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micro immuno exam 1 > Mucosal and Dermal immunity > Flashcards

Mucosal and Dermal immunity Flashcards

1
Q

Systemic Immune Response

A

no-local

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2
Q

What types of tissue are involved in Mucosal and Cutaneous Immunty

A

Mucosa and skin associated Lymphoid tissue

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3
Q

What makes up the Mucosa-associated Lymphoid tissue

A

GALT, BALT, NAlt

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4
Q

Relatively thin layers of Epithelial cells that line body passages

A

Mucosa

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5
Q

Surface area of Mucosa

A

400 square meters

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6
Q

Single Later of columnar Epithelial cells

A

Type I mucosa

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7
Q

Many layers, with top being squamous epithelial cells

A

Type II mucosa

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8
Q

Viscous solution of polysaccharides mixed with water

A

Mucus

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9
Q

What does Mucus cover

A

Apical membrane of epithelial cell

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10
Q

Mucus contains

A

Antimicrobial peptides, enzymes, antibodies…

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11
Q

Main Ab of Type I mucus

A

SIgA

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12
Q

Main Ab of Type II mucus

A

IgG

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13
Q

Non-inducible Defenses of GI

A

Acidity, Motility, Mucous Layer with under glycocalyx, Tight Junction

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14
Q

Where commensal bacteria for the gut hang out

A

in the lumen

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15
Q

What is found in the emithelial layer of the Gut

A

Intra-epithelial lymphocytes(gamma delta T cells), Goblet cells(mucus) and Paneth cells (for antimicrobial peptides)

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16
Q

M Cell roll in Gut

A

Antigen sensing

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17
Q

Where Imune cells are found in the gut

A

In the Lamina Proprea

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18
Q

Firs cells to touch Pathogen

A

Intestinal Epithelial cells

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19
Q

Area under the epithelial cells

A

Lamina Propria

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20
Q

Lamina Propria contain

A

Macrophages, neutrophils, mast cells, immature DCs, Memory T and B cells, effector Th17 cells

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21
Q

Cell involved with Pyer’s patches in the gut for an immune response

A

M cell

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22
Q

Ag Sampling in the gut

A

M cells internalize to give to Dendritic cells

CD103 DC’s-elongate through epithelial layer to sample lumen

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23
Q

NALT and BALT provide defense against

A

Inhaled AG

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24
Q

NALT involves

A

Nasal submucosal glands, Tonsils, Epithelial Cells(type II), Follicles and Diffuse Lymphocytes

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25
Q

Balt involves

A

Bronchial submucosal glands, Epithelial cells(type I), Follicles and diffuse lymphocytes

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26
Q

Non-inducable mechanisms for NALT and BALT

A 
Nose Hairs(NALT only)
Mucus
Cilia
Coughing
Tonsils
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27
Q

why is it easy to sample Antigens in the NALT and the BALT

A

Environemnt is less caustic

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28
Q

What does the BALT have to sample Ag

A

M cells and follicle asssociated epithelia

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29
Q

DC’s in the NALT can process Ag and move where

A

Tonsils or diffuse lymphoid

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30
Q

How do macrophages recognize microbes

A

Via pattern recognition receptors

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31
Q

Macrophages recognizing microbes leads to

A

Activation of the macrophage and the ability to kill microbes

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32
Q

Activation of Pattern recognition receptors on macrophages initiates

A

Inflammatory response

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33
Q

The adaptive response in the gut is biased toward

A

SigA, to protect antigen from being degraded

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34
Q

If inflammatory response is needed in the gut what will be activated

A

Robust Th1/Th17 response

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35
Q

INductive site in the gut

A

Where an antigen is presented

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36
Q

Activation of the Inductive site leads to

A

Activation of the B cell and class swtiching and ends up in the effector site

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37
Q

Effector site role

A

Secretory portion of cells allow shit antibodies to go into the lumen

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38
Q

Where is SIgA found

A

Constitutively in mucus

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39
Q

Is SIgA Ag specific

A

yes, but can bind to adhesion molecules found on many pathogens

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40
Q

What kind of reactivity is 50% of SIgA in the gut

A

Cross-reactive

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41
Q

Does SigA activate its complement well

A

No, so it doesn’t trigger unnecessary inflammation

42
Q

Do host and microbial protesases affect SIgA

A

No

43
Q

When an Antibody reacts with something it normally is not made to react with

A

Cross-reaction

44
Q

Why not initiate inflammatory response in mucosal surfaces

A

Cytokines, such as TNF-alpha can disrupt tight junctions between epithelial cells

45
Q

What does Cutaneous Immunity

A

Skin-Associated Lymphoid Tissue: epidermis and dermis

46
Q

Cells involved in Cutaneous Immunity

A

DCs, mast cells, macrophages T cells, little/no b Cells(no mucus)

47
Q

Immune response of Cutaneous immunity

A

Activation of nearby memory T cells, or induction of systemic immunity (Th1/Th17-inflammatory)

48
Q

Ability of any bacterial speicies to cause disease in a susceptible human host

A

Pathogenicity

49
Q

Presumes pathogenicity, but allows expression of degrees from low to high

A

Virulence

50
Q

Why does Clinical disease result

A

When a pathogen is able to enter a host, colonize, survive immune system defense, and cause damage

51
Q

What is neccessary for primary pathogens

A

Breach human cellular and anatomic barriers
Avoid host defenses
And transmit to a new host

