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MICB 3301 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Two branches of adaptive immunity

A
  • Cell-mediated
  • Humoral
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2
Q

B cells are associated with ______ immunity

A

B cells are associated with humoral immunity. B cells make antibodies

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3
Q

T cells are associated with ______ immunity

A

B cells are associated with cell-mediated immunity

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4
Q

Humoral branch of the adaptive immune system defends against?

A

extracellular pathogens (those that get into the blood)

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5
Q

Cell-mediated branch of the adaptive immune system defends against?

A

intracellular pathogens and cancer cells

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6
Q

Which branch of the adaptive immune system defends against cancer cells?

A

cell-mediated

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7
Q

Which branch of the adaptive immune system defends against extracellular pathogens?

A

humoral

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8
Q

Which branch of the adaptive immune system defends against intracellular pathogens?

A

cell-mediated

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9
Q

How is antibody diversity generated?

A

Rearrangement of antibody gene segments

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10
Q

Give an example of how antibody gene segments are rearranged?

A

V(D)J joining

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11
Q

What does V(D)J joining do?

A

mechanism of genetic recombination that occurs only in developing lymphocytes during the early stages of T and B cell maturation. It involves somatic recombination, and results in the highly diverse repertoire of antibodies/immunoglobulins (Igs) and T cell receptors (TCRs) found on B cells and T cells, respectively. The process is a defining feature of the adaptive immune system

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12
Q

What enzymes play a key role in V(D)J recombination?

A

Rag enzyme (recombination activating genes)

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13
Q

What is the order of genetic recombination of regions of the V(D)J gene?

A

The D and J segments are recombined first, then recombined to a V segment

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14
Q

What is the order of the regions of a processed V(D)J mRNA?

A

V-D-J-Constant region

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15
Q

When does V(D)J recombination occur?

A

Before infection while B cells develop in the bone marrow

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16
Q

How/when are V(D)J recombinants selected?

A

B cells and their unique antibodies are selected twice:

  • First, through clonal selection (occurs during development in bone marrow), where B cells that recognise “self” antigens are removed to prevent immune system attack on the bode
  • Second, through infection (occurs on infection in lymphoid organs and tissues), when the B cell antibodies are “selected” by the antigens if and when they bind them. Once this happens, proliferation occurs, forming a cloned colony of B cells with the antibody for that antigen
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17
Q

clonal selection

A

“self tolerance” or the removal of B cells that recognise self antigens

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18
Q

When are T cells activated?

A

When their receptors bind antigens presented by antigen-presenting cells (APC)

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19
Q

What cells make cytokines that activate B cells, macrophages, or other T cells?

A

Helper (CD-4+) T cells that bind to the MHCII of the APC

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20
Q

What cells kill other cells expressing foreign antigens?

A

cytotoxic (CD8+) T cells

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21
Q

helper T cell

A

Helper (CD4+) T cell

  • make cytokines that activate B cells, macrophages, or other T cells
  • recognise MHC II antigen presenters found on antigen-presenting cells (APCs) that display exogenous antigens, which are typically longer in length than those presented by MHC I. The helper T cells then help to trigger an appropriate immune response which may include localized inflammation and swelling due to recruitment of phagocytes or may lead to a full-force antibody immune response due to activation of B cells
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22
Q

cytotoxic T cell

A

Cytotoxic CD8+ T cells

  • kill cells expressing forieng antigens using perforins (form pores in their membranes) or granzymes (induce apoptosis)
  • recognise MHC I antigen presenters found on all nucleated cells in the body that desplay endogenous non-self antigens to the cytotoxic T cells
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23
Q

What is the ratio of progenitor B cells to antibodies produced?

A

High, one progentior B cell can make many lymphocytes, each with different specificity

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24
Q

cluster of differentiation molecules

A

cluster of differentiation (CD) molecules reside on immune cells like T cells and function as coreceptors and are used to determine a cell’s identity

  • helper T cells: CD4+
  • cytotoxic T cells: CD8+
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25
Q

When do T cell receptors bind antigens?

A

When presented to them by a major histocompatibility complex (MHC)

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26
Q

Where are T cell receptor genes rearranged?

A

the thymus

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27
Q

What is the MHC called in humans?

A

human leukocyte antigen (HLA)

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28
Q

How are MHC genes inherited?

