Brainscape's Knowledge GenomeTM

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


See full index

BIOL 2005 > (Lectures 14-15, Chapter 17) Immune System > Flashcards

(Lectures 14-15, Chapter 17) Immune System Flashcards

1
Q

What do pathogens do in the body? What are some examples (types) of pathogens?

A

They activate immune responses.

Bacteria, viruses, fungi, parasites

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

Virulence

A

Ability of a pathogen to cause disease

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

What does immunity rely on to function?

A

Antigens; proteins, lipids, etc. on the pathogen that the body recognizes as foreign. The immune function recognizes/targets the antigen, which leads to attacking the pathogen.

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

Characteristics of innate immunity

A
  • Nonspecific; response is the same regardless of the type of pathogen
  • Present from birth
  • Prevents approach/denies entry/limits spread of microbes and environmental hazards
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do nonspecific defenses rely on to attack pathogens?

A

Pathogen-associated molecular patterns (PAMPs), which are found on pathogens

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

What binds to PAMPs, starting the immune response?

A

Pattern recognition receptors (PRRs), found on interferons and natural killer (NK) cells

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

What are the primary barriers of the immune function?

A
  • Skin; tightly-packed epithelial cells, layers are always shed/regenerated, outer layer consists of dead cells
  • Sebaceous glands in the inner layers of skin make it oily and unfavourable for pathogens
  • Mucous membranes; mucous is very viscous and traps foreign matter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When does the 2nd line of defense work against pathogens?

A

After the first line is breached, they try to create an inhospitable environment for pathogens

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

Antimicrobial substances + examples

A
  • discourage microbial growth

- e.g. interferons, complements, iron-binding/antimicrobial proteins

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

Phagocytes

A
  • Intake pathogens and destroy them
  • Adhere to pathogens (PAMP/PRR) and ingest them
  • Pathogen is digested and killed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Phagosome

A
  • Lipid body in which a digested pathogen is packaged

- Combines with a lysosome, which has enzymes that act upon the pathogen

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

What is inflammation?

A

The accumulation of proteins, lipids, and phagocytes at a site of invasion/injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Steps of Inflammation

A
  1. Macrophages engulf debris and foreign matter
  2. Capillaries dilate due to release of histamine, increasing their permeability (proteins and fluid diffuse out and to the site of the injury)
  3. Foreign matter is contained
  4. More leukocytes migrate to the area
  5. Leukocytes clear the infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do clotting proteins do? Why is this important?

A

Clotting proteins prevent breaches by other pathogens, which allows the immune function to deal with just the current infection/injury.

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

Do all of the leukocytes involved in inflammation have the same purpose?

A

No; some are involved with the digestion of foreign matter, others signal to recruit more leukocytes to the area

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

T/F: Overall, inflammation is a very quick process, and the return to normal occurs soon after an infection.

A

False; while it starts quickly, the return to normal is slow.

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

Fever

A

Temporary rise in body temperature in response to an infection, which creates an unfavourable environment for pathogens.

  • Intensifies effects of interferons
  • Inhibits microbe growth
  • Speeds up body reactions that aid repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Regarding fevers, what are two things that can be dangerous to us?

A
  • Prolonged fever

- Body temperature above 40.5C

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

Interferons

A

Slow the spread of viral infection by interfering with viral replication.

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

How do interferons work? (steps)

A
  1. Virus-infected leukocyte produces interferons and releases them before dying
  2. Interferons bind to nearby cells, which start producing antiviral proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

T/F: the antiviral proteins produced after interferons bind to cells prevent the entry of viruses into the cell.

A

False; they affect viral replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Natural Killer (NK) Cells

A
  • Non-specifically target infected and cancerous cells
  • NK cells produce and release granzymes that then release perforin
  • Perforin attaches to the plasma membrane of target cells, creating pores that make it leaky/unstable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why does the creation of pores in the plasma membrane of target cells by perforin end up killing the cells?

A

No more homeostatic balance; internal environment is no longer separated from the external environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Complement System

A

Complements (proteins) bind to antibody proteins that are bound to pathogens, complementing the response of the latter by creating a protein cascade. This makes is easier for phagocytes to find and destroy pathogens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where are complements found?

A

Circulating in the blood plasma, in an inactive state.

26
Q

Characteristics of adaptive immunity

A
  • Selective for target; protects against specific threats
  • Develops/adapts after antigen exposure, becomes stronger w/subsequent exposure (i.e. uses “learned” defenses)
  • Engages after innate immunity starts/innate defenses are breached
  • Dependent on activity of lymphocytes (B and T cells)
27
Q

T/F: B and T cells form in the bone marrow, and emerge from it fully mature.

A

False: this is only true of B cells. T cells go to the thymus and mature there.

28
Q

Immunocompetence

A
  • Ability to adapt and respond to various pathogens
  • Cells can modify response based on the pathogens they encounter
  • Cells start expressing receptors, letting them recognize pathogens through antigens
  • Gained by B/T cells once they mature
29
Q

Antibody-Based/Humoral Immunity

A
  • B cells produce plasma cells

- Plasma cells secrete antibodies that attack pathogens in body fluids outside the cell

30
Q

Cell-Based Immunity

A

T cells defend against pathogens by lysing (killing/breaking up) infected body cells

31
Q

What are 4 characteristics that are shared by antibody- and cell-based immunity?

A
  • Specificity
  • Diversity
  • Memory
  • Self-Tolerance
32
Q

Clonal Selection

A
  • Lymphocyte proliferates and specializes to a specific antigen
  • When a pathogen first invades, its antigens outnumber the T/B cells that can recognize them because cells have yet to adapt
  • Once a lymphocyte gets a copy of an antigen, it’s stimulated to produce more lymphocytes for the same antigen
  • Process is slow to start
33
Q

In clonal selection, do all T cells attack the pathogen?

