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Immunology/Vaccination Flashcards

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Biology 101 flashcards
1
Q

Immunity

A

The active ability of an organism to resist infection

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2
Q

Innate immunity

A

The body’s built-in ability to recognize and destroy pathogens or their products

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3
Q

Adaptive immunity

A

The acquired ability to recognize and destroy a pathogen and its products
Activated by exposure of the immune system to the pathogen

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4
Q

Immunity results from the actions of cells that circulate through the

A

blood and lymph

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5
Q

Normal Microbiota helps host resist pathogens, particularly on the

A

skin and in the gut (competitive exclusion).

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6
Q

Name the physical and chemical barriers to infection

A

Mucosal membranes are coated with a thick layer of mucus.

Stomach acid inhibits bacterial growth.Skin is salty and acidic, limiting bacterial growth.

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7
Q

The lymphatic system is a

A

separate circulatory system that drains lymph fluid from extravascular tissues

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8
Q

Blood is pumped through what and returns from the body through what

A

arteries and capillaries and returns from the body through veins.

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9
Q

In capillary beds

A

leukocytes and solutes pass from blood into the lymphatic system.

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10
Q

Lymph nodes contain high concentrations of

A

lymphocytes and phagocytes

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11
Q

0.1 percent of blood cells are

A

leukocytes.

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12
Q

Leukoctyes include

A

include phagocytes and lymphocytes

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13
Q

Cytokines influence

A

the development of stem cells.

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14
Q

Whole blood is composed of

A

plasma and cells.

Plasma contains proteins and other solutes.

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15
Q

Serum is the portion

A

of blood that is not cells or clotting proteins.

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16
Q

Lymphocytes are specialized

A

leukocytes involved exclusively in adaptiveimmune response.

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17
Q

Leukocytes are

A

nucleated white blood cells.

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18
Q

Name the two types of lymphocytes

A

B and T cells

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19
Q

B cells

A

originate and mature in bone marrow.

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20
Q

T cells

A

originate in bone marrow, but mature in thymus.

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21
Q

Bone marrow and thymus

A

primary lymphoid organs

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22
Q

Lymphoid stem cells produce

A

T cells, B cells and NK cells.

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23
Q

Each lymphocyte produces a unique

name each for T and B cell

A

protein that interacts with a single antigen.
T cells: T cell receptors (TCRs)
B cells: antibodies or immunoglobulins (Igs)

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24
Q

Myeloid cells works

A

work as part of innate immune response

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25
Q

Antigen presenting cells (APCs) (myeloid)

A

engulf, process and present antigens to lymphocytes

Monocytes: macrophages and dendritic cells

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26
Q

Granulocytes (myeloid)

A

contain toxins or enzymes that are released to kill target cells
neutrophils, basophils, eosinophils

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27
Q

Microbial invasion:

A

bility of a pathogen to enter host cells or tissues, multiply, spread, and cause disease.

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28
Q

Invasion:

A

ability of a pathogen to enter host cells or tissues, multiply, spread, and cause disease.

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29
Q

Tissue damage triggers

A

the recruitmentof a large number of phagocytes.

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30
Q

Tissue damage and chemokine release

A

Resident leukocytes and damaged cells release cytokines, or chemical mediators, that allow communication between white blood cells. (Figure 26.5a)Cytokinesinclude chemokinesand interleukinsare specialized chemokinesRelease of cytokines(general communication) and chemokines(a cytokine that specifically attracts) draws macrophages and neutrophils to the area as they leave circulation (extravasation). (Figure 26.5b, c)

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31
Q

Innate immune response

A

is the first line of defense
Begins when phagocyte encounters a pathogen or pathogen product
Inflammation can result

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32
Q

Phagocytes

A

engluf and destory pathogens

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33
Q

Name the phagocytes

A

Include macrophages, monocytes, and neutrophils

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34
Q

How do phagocytes move

A

Move by amoeboid action and have lysosomes

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35
Q

Phagocytes recognize a pathogen using

A

pattern recognition molecules (PRM)

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36
Q

Membrane-bound phagocyte proteins that recognize

A

pathogen associated molecular patterns (PAMPs)

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37
Q

??? on phagocytes recognize PAMPs

A

Toll-like receptors (TLRs)

Note: this is different than the antibody-mediated adaptive response

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38
Q

Phagocytic cells use toxic

A

oxygen to kill ingested bacterial cells by oxidizing key cellular constituents

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39
Q

Explain innate immune response

A

Membrane-spanning TLR-2 interacts with peptidoglycan from gram+ pathogens. •Interaction stimulates signal transduction, activates transcription factors in nucleus.•Result: transcription of genes that induce inflammation and other phagocyte activities