A

Both genes from both parents are expressed, so each individual has two types of each MHC

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29
Q

What gene must be accounted for in organ transplants?

A

the major histocompatibility complex, the closer two people are related the more similar their HLAs (human leukocyte antigens)

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30
Q

major histocompatibility complex class I

A

found on all nucleated cells in the body that desplay endogenous non-self antigens to the cytotoxic (CD8+) T cells

Class I MHC molecules bind peptides generated mainly from degradation of cytosolic proteins by the proteasome. The MHC I:peptide complex is then inserted via endoplasmic reticulum into the external plasma membrane of the cell. The epitope peptide is bound on extracellular parts of the class I MHC molecule. Thus, the function of the class I MHC is to display intracellular proteins to cytotoxic T cells (CTLs). However, class I MHC can also present peptides generated from exogenous proteins, in a process known as cross-presentation

31
Q

major histocompatibility complex class II

A

found on antigen-presenting cells (APCs) that display exogenous antigens, which are typically longer in length than those presented by MHC I. Present to helper (CD4+) T cells

Loading of a MHC class II molecule occurs by phagocytosis; extracellular proteins are endocytosed, digested in lysosomes, and the resulting epitopic peptide fragments are loaded onto MHC class II molecules prior to their migration to the cell surface

32
Q

Describe the process by which a dendritic cell (an antigen-presenting cell) presents an antigen

A
  • Pathogen is taken up for degredation
  • Pathogen is taken apart inside the cell
  • Pathogen proteins are unfolded and cut into small pieces
  • Peptides bind to MHC II molecules and the complexes go to the cell surface
  • T cell receptors (plus CD4+) of helper T cell bind to the peptide:MHC complex on the dendritic cell
33
Q

Describe the process by which a nucleated cell presents an antigen

A
  • nucleated cells use the endogenous pathway for presentation. The non-self antigens are already present in the infected cell, so it associates with MHC class I and is transported to the surface
  • antigen:MHC I and T cell receptor (plus CD8+) recognise and bind, alerting the cytotoxic T cell to an infection
34
Q

pathogen

A

organism that produces disease

35
Q

opportunistic pathogen

A

organism that infects hosts with weakened (compromised) immune systems

36
Q

carrier

A

infected individual, potential source of infection

  • no obervable symptoms
37
Q

zoonoses

A

diseases transmitted to humans from animals

38
Q

vectors

A

organisms (usually insects) that transmit diseases to humans

  • mosquitos, ticks, fleas
39
Q

virulence factors or determinants

A

genetic, biochemical, structural features that contribute to virulence in a strain

40
Q

pathogenicity

A

ability to produce disease

41
Q

virulence

A

degree of pathogenicity (ability to produce disease)

42
Q

latency

A

refers to a phase where the pathogen stops producing but may become active again

43
Q

pathogenicity islands

A
  • large groups of genes that encode virulence determinants
  • present in virulent strains, absent in non-virulent strains
  • DNA base composition differs from the rest of the genome, often flanked by phage DNA which suggests regions are mobile and susceptible to horizontal gene transfer
44
Q

Definition:

organism that produces disease

A

pathogen

45
Q

Definition:

organism that infects hosts with weakened (compromised) immune systems

A

opportunistic pathogen

46
Q

Definition:

infected individual, potential source of infection

  • no obervable symptoms
A

carrier

47
Q

Definition:

diseases transmitted to humans from animals

A

zoonoses

48
Q

Definition:

organisms (usually insects) that transmit diseases to humans

  • mosquitos, ticks, fleas
A

vectors

49
Q

Definition:

genetic, biochemical, structural features that contribute to virulence in a strain

A

virulence factors or determinants

50
Q

Definition:

ability to produce disease

A

pathogenicity

51
Q

Definition:

degree of pathogenicity (ability to produce disease)

A

virulence

52
Q

Definition:

refers to a phase where the pathogen stops producing but may become active again

A

latency

53
Q

Definition:

  • large groups of genes that encode virulence determinants
  • present in virulent strains, absent in non-virulent strains
  • DNA base composition differs from the rest of the genome, often flanked by phage DNA which suggests regions are mobile and susceptible to horizontal gene transfer
A

pathogenicity islands

54
Q

how is virulence measured?