52
Q

Vector Borne transmission

A

Like a tick biting you

53
Q

Do all pathogens need the same amount of the pathogen to get you sick

A

No

54
Q

3 stages to establish an infection

A

Adherence, Coloniziation/invation

Damage

55
Q

How would a pathogen breach host innate defenses to colonize

A

Attach to unique host molecules
IgA Protease
Inherent resistance to lysozymes
Mechanisms to sequester iron

56
Q

How pathogens bind to host cells

A

Though Pili and protein adhesins

57
Q

Pili can bind to what cells

A

bind to cell-specific receptors present in material covering the host cell

58
Q

Roll of Pili for pathogens

A

Allow inital attachment, bringing organism closter to cell so second Adhesin can bind

59
Q

Attachment mech of bacterial pathogens

A

Pili or Fimbriae, Biofilms

60
Q

Cleaves SIgA in the hinge region to release the Fc portion from the Fab fragment

A

SIgA protease

61
Q

How some cells avoid lysozymes

A

Outer membrane of Gram negative bacteria prevent penetration of lysozymes

62
Q

How bacteria fight the low levels of iron needed to grow

A

Produce Siderophores to compete with human proteins for iron

63
Q

Sequesters iron

A

Lactoferrin

64
Q

ways a pathogen avoids immune system

A

Invade and survive in host cells
avoid contact with phagocytes
Inhibit phagocytic engulfment

65
Q

PAthogen that cannot invade host cells

A

Extracellular

66
Q

Pathogen that can invade host cells, but can survive extracellular

A

Facultative intracellular bacteria

67
Q

Require host cells for surival

A

Obligate intracellular bacteria

68
Q

Facultative intracellular bacteria prefer to enter

A

Macrophages

69
Q

OBligate intracellular bacteria prefer to not enter

A

Macrophage

70
Q

Any protein produce by bacteria that allows the bacteria to invade non-phagocytic host cells/tissue

A

Invasins

71
Q

Examples of Invasins

A

Effector Proteins injected by type III secretion
Secreted enzymes that interupt tight juntion
Proteins that bind integrins on host cell and facilitate uptake

72
Q

Action of Effector Proteins

A

Promote invation of host cell

suppress host cell defenses

73
Q

Endosomes normal action

A

Fuse with lysosomes to digest contents

74
Q

Invasive pathogens that enter through endosomes must be able to

A

Disrupt normal cell vesicle trafficking, escape endosome in cytoplasm

75
Q

How pathogens avoid being killed once in the cell

A

Modify endosome for survial
Escape endosome and replicate
Block endosome-lysosome fusion

76
Q

How can a pathogen avoid phagocytosis by a macrophage and PMN

A

Capsule that interferes with complement deposition on bacteria

77
Q

How a capsule aids in avoiding innate host defense

A

Binds factor H present in serum-degrades complement protein C3b preventing it’s deposition on bacterial cell surface

78
Q

How a pathogen will avoid contact with phagocytes

A

Invade location not surveilled phagocytes
avoid inducing inflammation
Inhibit phagocyte chemotaxis
Bind host molecules to hide antigenic surface

79
Q

How can a pathogen Inhibit phagocytosis

A 
Polysaccharide Capsule
M protein and fimbriae
O Polysaccharide
K Antigen
Cell-bound Protein A
80
Q

How Cell-bound Protein A inhibits phagocytosis

A

Binds to Fc region of IgG and blocks Ab binding(prevents opsonization)

81
Q

How can a pathogen munipulat PAMPS and AMPS

A

Have poorly recognized Lipid A portion of LPS (TLR-4)
Lipid A modification-changes surface(prevent AMPS)
Alter cell wall with Teichoic acid(prevents TLR signalling

82
Q

What does Varying surface antigens on pathogens do

A

Prevent PAMPS from being recognized

83
Q

Why pathogens would kill host cells

A

Decrease number of defenders and prevent the alarm bells from sounding

84
Q

Roll of strptolysin and Leukocidin

A

Target neutrophils to release lysozomal content into cytoplasm

85
Q

Roll of Exotoxin A

A

Targets and kills Macrophages

86
Q

Ways baceria can injur host

A

Exotoxin, endotoxin, hydrolytic enzymes, superantigen exotoxins
Inflammation

87
Q

Bacterial secreted proteins

A

Exotoxins

88
Q

Lipid A portion of LPS of Gram-negative bacteria that stimulates cytokine release(inflammation)

A

Endotoxin

89
Q

Facilitate tissue invasion

A

Hydrolytic enzymes

90
Q

Stimulate massive sytokine secretion (toxic shock)

A

superantigen exotoxins

91
Q

Prolonged immune response to bacteria can damage host tissues

A

Inflammation

92
Q

What can be exotins

A

Local or Systemic if in blood

93
Q

What can exotoxins bind to

A

Host cell specific-bind to specific cell receptors

94
Q

Effect of Exotoins

A

Depends on target but may inhibit, stimulate, or kill

95
Q

A- B exotoxin parts

A

B=bind to host cell surface receptor glycoproteins or glycolipids
A=transported by direct fusion or endocytosis into host to act on target

96
Q

Create pores in host cell membrane(DAMPS)

A

Membrane active exotoxins

97
Q

Lipid A portion of LPS

A

Endotoxin

98
Q

How endotoxin induces fever

A

macrophages release IL-1 and TNF

99
Q

Useing antibiotics on Endotoxin

A

Makes it worse because Lipid A is released

100
Q

Binds to MHC II, activating T cell non specifically, causing them to release Cytokines IL-1 and TNF to cause shock/inflammation

A

Superantigen

101
Q

Chronic infection can cause

A

delayed type hypersensitivity reaction

micro immuno exam 1 (8 decks)

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