BIOL 435 Ch. 1 (Overview of the Immune System) Flashcards

1
Q

immunity

A

-state of protection against foreign pathogens or substances (antigens)
>sometimes not foreign (ex. cancer)
-“exempt”

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

observations of immunity

A
  • go back over 2000 years

- noticed that those recovered from the plague could safely nurse the currently ill

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

vaccination

A
  • prepares the immune system to eradicate on infectious agent before it causes disease
  • widespread use has saved many lives
    ex. rabies vaccination and eradication of small pox
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Louis Pasteur

A
  • ‘old’ (attenuated) bacteria into chickens and didn’t die

- could inoculate and prevent disease

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

virulation

A
  • dried puss into cuts

- became immune by getting a milder case

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

attenuation

A

-weakened strength or ability to cause disease

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

immune system components

A
  1. Innate
  2. Adaptive
    * don’t work independently
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

innate immunity

A

-very fast (minutes to hours)
-limited and fixed
-same response each time
Major components:
-barriers (eg. skin)
-phagocytes
-pattern recognition molecules
-can work independently

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

adaptive immunity

A

-slower response
-highly diverse and adapts
-different response each time (more rapid and effective)
-can’t work independently
-not in everyone
Major components:
-T and B lymphocytes
-antigen-specific receptors
-antibodies (Ab)

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

cooperatively

A
  • innate and adaptive immunity
  • activation of innate(+adaptive) produces signal molecules (cytokines and chemokines:’trail of bread crumbs’)
  • these molecules stimulate and direct adaptive immune responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

innate immune responses

A

-first line of defence
>fast, relatively nonspecific
-uses germ-line encoded (inherited) pattern recognition receptors (PRR)
-also uses phagocytic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PRR

A
  • pattern recognition receptors
  • bind to PAMPs
  • target something that will always be on pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PAMPs

A
  • pathogen-associated molecular patterns
  • generic molecules found on many different types of pathogens
  • eg. peptidoglycan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

adaptive immune responses

A
  1. Humoral responses (B-cells)
  2. Cell-mediated responses (T-cells)
    - slower to develop (5-6days)
    - use randomly generated antigen receptors
    - highly specified to individual antigen molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

randomly generated antigen receptors

A

-these bind to very specific antigens, rather than molecules found on many pathogens
>ex. bind to a single component of peptidoglycan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

memory

A
  • the hallmark of adaptive immunity

- NOT present in innate immunity

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

primary response (memory)

A
  • initiated upon first exposure to an antigen

- memory lymphocytes are left behind after antigen is cleared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

secondary response (memory)

A
  • initiated upon second exposure to the same antigen that stimulates memory lymphocytes
  • stimulation yields faster, more significant, better adaptive response
19
Q

humoral immunity

A
  • combats pathogens via antibodies (Ab)
  • Ab produced by B-lymphocytes
  • Ab can be transferred between individuals to provide passive immunity
20
Q

cell-mediated immunity

A

-involves primarily T lymphocytes

>can eradicate pathogens, clear infected self-cells or aid other cells in inducing immunity

21
Q

surface receptors

A
  • used in humoral and cell-mediated immunity
  • B-cell receptors (BCR)
  • T-cell receptors (TCR)
  • randomly generated by gene segment rearrangements in B and T cells (rearranging the DNA)
  • once released from membrane=Ab
22
Q

B-cells encounter antigen

A

-produce antibodies matching the specificity of their BCR

>cell membrane immunoglobin

23
Q

T-cell receptors

A

-bind specific peptides displayed on the surface of other cells
>peptides must be bound to special presentation molecules called MHC (self) and peptide (non-self)
-positive and negative selection

24
Q

individual B and T cells

A
  • have an individual specificity for a single antigen

- due to having many copies of a receptor on their surface that only binds to one type of antigen

25
Q

B- and T-cell interacts with unique antigen

A

-it is selected and becomes activated

>results in a proliferation (producing a large number of clones)

26
Q

each clone

A
  • reactive against the same antigen that initially stimulated the original lymphocyte
  • each produces antibodies and releases them to fight the pathogen
27
Q

4 major categories of pathogens

A

-viruses
-bacteria
-fungi
-parasites
*immune responses are quickly tailored to the type of organism involved
>depends on structure of pathogen and location

28
Q

SARS-CoV-2

A

-severe acute respiratory syndrome coronavirus 2

29
Q

tolerance

A
  • ensures that the immune system avoids destroying host tissue
  • helps keep anti-self recognition molecules (due to random rearrangement) from circulating in bloodstream
30
Q

negative selection process

A
  • cells too reactive to ‘self’ are culled

- important that it works, otherwise we get auto-immunity

31
Q

tolerance mechanisms

A
  • any cells or receptors that respond to self are eliminated
  • host should always know difference between self and non-self
  • danger/damage vs. safe (not as much self vs. non-self)
32
Q

dysfunctions of immunity categories

A
  1. Overly active

2. Immunodeficiency

33
Q

overly active

A
  • or misdirected immune response
  • allergies
  • asthma
  • autoimmune disease (eg. MS, Crohn’s)
34
Q

immunodeficiency

A
  • primary loss of immune function (genetic)

- secondary loss of immune function (acquired)

35
Q

secondary (acquired) loss of immune function

A
  • opportunistic infections can occur in people with impaired immune responses
    ex. oral thrush and HIV
36
Q

transplanted tissues

A
  • a rare case where we want to AVOID an immune response
  • don’t want rejection
  • body’s natural response to foreign tissue is to attack it and destroy it
37
Q

cancer

A
  • situation where the dangerous cells we want to target are our own self-cells
  • generally tolerated and hard to generate immunity against
38
Q

the microbiome

A
  • community of commensal organisms that live in and on us the cause no harm
  • function in homeostasis (metabolic and immune balance)
39
Q

imbalance or dysbiosis

A
  • leads to immune overstimulation resulting in inflammation

- due to dietary changes or environmental factors (ex. stress)

40
Q

inflammation

A
-cause of many things
>CVD
>diabetes
>obesity 
>allergies
41
Q

symbiosis

A

-gut barrier integrity
-gut-brain-immune homeostasis
>balanced immune function
>neurologic homeostasis
>metabolic regulation

42
Q

antigen (Ag)

A
  • any molecule that will specifically stimulate B- and T- cells and produce an adaptive immune response
  • general: anything that produces an immune response
43
Q

humoral

A

-blood borne

44
Q

passive immunity

A
  • not very long
  • not as good as active immunity
    ex. injecting antibodies into a human to treat a snake bite