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40
Q

Phagocytic cells contain bacteriocidal materials

A

lethal oxidative reactions KNOW THEM

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41
Q

Some pathogens have developed mechanisms for neutralizing toxic phagocyte products
NAME THEM

A

S . aureus and M. tuberculosis

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42
Q

Some intracellular pathogens produce leukocidins

what is that and what are they

A

kill the phagocyte (forms pus)

43
Q

Some bacteria produce a capsule resistant to phagocytosis name a bacteria

A

S. pneumoniae

44
Q

Inflammation

A

is a nonspecific reaction to noxious stimuli

Redness, swelling, pain, and heat localized at site of infection

45
Q

Molecular producers of inflammation are proteins:

A

cytokinesand chemokines(produced by phagocytes and lymphocytes i.e. T cells)

46
Q

Inflammation also

whats the downside

A

Isolates and limits tissue damage, destroying damaged cells and pathogens
Downside: Inflammation can result in considerable damage to healthy tissue

47
Q

are the first to arrive at scene of infection

A

Neutrophils

48
Q

Attracted to site by

A

interleukins (a cytokine/chemokine that is released from damaged host cell)

49
Q

Activated neutrophils release

A

chemokines to recruit macrophages by guiding them along a chemokine gradient

50
Q

Usual outcome of inflammation is a

A

rapid localization and destruction of pathogen

51
Q

In some cases inflammation fails to

A

localize pathogen and the reaction becomes widespread

Can lead to septic shock,a life-threatening condition

52
Q

Septic shock can be

A

more dangerous than the initial infection

53
Q

T lymphocytes

A

recognize peptide or carbohydrate antigens through cell surface T cell receptors (TCRs)

54
Q

Cell-mediated immunity

A

leads to killing of pathogen-infected host cells through recognition of pathogen antigens found on infected host cells

55
Q

Antibody-mediated (humoral) immunity

A

is effective against extracellular pathogens such as bacteria and soluble pathogen products

56
Q

Antigens

A

are substances that react with antibodies or TCRs

57
Q

T cell receptor (TCR)

A

is a membrane protein

Each T cell has thousands of copies of the same TCR on its surface

58
Q

Major Histocompatibility Complex (MHC)

A

Initially identified as being responsible for immune-mediated organ transplant rejection
Now know they function as antigen-presenting molecules
MHC-I proteins present items from inside cells, found on all nucleated cells, mainly react with cytotoxic T cells
MHC-II proteins present items from inside cells, found only on B lymphocytes, macrophages and dendritic cells (the antigen-presenting cells APCs), mainly react with T helper cells

59
Q

MHC-I proteins expressed on the

A

cell surface reflect the composition of the proteins inside the cell

60
Q

T cells don’t interact with a foreign antigen unless

A

it is presented in the context of a MHC protein

61
Q

T-cytotoxic cells (CTLs or Tc)are T cells (T-lymphocytes) that

A

kill cells displaying foreign antigens (in MHC-I)

62
Q

T-cytotoxic cells (CTLs or Tc)

A

contact target; granules contain enzyme that perforates target cell membrane
Other enzymes cause apoptosis

63
Q

Natural killer cells (NK cells)are not

A

T cells or B cells

Kill targets in the absence of a specific protein

64
Q

Natural killer cells (NK cells)

A

Lack of normal MHCs result in killing

65
Q

TH1 subset

A

activates macrophages by secreting cytokines (including interferon gamma and others)
Also play a role in inflammation and transplanted organ rejection

66
Q

TH2 subset

A

plays a crucial role in B cell activation and antibody production

67
Q

Antibodies or Immunoglobulins (Ig)

A

are protein molecules that interact specifically with antigens

68
Q

Antibodies or Immunoglobulins (Ig)

A

Found in serum, milk, and gastric secretions

5 major classes (IgG, IgA, IgM, IgD, andIgE)

69
Q

is the most common antibody circulating in the body

A

IgG

70
Q

IgG

A

4 polypeptide chains (2 heavy and 2 light chains)
Antigen-binding site results from interaction between heavy and light chains
We all produce billions of different antigen-binding sites

71
Q

All five classes

A 
have different structural characteristics, expression patterns, and functional roles
The heavy chains of a given antibody define its class based on amino acid sequence
72
Q

Each person can

A

produce billions of different antibodies and T cell receptors (TCRs)

73
Q

Antibody production

A

responds to antigen exposureInvolves interactions between B cells and T cells

74
Q

Antibody production:

A

Antigen-stimulated B cells multiply and differentiate to form antibody-secreting plasma cells and memory cells (primary antibody response)

