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Microbiology > Chapter 17- Exam 3 > Flashcards

Chapter 17- Exam 3 Flashcards

1
Q

Defenses against any pathogen

A

innate immunity

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2
Q

Induced resistance to a specific pathogen

A

adaptive immunity

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3
Q

Describe the story of how Louis Pasteur discovered immunity

A

Made numerous advances in microbiology and immunology. Told his assistant to inoculate some
chickens with chicken cholera while he left for vacation.
The assistant went on vacation himself and didn’t inoculate the chickens until he got back.
The the month-old bacterial culture made the chickens only a little ill, but also made them immune to
chicken cholera.

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4
Q

Emil Von Behring (1854-1917)

A

“savior of children” Won the first Nobel Prize in Physiology or Medicine. Discovered that bacterial toxins
generated the production “antitoxins” in serum. Antitoxin sera mixed with toxin could be given to prevent diphtheria, a common cause of
childhood death.

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5
Q

Paul Ehrlich (1854-1915)

A

A pioneer in microbiology and immunology
A friend of Koch and collaborator
He determined that the body produces an excess of
antitoxins which last beyond the initial exposure.
He called this “immunization”. Antitoxins turned out to be antibodies.

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6
Q

Michael Heidelberger (1888-1991)

A

“The Father of Modern Immunology”
A chemist showed that antigens of pneumococcus are
polysaccharides. Showed that antibodies are proteins.

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7
Q

Gerald Edelman (1929- 2014)https://www.brainscape.com/packs?makeflashcards=true

A

Nobel Prize, 1972

Worked out the general structure of antibodies

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8
Q

Susumu Tonegawa

1939-

A

Nobel Prize, 1987
Worked out how genes in B cells produce the many
different antibodies to virtually any antigen.

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9
Q

Serology

A

The study of reactions between antibodies and antigens

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10
Q

Antiserum

A

The generic term for serum that contains antibodies

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11
Q

Globulins

A

serum proteins

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12
Q

Gamma (γ) globulin

A

serum fraction containing antibodies

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13
Q

Immunoglobulins (Ig)

A

antibodies

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14
Q

Hematopoeisis

A

making blood cells

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15
Q

Immunoglobulins, or antibodies, are among the _______ globulins.

A

gamma

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16
Q

A single antigen may possess multiple ________ _________ (_________).

A

antigenic determinants (epitopes)

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17
Q

A substance that causes the body to

produce specific antibodies or sensitized T cells

A

antigen

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18
Q

Typically what is the biochemical make up of an antigen?

A

typically a protein or polysaccharide, >10kD in size

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19
Q

interact with epitopes or antigenic determinants

A

antibodies

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20
Q

What is a hapten?

A

An antigen too small to be recognized by
the immune system that can be recognized when
combined with a carrier protein.

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21
Q

_________ is not immunogenic on its own. It covalently attaches to proteins in the blood, and the combination makes it recognizable by the immune system.

A

Penicillin

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22
Q

What is the carrier molecule for penicillin?

A

albumin

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23
Q

What is KLH?

A

Keyhole Limpet Hemocyanin: Keyhole limpet hemocyanin (KLH) is a large, multisubunit, oxygen-carrying, metalloprotein that is found in the hemolymph of the giant keyhole limpet (marine mollusc). Haptens can be coupled to KLH using several methods.The KLH protein is potently immunogenic, but does not cause an adverse immune response in humans. It is therefore highly prized as a vaccine carrier protein. Because of its size and glycosylation, KLH protein cannot be reproduced synthetically; it is available only as a purified biological product from the keyhole limpet Megathura crenulata.

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24
Q

________ are covalently linked to the carrier

protein

A

Haptens

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25
Q

Each _________ produces a unique antibody

A

B-cell

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26
Q

generate unique antibody genes in each cell

A

chromosomal rearrangement

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27
Q

random combinations of gene segments generate a different ___ chain and ___ chain in each B cell

A

L and H

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28
Q

How do antibodies differ from each other? What are the main classes of antibodies?

