

42
Q

what are physiological signs of acute inflammation?

A
  • dilation of small blood vessels so increased blood flow & cell accumulation & increased cell metabolism
    = redness (rubor) and heat (calor)

-permeability of post-capillary venules (fluid accumulates in extracellular spaces)
= swelling (tumor)

nerve damage
= loss of function & pain

43
Q

what are white blood cells activity in healthy tissue?

A
  • they’re constantly flowing through at high speed through post capillary venules
    -no inflammatory mediators
    -normal vasculature
    -circulating neutrophils
44
Q

Describe inflammation response

A
  • vasodilation & gaps in endothelial cells allow cells & molecules to be carried in the circulatory system to escape inflamed tissue
    -pro-inflammatory stimuli increase (slows down blood flow & slows white blood cells to allow more time to bind & attach)
    -recruitement & activation of neutrophils (trans-endothelial migration)
    -bacteria & innate immune response cells produce chemical signals that attract neutrophils to site of infection
45
Q

what is the process of trans-endothelial migration?

A
  1. margination (adhesion) of neutrophils to endothelium near sites of tissue dmage/infection
  2. binding of neutrophils to adhesion molecules (selectins & ICAM-1) on the endothelial cells
  3. migration of neutrophils across endothelium
  4. movement of neutrophils within tissue via chemotaxis (take to site of infection)
  5. activation of neutrophil by PAMP and TNF alpha (cytokine produced by macrophage)
46
Q

what are the 3 ways neutrophils kill?

A
  1. phagocytosis
  2. degranulation
  3. NET’s
47
Q

describe phagocytosis of neutrophils

A

-1.in infected tissues, pathogens release chemical signals that attract neutrophils
2.neutrophils use PRR’s to recognise PAMPs and bind to & phagocytose pathogens
3.they then kill pathogens via 2 distinct mechanisms: phagolysosomal killing & ROS-dependant killing (oxidative burst)

48
Q

describe phagolysosomal killing?

A
  1. bacterium is phagocytosed by neutrophil
  2. phagosome fuses with specific granules & azurophilic granules
  3. pH of phagosome rises, antimicrobial response is activated & bacterium killed
  4. pH of phagasome decreases, fusion with lysosomes allow acid hydrolases to degrade bacterium completely
49
Q

describe ROS-dependant killing

A

= production of toxic reactive oxygen species, ROS (oxidative burst)
1. neutrophil activation (PAMPs, pro-inflammatory cytokines)
2. assembly of NADPH oxidase complex
3. production & release of ROS into phagolysosome

50
Q

what is degranulation?

A

release of anti-microbial proteins from neutrophil,basophils or mast cells granules directly into extracellular milieu
= direct killing of extracellular pathogens (bacteria & funghi)
= tissue damage & (potentially) systemic inflammation

51
Q

what is NET form of pathogen killing?

A

Neutrophil extracellular traps (NETs) are made of a network of extracellular strings of DNA& enzymes that surround and trap pathogenic microbes.
-described as neutrophil suicide
-neutrophils are short lived and undergoe NET as last resort
-build up causes pus - yellow/green colour due to iron as cofactor

52
Q

what are interferons alpha/beta (IFN alpha/beta)?

A

cytokines produced & released by virally infected cells

53
Q

what is function of interferon alpha/beta?

A

they can:
1. signal neighbouring uninfected cells to destroy RNA & reduce protein synthesis
2. signal neighbouring infected cells to undergo apoptosis
3. activate immune cells e.g. NK cells

54
Q

how do natural killer cells know to ONLY kill virally infected cells?

A
  • every cell in body expresses MHC class 1 and protein (peptide) can bind to MHC class 1 and be displayed
  • so NK moves around our tissue, it’s first response is to kill target cell so healthy cell has to tell NK “I’m healthy don’t kill me”
  • ligand receptor interaction sends inhibitory signal that inhibits NK response
  • so in infected cell or cancer cell - they don’t have MHC class 1 so no ligand receptor interaction so NK stays as killing cell (not inhibted) and by default it kills

Immunology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions