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Immunity > Innate Immunity I > Flashcards

Innate Immunity I Flashcards

1
Q

Our early and rapid system of defense against pathogens and other events or substances considered to be dangerous

A

Innate Immunity

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2
Q

Consists of molecules that recognize foreign or unusual molecules in the body, and molecules or cells that respond to this perceived threat by eliminating or neutralizing the perceived threat

A

Innate Immunity

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3
Q

Innate Immunity is the initial response to microbes that acts to prevent, control and eliminate

A

Infection

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4
Q

stimulates the subsequent adaptive immune response and can influence the nature of the response to tailor it to the specific type of microbe

A

Innate Immunity

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5
Q

Innate immunity can also recognize some products of damaged or dead host cells and can eliminate those cells and initiate tissue repair, often without causing

A

Inflammation

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6
Q

Innate immunity is always

A

Functional

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7
Q

Key molecules of innate immunity are encoded in the

-Thus are NOT the products of antigen-specific genetic rearrangements

A

Genome

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8
Q

Does not result in specific memory of antigens or pathogens previously encountered

A

Innate immunity

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9
Q

The molecules of innate immunity that recognize foreign or unusual molecules are generically referred to as

A

Pattern Recognition Receptors (PRRs)

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10
Q

The molecules on the pathogen, or produced by the pathogen, that are recognized by PRRs are referred to as

A

“Pathogen-Associated Molecular Patterns (“PAMPS”)

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11
Q

If these recognized patterns arise from “unmasked” or unusual host components, they are called

A

“Damage-Associated Molecular Patterns” (“DAMPS”)

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12
Q

PRRs may be located in the

A

Serum or Tissues

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13
Q

Cellular PRRs can be located on the cell membrane to sense

A

PAMPS outside of the cell

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14
Q

Cellular PRRs can be located on the endosomal membrane, to sense PAMPs that have been brought into the cell by

A

Endocytosis

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15
Q

Cellular PRRs can be located in the cytoplasm, where they sense

A

PAMPs

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16
Q

Can have several outcomes: (1) it may directly affect the pathogen; (2) it can trigger a cascade of molecular, cellular and global responses by the host

A

Binding of PRRs to pathogen

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17
Q

The two major global responses against pathogens are

A

Acute inflammation and the antiviral response

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18
Q

Can also arise in response to damaged or dead cells, or to the accumulation of abnormal substances in cells or tissues

A

Inflammatory response

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19
Q

However, while it’s useful to consider innate immune responses separately, a 3rd outcome of the innate response in many cases is the initiation of a longer-term, more specific

A

Adaptive Immune response

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20
Q

The initiation of a longer-term, more specific “adaptive immune response” causes the generation of

A

T and B cells and antibodies

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21
Q

Was first recognized in the late 1890s, and a number of other recognition molecules were discovered throughout the ensuing 100 years

A

Complement

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22
Q

A major landmark for our understanding of how the body recognizes pathogens came in the med-1990’s with the discovery of

A

Toll-like receptors

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23
Q

Bacteria, viruses and fungi have a number of unique molecules that serve as

A

Pathogen-Associated Molecular Patterns (PAMPs)

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24
Q

Damaged and dead cells, or cellular inclusions, may also be recognized by the immune system, and these are referred to as

A

“Damage-Associated Molecular Patterns” (DAMPS)

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25
Q

An important property of PAMPs is that these molecules are often essential for

A

Microbial survival

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26
Q

Produced by host cell damage from infection, injury, trauma, ischemia, etc

A

DAMPs

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27
Q

Note that these are cell debris resulting from apoptosis is efficiently cleared, so that inflammation does not result). Defects in the mechanisms of debris clearance from apoptotic cells can contribute to

A

Autoimmune disease

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28
Q

Found on a wide variety of cells

A

Cell-associated Pathogen Recognition Receptors (Cell-associated PRRs)

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29
Q

Express the greatest variety and amount of PRRs

-have direct and immediate roles in defense

A

Phagocytes (macrophages and neutrophils) and dendritic cells

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30
Q

However, other cell types, such as epithelial and endothelial cells that can play important but less direct roles in the immune response and regulation, may also express

A

PRRs

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31
Q

In both instances, binding to cell-associated PRRs most often activates signal transduction pathways that lead to

A

Anti-microbial and pro-inflammatory responses

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32
Q

A family of PRRs that are conserved through evolution, are expressed on many cell types, and are capable of recognizing a wide variety of PAMPs from different classes of pathogens

A

Toll-like Receptors (TLRs)

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33
Q

TLRs on the cell surface can recognize various structures from

A

Bacteria or Fungi

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34
Q

May be part of the intact pathogen, shed by the pathogen, or released following phagocytosis of pathogens by macrophages or killing by neutrophils

A

The PAMPs for TLRs

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35
Q

Pathogens that are endocytosed into endosomes, such as many viruses, may have components such as single- or double-stranded RNA, or bacterial DNA that are recognized by

A

Endosomal TLRs

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36
Q

A characteristic molecule of Gram-negative bacteria that is a ligand for TLRs

A

Lipopolysaccharide (LPS)

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37
Q

Once the PAMP binds to its cognate TLR, a series of molecules are recruited and activated in a

A

Signal Transduction Cascade

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38
Q

This signal transduction cascade results in the activation of

A

Transcription factors in the nucleus

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39
Q

For an inflammatory response, a very important transcription factor is

A

NF-kB (“NK-kappaB”)

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40
Q

Antiviral responses particularly work through transcription factors of the

A

Interferon Response Factor (IRF) family

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41
Q

These and other activated transcription factors turn on or off a host of genes that then feed into two main responses, the

A

Inflammatory Response and Antiviral Response

42
Q

Of particular interest, the activation of NF-kB helps turn on pro-inflammatory responses through the production and secretion of the “pro-inflammatory cytokines”

A

Tumor necrosis factor (TNF) α, interleukin 1 (IL-1) β, and interleukin 6

43
Q

Similarly, during viral infections, activation of IRF-family transcription factors lead, among other outcomes, to the production and secretion of

A

Type I and Type III interferons

44
Q

The most common forms of Type I and Type III interferons are the

A

Alpha interferons (IFN-α) and interferon beta (IFN-β)

45
Q

The Type I and Type III IFNs are crucial to early

A

Antiviral Defense

46
Q

Interferons are protein signals called

A

Cytokines

47
Q

Thus, the molecular events triggered through the TLRs (and other PRRs) begin to determine whether the host mounts an

A

Appropriate Response

48
Q

In addition to these membrane-associated PRRs, there are also receptors and recognition molecules for PAMPs and DAMPs in the

A

Cytoplasm

49
Q

These are important because some pathogens, including many viruses, have parts of their life-cycle in the

A

Cytoplasm

50
Q

One major family of cytoplasmic PRRs is called the

A

NOD-like receptors (NLRs)

51
Q

Occur in a variety of cell types, including immune, inflammatory and epithelial barrier cells

A

NLRs

52
Q

The binding of NLRs to their PAMPs or DAMPs initiates an intracellular signaling cascade. As with the TLRs, one important outcome is the activation of the key transcription factor for the

A

Inflammatory genes, NF-kB, and the activation of the pro-inflammatory cytokine IL-1

53
Q

Genetic evidence suggests that mis-regulation of some NLRs may be involved in the pathogenesis of gut diseases, particularly

A

Inflammatory Bowel Disease (IBD)

54
Q

Other inflammatory diseases, such as gout, pseudo-gout or lung disease related to silica or asbestos exposure may be related to the activation of NLRs and inflammatory cytokines such as

A

IL-1

55
Q

In addition to the NLRs in the cytoplasm, there are important cytoplasmic sensors for both

A

RNA and DNA

56
Q

As an example of how an RNA sensor can distinguish between cellular and viral RNA, requires that there be a triphosphate on the 5-prime end of the RNA

A

RIG-I RNA sensor

57
Q

Cellular mRNAs have the specially modified “cap” (modified guanine residue) at their 5-prime end, and do not bind to

A

RIG-I

58
Q

Some cell membrane receptors recognize bacterial carbohydrates that do not have equivalents on host cells. These carbohydrate receptors are in the

A

C-lectin Family

59
Q

Proteins that bind carbohydrates

A

Lectins

60
Q

For their binding, C-lectins depend on

A

Calcium

61
Q

Can aid in the phagocytosis of microbes and some can also stimulate signaling pathways

A

C-Lectins

62
Q

One example of a C-lectin receptor is the

A

Mannose receptor

63
Q

A diverse collection of cell surface receptors. Some have very broad specificity, including the recognition or oxidized lipoproteins

A

Scavenger receptors

64
Q

May mediate phagocytosis of microorganisms

A

Scavenger receptors

65
Q

Responds to the N-terminus of bacterial proteins

A

FMLP (f-Met-Leu-Phe) receptor

66
Q

Recall that the first amino acid at the N-terminus of most bacterial proteins is

A

f-Met

67
Q

Some mammalian cells, including macrophages and neutrophils, have a specific receptor that recognizes peptides with a terminal

A

f-Met

68
Q

Unlike other receptors we’ve discussed, these are in the family of

A

G-protein coupled receptors (GPCRs)

69
Q

What are the four main cells involved in innate immunity?