A 
Different antibody classes differ in the constant
region of the heavy chain, two of which form the Fc
portion of the antibody molecule. 
IgG
IgM
IgA
IgD
IgE
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29
Q

IgG Antibodies

A
  • Monomer
  • 80% of serum Abs
  • Fix complement
  • In blood, lymph, and intestine
  • Cross placenta
  • Enhance phagocytosis; neutralize toxins and viruses; protects fetus and newborn
  • Half-life = 23 days
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30
Q

IgM Antibodies

A
  • Pentamer
  • 5–10% of serum Abs
  • Fix complement
  • In blood, in lymph, and on B cells
  • Agglutinates microbes; first Ab produced in response to infection
  • Half-life = 5 days
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31
Q

IgA Antibodies

A
  • Dimer
  • 10–15% of serum Abs
  • In secretions
  • Mucosal protection
  • Half-life = 6 days
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32
Q

IgD Antibodies

A
  • Monomer
  • 0.2% of serum Abs
  • In blood, in lymph, and on B cells
  • On B cells, initiate immune response
  • Half-life = 3 days
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33
Q

IgE Antibodies

A
  • Monomer
  • 0.002% of serum Abs
  • On mast cells, on basophils, and in blood
  • Allergic reactions; lysis of parasitic worms
  • Half-life = 2 days
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34
Q

How does class switching work?

A

A single B-cell can produce different classes of antibodies over time. More DNA recombination causes the switch from one Ig class to another.

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35
Q

Can B cells keep their antigen specificity even if they class switch?

A

Yes. B cells can switch Ig class and keep their antigen specificity.

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36
Q

All ________ B cells express antibodies on their

surface.

A

mature

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37
Q

What happens to B cells that make autoantibodies?

A

they are eliminated

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38
Q

What happens to B cells that don’t immediately interact with antigens?

A

Some do not immediately interact with antigens
and survive.
Some later encounter antigen.

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39
Q

What happens to B cells that interact with

T cells?

A

If those that have encountered antigen are

activated by T-cells, they proliferate.

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40
Q

What happens to proliferating B cells?

A

They become plasma cells or become memory B cells

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41
Q

__ cells activate __ cells to secrete Ab. Based on what conditions?

A

T cells; B cells
The B cell is activated to secrete antibodies only if it
and a T cell can recognize the same antigen.

42
Q

Clonal deletion vs. Clonal selection

A

deletion: eliminates harmful B cells
selection: expands active B cells

43
Q

Can B cells be activated without a T cell?

A

Yes, Sometimes B cells may be activated without help
from T cells. For example, a polysaccharide can be a T independent antigen that binds its epitopes to the B cell receptors.

44
Q

What is another name for B cell receptors?

A

membrane bound antibodies

45
Q

Once the antigen epitope is recognized by the antibody, what cellular responses can occur?

A
  • Agglutination
  • Opsonization
  • Complement fixation
  • Antibody-dependent cell-mediated immunity (ADCC)
  • Neutralization
46
Q

Agglutination

A
  • reduces number of infectious units to be dealt with
  • a reaction in which particles (as red blood cells or bacteria) suspended in a liquid collect into clumps and which occurs especially as a serological response to a specific antibody.
  • Agglutination is the process that occurs if an antigen is mixed with its corresponding antibody called isoagglutinin.
47
Q

Opsonization

A
  • coating an antigen with antibodies enhances its phagocytosis
  • Opsonization is a term that refers to an immune process where particles such as bacteria are targeted for destruction by an immune cell known as a phagocyte .
  • The process of opsonization is a means of identifying the invading particle to the phagocyte.
48
Q

Complement fixation

A
  • causes inflammation and cell lysis
  • the process of binding serum complement to the product formed by the union of an antibody and the antigen for which it is specific
  • occurs when complement is added to a mixture (in proper proportion) of such an antibody and antigen.
49
Q

Antibody-Dependent Cell-Mediated Immunity

A
  • antibodies attached to target cell cause destruction by macrophages, eosinophils, and NK cells
  • This process is carried out by macrophages, eosinophils, and Natural Killer (NK) cells
50
Q

Neutralization

A
  • blocks adhesion of bacteria and viruses to the mucosa
  • blocks attachment of the toxin
  • the ability of specific antibodies to block the site(s) on viruses that they use to enter their target cell.
51
Q

what is the dual nature of adaptive immunity?