Memory B cells generated may live for years and quickly transform into antibody-secreting cells (secondary antibody response)

75
Q

Complement

A

is a group of sequentially interacting proteins
Roles in innate and adaptive immunity
Cause lysis of pathogens or mark them for recognition by phagocytes

76
Q

Complement lyses

A

many gram-negative bacteria

77
Q

Opsonization

A

A bacterial cell is more likely to be phagocytized if it has been bound by an antibody
Complement binds antibody-antigen complex, increases likelihood of phagocytosis further

78
Q

Superantigens

A

Proteins capable of eliciting a strong response because they activate more T cells than a normal immune response
Produced by many viruses and bacteria that interact with TCRs
Superantigen-activated T cells may produce diseases characterized by systemic inflammatory reactions

79
Q

Natural active immunity

A

By acquiring an infection that initiates an adaptive immune response

80
Q

Natural passive immunity

A

Through antibody transfer across the placenta or in breast milk

81
Q

Artificial induction of immunity

A

to individual infectious diseases is a major weapon for the treatment and prevention of diseases

82
Q

Artificial active immunity (vaccination)

A

Can be achieved through exposure to a controlled dose of a harmless antigen to induce formation of antibodies

83
Q

Artificial passive immunity

A

Can be achieved through injection of an antiserum derived from an immune individual

84
Q

Immunization

A

The process of generating an artificial active immune response by exposure to an antigen or antigen mixture (vaccine)

85
Q

Immunization with live cells or virus is usually

A

more effective than that with dead or inactivated material

86
Q

nATURES OF vaccines

A

The importance of immunizations in controlling infectious diseases is well established, and the Center for Disease Control has specific recommendations for children in the United States. (Figure 28.25)
Immunizations usually involve a series of secondary immunizations or “booster” immunizations to produce a secondary response and a higher antibody titer.

87
Q

Synthhetic vaccines

A

Synthetic vaccines are the product of genetically engineering antigenic components to stimulate the immune response.
Conjugate vaccines attach a smaller antigenic protein to a larger carrier protein to improve immune response to the protective antigen.Attaching a polysaccharide to a toxoid improves the immune response of polysaccharides, which are not as immunogenic as proteins.
Pneumococcal vaccines are made this way. (Figure 28.26)

88
Q

DNA vaccines

A

Target proteins are cloned into plasmid vectors and injected intramuscularly.
The DNA is taken up by host cells, and proteins are expressed.
The host then mounts an immune response to the protein.

89
Q

DNA vaccines:

A

based on expression of cloned genes in host cells

90
Q

Antiviral drugs

A

Most antiviral drugs also target host structures, resulting in toxicity

  • Most successful and commonly used antivirals are the nucleoside analogs.(e.g., AZT)
  • block reverse transcriptase and production of viral DNA
  • also called nucleoside reverse transcriptase inhibitors (NRTIs)
91
Q

Nonnucleosidereverse transcriptase inhibitors (NNRTIs)

A

bind directly to RT and inhibit reverse transcription.

92
Q

Protease inhibitors

A

inhibit the processing of large viral proteins into individual components.

93
Q

Fusion inhibitors

A

prevent viruses from successfully fusing with the host cell.

94
Q

Nevirapine

A

Nonnucleoside reverse transcriptase inhibitor
•Binds directly to catalytic site of HIV reverse transcriptase
•Inhibits chain elongation

95
Q

Azidothymidine(AZT) aka zidovudine

A

Nucleoside reverse transcriptase inhibitor (inhibits virus replication)

  • Nucleoside analog missing the –OH group on the 3’-carbon
  • Causes nucleotide chain elongation to terminate when analog incorporated
96
Q

Neuraminidase

A

Nicks sialic acid to cut loose from the cell (exit)

97
Q

Hemagglutinin

A

Holds onto sialic acid to enter host cells

98
Q

T-cytotoxic (Tc) cells

A

Recognize the antigen presented by an MHC I protein on an infected cellKill antigen-bearing target cells directly

99
Q

T-helper (TH) cells

A

Interact with peptide-MHC II complexes on the surface of antigen-presenting cellsAct through cytokines to promote immune reactions

100
Q

TH1 cells

A

Initiate inflammation and immunity by activating macrophage

101
Q

Antibodies (immunoglobulins)are soluble proteins made by

A

vB cells in response to exposure to nonself antigens that are part of pathogens or their products

102
Q

B cells display antibodies on their cell surfaces that directly

A

interact with antigens to cause B cells to ingest pathogen via phagocytosis

103
Q

B cells then produce many pathogen-derived

A

peptide antigens that are presented to antigen-specific TH2 cells

Microbiology (12 decks)

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