A

No; some form memory cells that stimulate T cell production if the antigen returns. The ones that attack the pathogen are effector cells.

34
Q

What happens to effector cells (T cells) that attack pathogens?

A

They die/are eliminated from the body after the antigen is dealt with

35
Q

What are two characteristics of antigens?

A
  1. Immunogenecity: ability to provoke an immune response by stimulating antibody production
  2. Reactivity: antibodies bind specifically to the antigen(s) that provoked them
36
Q

T/F: all antigens are proteins

A

False; can be any substance that the body recognizes as foreign

37
Q

Epitopes

A
  • Parts of an antigen

- Recognition sequences (i.e. binding regions for immune cells)

38
Q

How are antigens involved in the immune response?

A
  • Antigens are processed by immune cells and expressed on their membranes
  • Other cells are then able to recognize the antigen (i.e. something that’s foreign to the body)
39
Q

What’s the difference between adaptive natural immunity and adaptive artificial immunity?

A

Natural immunity is gained from/produced by the human body, while artificial immunity is gained from outside sources.

40
Q

Give an example of:

  1. Passively-gained natural immunity
  2. Actively-gained natural immunity
  3. Passively-gained artificial immunity
  4. Actively-gained artificial immunity
A
  1. Breastfeeding or from the womb
  2. Immune response from direct exposure to a pathogen (e.g. chicken pox rashes)
  3. Injection with antibodies (e.g. antivenom)
  4. Vaccination - receiving antigens (dead/attenuated pathogens) to stimulate antibody production
41
Q

T/F: once produced, antibodies last in the body forever

A

False; they’re proteins, so they degrade after some time

42
Q

Describe antibody concentrations over time in passively- and actively-gained immunity.

A

Passively-Gained: starts with high antibody count, but it drops over time
Actively-Gained: there are little/no antibodies until B cells start producing them

43
Q

Between the primary and secondary response to pathogen exposure, which is faster/stronger?

A

Secondary response

44
Q

Features of adaptive immunity - specificity

A
  • Comes from antigens, which stimulate B cells to generate antibodies
  • Antibodies have binding sites for pathogens and B/T cells
  • B cells make/release antibodies + express them on their membranes
  • T cell receptors (TCRs) on T cell membranes have antigen binding sites
  • TCRs are for targeting/processing; they are NOT secreted
45
Q

Features of adaptive immunity - diversity

A
  • there are millions of antigens that lymphocytes can recognize; lymphocyte proliferates and differentiates after interacting with an antigen (clonal selection!)
46
Q

Effector Cells (immune system)

A

Short-lived lymphocytes that directly attack antigens and secrete antibodies

47
Q

Memory Cells

A

Long-lived lymphocytes that carry antibodies for a specific antigen on their membranes

48
Q

Features of adaptive immunity - memory

A
  • (faster, stronger, longer-lasting) Immune response can be produced when secondary exposure to an antigen occurs
  • this is due to memory cells, which are inactive during the primary response
49
Q

Features of adaptive immunity - self-tolerance

A
  • B/T cells only attack cells/pathogens that are recognized as not-self (i.e. not part of the body)
  • tolerance lasts as long as exposure continues
50
Q

What kind of diseases arise from the failure of self-tolerance?

A

Autoimmune diseases

51
Q

What is another name for antibodies?

A

Immunoglobins (Ig)

52
Q

T/F: Antibodies are Y-shaped, with antigen-binding sites on their two ‘arms’

A

True

53
Q

Five antibody classes

A
  1. IgM (large pentamer, good for clumping things together)
  2. IgA (found in mucous and other secretions)
  3. IgD (found on B cells, acts as antigen receptor)
  4. IgG (most abundant, involved in primary + secondary immune responses)
  5. IgE (involved with release of histamine/mast cells in the allergic response)
54
Q

T/F: Antibodies do not destroy antigens

A

True: they inactivate/tag them instead

55
Q

5 defense mechanisms used by antibodies

A
  1. Neutralization
  2. Agglutination
  3. Precipitation
  4. Complement Fixation/Activation
  5. Opsonization
56
Q

Antibody defense mechanisms - neutralization

A
  • Antibodies prevent antigens from binding to receptors on tissue cells by blocking sites on pathogens
  • leads to phagocytosis of antigen-antibody complex
57
Q

Antibody defense mechanisms - agglutination

A
  • Cross-linking of antigen-antibody complexes into large, lattice-like clumps (recall that each antibody has two arms with regions to bind antigens)
  • Pathogens are ‘disabled,’ making it easier for phagocytes to find and engulf them
58
Q

Antibody defense mechanisms - precipitation

A
  • Soluble molecules (not cells) are cross-linked into complexes, which then precipitate out of solution
  • Easier for phagocytes to engulf them
59
Q

Antibody defense mechanisms - complement fixation/activation

A
  • Main antibody defense against cellular antigens (e.g. bacteria, mismatched RBCs)
  • Many antibodies bind close together on an antigen, with the binding sites on their stem regions aligned
  • Alignment of complement-binding sites on stem regions triggers complement fixation, which causes cell lysis, etc.
  • e.g. amplification of inflammatory response, opsonization
60
Q

Antibody defense mechanisms - opsonization

A
  • Pathogens are coated by opsonins (proteins), making it easier for phagocytes to engulf/destroy them
  • Antibody binding opsonizes a pathogen
61
Q

What is immunological surveillance?

A

The ability to identify tumour-specific antigens and destroy cancer cells.

BIOL 2005 (8 decks)

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