A

It is divided into 2 parts, each responsible for dealing with pathogens in different ways. Humoral immunity (antibody-mediated immunity) is directed at freely circulating pathogens and depends on B cells. Cellular immunity, also called cell-mediated immunity depends on T cells to eliminate intracellular pathogens, reject foreign tissue recognized as non-self, and destroy tumor cells. These two systems function interdependently to keep the body free of pathogens.

52
Q

Where do T cells mature?

A

In the thymus

53
Q

How do T cells respond to antigen?

A

T cells respond to antigen by T-cell receptors

(TCRs), the T cell version of antibodies.

54
Q

What is the other cell type that works in conjunction with T cells?

A

T cells require antigen-presenting cells (APCs)

55
Q

What MUST T cell receptors interact with?

A 
T cell receptors must interact with Major
Histocompatibility Complex (MHC) molecules
56
Q

What are some examples of professional antigen presenting cells?

A

B cells
Dendritic cells
Macrophages

57
Q

What organism is MHC found on? What does MHC stand for?

A

Mouse: Major Histocompatibility Complex

58
Q

What organism in HLA found on? What does HLA stand for?

A

Human: Human Leukocyte Antigens

59
Q

What are MHC and HLA?

A

Transmembrane cell surface proteins that hold

antigens for presentation

60
Q

What is responsible for transplant rejection?

A

Different MHC between the donor and recipient

61
Q

T cell that activate the antibody response

A

T Helper Cells (TH) (CD4+)

62
Q

T cell that directly target host cells

A

T Cytotoxic Cells (TC) (CD8+)

63
Q

T cell that keep the immune system in check

A

T Regulatory Cells (TReg)

64
Q

T Helper Cells

A

CD4+ or TH cells activate B cells
TCRs recognize antigens with MHC class II on antigen presenting cells (APCs)
TH cells produce cytokines and differentiate into
−TH1 cells (Type 1 TH cells)
−TH2 cells (Type 2 TH cells)
−TH17 cells
−Memory T cells

65
Q

What type of interferon do TH1 cells produce?

A

TH1 cells produces IFN-γ (gamma interferon)

66
Q

What is the function of IFN-γ (gamma interferon)?

A

which activates cells related to cell-mediated
immunity, macrophages, and antibodies; effective
against intracellular pathogens

67
Q

What do TH2 cells activate?

A

TH2 cells activate eosinophils and B cells to

produce IgE

68
Q

What is the function of IgE production?

A

important in allergic reactions;

effective against helminths (worms)

69
Q

What do TH17 cells produce?

A

TH17 cells produce large amounts of cytokine IL-17

70
Q

What is the function of IL-17?

A

recruit neutrophils, and work against certain

extracellular bacteria and fungi

71
Q

Describe the process of activating Helper T cells

A
  • Antigen Presenting Cell (APC) encounters antigen
  • APC processes antigen protein into short peptide
    fragments
  • APC presents antigen fragment with MHC II
  • TH cell encounters APC presenting antigen
  • TCR recognizes antigen fragment with MHC II
  • co-stimulatory signal is needed to activate T cells that have not previously encountered antigen
  • TH cell is activated and produces cytokines
72
Q

examples of APCs

A

B cells, Dendritic cells, Activated macrophages

73
Q

What is the purpose of APCs?

A 
Digest antigen
Present fragments on APC surface with MHC class II
74
Q

What do pathogens entering the gastrointestinal or respiratory tracts pass through? Why?

A

M (microfold) cells over Peyer’s patches, which contain APCs so that pathogens can get cleared before they enter the GI or respiratory tracts

75
Q

M cells facilitate contact between what?