A

Two ways:

  • ID50 (infectious dose 50): number of pathogens required to cause clinical disease in 50% of hosts innoculated
  • LD50 (lethal dose 50): number of pathogens required to kill 50% of hosts innoculated
55
Q

number of pathogens required to cause clinical disease in 50% of hosts innoculated is called the

A

ID50

(infectious dose 50)

56
Q

number of pathogens required to kill 50% of hosts innoculated is called the

A

LD50

(lethal dose 50)

57
Q

Which strain is more virulent?

A

Strain A, the percent infected is higher with a smaller dose

58
Q

Breifly list the steps of the viral replication cycle

A
  • attatchment
  • entry
  • uncoating
  • genome replicaiton
  • gene expression
  • assembly
  • release (through budding)
59
Q

How do viruses attatch to host cells?

A

capsid and spike proteins mediate attatchment, ex: GP120 on HIV binds CD4 and CCR5 receptors of leukocytes

60
Q

What parts of the virion (virus particle) are visible, and where are they made?

A
  • capsid and spike proteins made by the virus
  • cell envelope from the infected host
61
Q

Hemagglutinin

A

a spike protein of a virus, in the case of influenza, hemagglutinin binds salic acid

62
Q

what type of virus is influenza?

A

a segmented RNA virus

63
Q

How do viruses spread?

A
  • viruses spread via blood, neuronal, or lymphatic systems, but because they have no flagella, their movements must be facilitated by the host
64
Q

viral tropism

A

Viruses and other pathogens affect what is called “host tropism”, “tissue tropism”, or “cell tropism”, or in which case tropism refers to the way in which different viruses/pathogens have evolved to preferentially target specific host species, specific tissue, or specific cell types within those species. Tropisms are usually named for the stimulus involved (for example, a phototropism is a reaction to sunlight) and may be either positive (towards the stimulus) or negative (away from the stimulus).

65
Q

compliment system

A

The complement system is a part of the innate immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear pathogens from an organism. It can be recruited and brought into action by the adaptive immune system.

The complement system is a signal cascade produced by cleaving blood serum precursors. End products achieve four functions:

Opsonisation – enhancing phagocytosis of antigens. C3b has most important opsonizing activity

Chemotaxis – attracting macrophages and neutrophils

Cell Lysis – rupturing membranes of foreign cells

Agglutination – clustering and binding of pathogens together (sticking)

66
Q

opsonin

A

An opsonin (from the Greek opsōneîn, to prepare for eating) is any molecule that enhances phagocytosis by marking an antigen for an immune response or marking dead cells for recycling.

Opsonisation is the molecular mechanism whereby molecules, microbes, or apoptotic cells are chemically modified to have stronger interactions with cell surface receptors on phagocytes and NK cells. With the antigen coated in opsonins, binding to immune cells is greatly enhanced. Opsonization also mediates phagocytosis via signal cascades from cell surface receptors.

67
Q

How do viruses evade the innate immune system?

A
  • block, breakdown compliment system (blood serum system of many proteins that recruits immune response and combats pathogens)
  • block interferon production (antiviral agents and immune system modulators made by T helper cells)
68
Q

How do viruses evade the adaptive immune responses?

A
  • block antigen procesing, MHC export (cells can’t present antigens to T cells)
  • evade antibodies through antigenic variation (amino acid changes in virion spikes, common in RNA viruses with high mutation rates, reason for new flu shots…)
69
Q

What are the mechanisms of bacterial pathogenicity?

A
  • Attatchment (with pili, EPS capsules)
  • Invasion and spread
  • Colonisation (establishing a site of microbial reproduction on or in the host)
  • Evading innate and adaptive immune responses
70
Q

multifactoral pathogenicity

A

Not relying on one virulence determinant is the key to being a sucessful pathogen!

71
Q

Methods of bacterial attachment

A

pili, capsules

72
Q
A
73
Q

capsules

A

capsules

examples:

  • Streptococcus pneumoniae*
  • Haemophilus influenzae*
  • Neisseria meningitidis*

Vaccines exist for these strains that attack the capsules

(Shown: mucoid strain of P. aeruginosa that produces capsules and is an opportinistic pathogen in burn and cystic fibrosis patients)

MICB 3301 (14 decks)

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