A

Phagocytes. dendritic cells, Natural Killer (NK) cells, and mast cells

70
Q

Once thought to be inert barrier cells, contain a large complement of diverse PRRs, including many of the TLRs and some NOD-like receptors, and thus are important outer sentinels

A

Keratinocytes

71
Q

Among the more important anti-microbial molecules of the epithelial barrier are a class of small peptides called

A

Defensins

72
Q

The skin and mucosa of the respiratory, gastrointestinal, and genitourinary tracts are referred to as the

A

Epithelial Barriers

73
Q

Have direct antimicrobial toxicity, and can activate cells involved in the inflammatory response

A

Defensins

74
Q

A second class of molecules that also have microbicidal activity and immune activation functions is the

A

“cathelicidins”

75
Q

Among the important immune cells in the skin and mucosal epithelia are

A

Intrepithelial T-lymphocytes

76
Q

Although we generally consider T lymphocytes as element s of adaptive immunity, at least some intraepithelial T lymphocytes seem to be pre-programmed with a fixed and limited antigen specificity to recognized common

A

PAMPs

77
Q

Cells with the ability to engulf, kill and otherwise process microbes, and represent a powerful cellular defense against microbes that breach the physical barriers

A

Phagocytes

78
Q

The two primary types of phagocytes are

A

Macrophages and Neutrophils

79
Q

Arise from circulating blood monocytes that migrate into tissues and undergo differentiation

A

Macrophages

80
Q

Macrophages arise from circulating blood monocytes that migrate into tissues and undergo differentiation into macrophages, where they are generically known as

A

Resident Macrophages

81
Q

The first function of these macrophages is

A

Surveillance

82
Q

Can be activated by several mechanisms such as binding of microbes to Toll-like receptors (TLRs), or to other cell-surface PRRs on the macrophages, such as a receptor for complement

A

Resident Macrophages

83
Q

Can be activated by signaling from other activated immune cells, such as the cytokine gamma interferon (IFN-γ), which can be released from natural killer (NK) cells

A

Resident Macrophages

84
Q

“Activation” has many facets: phagocytosis is made more efficient, for instance by expression of additional cell-surface

A

PRRs

85
Q

Included in these mechanisms are the up-regulation of enzymes that produce

A

ROS and Nitric Oxide

86
Q

In addition, activated macrophages produce a number of “pro-inflammatory cytokines”, including

A

Tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin 6 (IL-6)

87
Q

Help activate and mobilize other immune cells, change the vascular permeability properties of nearby vasculature, and other functions related to initiating or propagating an inflammatory response

A

TNF, IL-1, and IL-6

88
Q

During infection, monocytes can be attracted to sites of infection in increase and replenish the

A

Macrophage population

89
Q

About 60% of the white cells in blood, and their abundance can increase during infections

A

Neutrophils

90
Q

The first cells to infiltrate areas of bacterial and fungal infection, and are the dominant cells in tissue with acute inflammation

A

Neutrophils

91
Q

Basically, they are killing machines with a short half life (several hours) in tissues, so they do not provide long-lasting defense

A

Neutrophils

92
Q

Neutrophils also are used for clearance of cell debris at sites of tissue damage not related to

A

Infection

93
Q

Low neutrophil counts, such as in patients undergoing chemotherapy, is a cause of high rate of

A

Bacterial and Fungal infections

94
Q

Can sense and kill infected cells, with a second function of producing the cytokine interferon-γ (IFN-γ) to activate macrophages

A

NK Cells

95
Q

Unlike most cells of innate immunity, NK cells are in the lymphocyte lineage that includes

A

B and T cells

96
Q

Large lymphocytes with numerous cytoplasmic granules, whose contents are primarily used for killing target cells

A

NK Cells

97
Q

How do NK cells distinguish infected or damaged host cells from healthy host cells? NK cells have both

A

Inhibitory and Activatory receptors

98
Q

Most inhibitory receptors recognize

A

Class I MHCs

99
Q

However, many viruses and other causes of cell stress lead to down-regulation of MHC surface molecules that are involved in

A

Antigen presentation

100
Q

In such cases, the inhibitory receptors are not efficiently engaged, and the balance of signals will favor cellular

A

Activation and killing

Immunity (33 decks)

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