A

M cells facilitate contact between antigens passing through the intestinal tract and cells of the body’s immune system

76
Q

Describe the process of Activating CD4 T Helper Cells

A
  1. An APC encounters and ingests a microorganism. The antigen is enzymatically process into short peptides, which combine with MHC Class II molecules and are displayed on the surface of the APC
  2. A receptors (TCR) on the surface of the CD4 T helper cell (Th cell) binds to the MHC- antigen complex. If this includes a TLR the APC is stimulated to secrete a costimulatory molecule. These two signals activate the Th cell, which produces cytokines.
  3. The cytokines cause the Th cell to proliferate and to develop its effector functions
  4. A T cell that recognizes a dendritic cell that is producing costimulatory molecules becomes activated, allowing proliferation and development of effector functions
77
Q

T Cytotoxic Cells

A
  • CD8+ or TC cells
  • Target cells are “self” with endogenous antigens
  • Activated into cytotoxic T lymphocytes (CTLs)
  • MHC class I molecules are on all cells of the body
  • CTLs recognize antigen with MHC class I
  • Induce apoptosis in target cell
  • CTL releases perforin and granzymes
78
Q

Describe the process of Cytotoxic T cell activation

A
  1. A normal cell will not trigger a response by a CTL but a virus infected cell or a cancer cell produces abnormal endogenous antigens
  2. The abnormal antigen is presented on the cell surface in association with MHC class I molecules, CD8 T cells with receptors for the antigen are transformed into CTLs
  3. The CTL induces destruction of the virus-infected cell by apoptosis
79
Q

T regulatory cells

A
  • TReg cells are similar to TH cells
  • Have CD4 and CD25 on their surface
  • Suppress T cells that act against “self” antigens
    to block their potentially destructive activity
    TCRs that are like autoantibodies
80
Q

NK cells

A
  • Extracellular killing by the immune system
  • NK cells are granular leukocytes
  • destroy any cells that don’t express MHC I
  • kill virus-infected and tumor cells
  • attack parasites
81
Q

ADCC

A
  • Antibody-dependent cell-mediated cytotoxicity
  • antibodies stimulate NK and other cells to kill
  • Require Fc receptors on the killing cell
82
Q

What happens to organisms that are too large for ingestion by phagocytes?

A

Must be attacked externally by ADCC

83
Q

Cytokines

A

Cytokines are chemical messengers

84
Q

What happens when cytokines are overproduced?

A

Overproduction leads to “cytokine storm” and signaling gets out of control which can cause significant damage to tissues. This is part of pathology of many diseases.

85
Q

Diseases that are caused by cytokine overproduction

A

− influenza
− graft-versus-host disease
− sepsis

86
Q

Interleukin-1 (IL-1)

A

Stimulates TH cells in presence of

antigens; attracts phagocytes

87
Q

Interleukin-2 (IL-2)

A 
Proliferation of antigen-stimulated
CD4+ T helper cells, proliferation
and differentiation of B cells;
activation of CD8+ T cells and NK
cells
88
Q

Interleukin-12 (IL-12)

A

Inhibits humoral immunity;

activates TH1 cellular immunity

89
Q

Chemokines

A

Induce the migration of leukocytes

90
Q

TNF-alpha

A

Promotes inflammation

91
Q

Hematopoietic cytokines

A

Influence differentiation of blood

stem cells

92
Q

IFN- alpha and beta

A

Response to viral infection;

interfere with protein synthesis

93
Q

IFN- gamma

A

Stimulates macrophage activity

94
Q

Antibody titer

A

is the amount of antibody in

serum

95
Q

Primary response

A

occurs after initial contact

with antigen

96
Q

Secondary or memory response (anamnestic)

A

occurs after second exposure

97
Q

immunological memory

A

a distinct characteristic of the immune system and it relates to its ability to remember antigens on pathogens, tumour cells, tissue of the immunological self, and cells and tissues derived from other individuals of the species and mount an immunological response of greater magnitude. This is why vaccinations work

98
Q

Which antibody has a greater immune response to an antigen during the second exposure and which has the same immune response?

A

IgG- greater

IgM- same

99
Q

Does antibody titer increase post- vaccination?

A

Yes, for example when rubella virus vaccination occurred in school girls in India, in 2008 the IgG antibody titers increased significantly (almost 10k fold)

100
Q

What are the four types of adaptive immunity? Provide examples of each

A 
1. Naturally acquired active immunity
Resulting from infection
2. Naturally acquired passive immunity
Transplacental or via colostrum
3. Artificially acquired active immunity
Injection of Ag (vaccination)
4. Artificially acquired passive immunity
Injection of Ab

Microbiology (15 decks)

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