Mucosal and Dermal immunity Flashcards
1
Q
Systemic Immune Response
A
no-local
2
Q
What types of tissue are involved in Mucosal and Cutaneous Immunty
A
Mucosa and skin associated Lymphoid tissue
3
Q
What makes up the Mucosa-associated Lymphoid tissue
A
GALT, BALT, NAlt
4
Q
Relatively thin layers of Epithelial cells that line body passages
A
Mucosa
5
Q
Surface area of Mucosa
A
400 square meters
6
Q
Single Later of columnar Epithelial cells
A
Type I mucosa
7
Q
Many layers, with top being squamous epithelial cells
A
Type II mucosa
8
Q
Viscous solution of polysaccharides mixed with water
A
Mucus
9
Q
What does Mucus cover
A
Apical membrane of epithelial cell
10
Q
Mucus contains
A
Antimicrobial peptides, enzymes, antibodies…
11
Q
Main Ab of Type I mucus
A
SIgA
12
Q
Main Ab of Type II mucus
A
IgG
13
Q
Non-inducible Defenses of GI
A
Acidity, Motility, Mucous Layer with under glycocalyx, Tight Junction
14
Q
Where commensal bacteria for the gut hang out
A
in the lumen
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)
16
Q
M Cell roll in Gut
A
Antigen sensing
17
Q
Where Imune cells are found in the gut
A
In the Lamina Proprea
18
Q
Firs cells to touch Pathogen
A
Intestinal Epithelial cells
19
Q
Area under the epithelial cells
A
Lamina Propria
20
Q
Lamina Propria contain
A
Macrophages, neutrophils, mast cells, immature DCs, Memory T and B cells, effector Th17 cells
21
Q
Cell involved with Pyer’s patches in the gut for an immune response
A
M cell
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
23
Q
NALT and BALT provide defense against
A
Inhaled AG
24
Q
NALT involves
A
Nasal submucosal glands, Tonsils, Epithelial Cells(type II), Follicles and Diffuse Lymphocytes
25
Balt involves
Bronchial submucosal glands, Epithelial cells(type I), Follicles and diffuse lymphocytes
26
Non-inducable mechanisms for NALT and BALT
```
Nose Hairs(NALT only)
Mucus
Cilia
Coughing
Tonsils
```
27
why is it easy to sample Antigens in the NALT and the BALT
Environemnt is less caustic
28
What does the BALT have to sample Ag
M cells and follicle asssociated epithelia
29
DC's in the NALT can process Ag and move where
Tonsils or diffuse lymphoid
30
How do macrophages recognize microbes
Via pattern recognition receptors
31
Macrophages recognizing microbes leads to
Activation of the macrophage and the ability to kill microbes
32
Activation of Pattern recognition receptors on macrophages initiates
Inflammatory response
33
The adaptive response in the gut is biased toward
SigA, to protect antigen from being degraded
34
If inflammatory response is needed in the gut what will be activated
Robust Th1/Th17 response
35
INductive site in the gut
Where an antigen is presented
36
Activation of the Inductive site leads to
Activation of the B cell and class swtiching and ends up in the effector site
37
Effector site role
Secretory portion of cells allow shit antibodies to go into the lumen
38
Where is SIgA found
Constitutively in mucus
39
Is SIgA Ag specific
yes, but can bind to adhesion molecules found on many pathogens
40
What kind of reactivity is 50% of SIgA in the gut
Cross-reactive
41
Does SigA activate its complement well
No, so it doesn't trigger unnecessary inflammation
42
Do host and microbial protesases affect SIgA
No
43
When an Antibody reacts with something it normally is not made to react with
Cross-reaction
44
Why not initiate inflammatory response in mucosal surfaces
Cytokines, such as TNF-alpha can disrupt tight junctions between epithelial cells
45
What does Cutaneous Immunity
Skin-Associated Lymphoid Tissue: epidermis and dermis
46
Cells involved in Cutaneous Immunity
DCs, mast cells, macrophages T cells, little/no b Cells(no mucus)
47
Immune response of Cutaneous immunity
Activation of nearby memory T cells, or induction of systemic immunity (Th1/Th17-inflammatory)
48
Ability of any bacterial speicies to cause disease in a susceptible human host
Pathogenicity
49
Presumes pathogenicity, but allows expression of degrees from low to high
Virulence
50
Why does Clinical disease result
When a pathogen is able to enter a host, colonize, survive immune system defense, and cause damage
51
What is neccessary for primary pathogens
Breach human cellular and anatomic barriers
Avoid host defenses
And transmit to a new host
52
Vector Borne transmission
Like a tick biting you
53
Do all pathogens need the same amount of the pathogen to get you sick
No
54
3 stages to establish an infection
Adherence, Coloniziation/invation
| Damage
55
How would a pathogen breach host innate defenses to colonize
Attach to unique host molecules
IgA Protease
Inherent resistance to lysozymes
Mechanisms to sequester iron
56
How pathogens bind to host cells
Though Pili and protein adhesins
57
Pili can bind to what cells
bind to cell-specific receptors present in material covering the host cell
58
Roll of Pili for pathogens
Allow inital attachment, bringing organism closter to cell so second Adhesin can bind
59
Attachment mech of bacterial pathogens
Pili or Fimbriae, Biofilms
60
Cleaves SIgA in the hinge region to release the Fc portion from the Fab fragment
SIgA protease
61
How some cells avoid lysozymes
Outer membrane of Gram negative bacteria prevent penetration of lysozymes
62
How bacteria fight the low levels of iron needed to grow
Produce Siderophores to compete with human proteins for iron
63
Sequesters iron
Lactoferrin
64
ways a pathogen avoids immune system
Invade and survive in host cells
avoid contact with phagocytes
Inhibit phagocytic engulfment
65
PAthogen that cannot invade host cells
Extracellular
66
Pathogen that can invade host cells, but can survive extracellular
Facultative intracellular bacteria
67
Require host cells for surival
Obligate intracellular bacteria
68
Facultative intracellular bacteria prefer to enter
Macrophages
69
OBligate intracellular bacteria prefer to not enter
Macrophage
70
Any protein produce by bacteria that allows the bacteria to invade non-phagocytic host cells/tissue
Invasins
71
Examples of Invasins
Effector Proteins injected by type III secretion
Secreted enzymes that interupt tight juntion
Proteins that bind integrins on host cell and facilitate uptake
72
Action of Effector Proteins
Promote invation of host cell
| suppress host cell defenses
73
Endosomes normal action
Fuse with lysosomes to digest contents
74
Invasive pathogens that enter through endosomes must be able to
Disrupt normal cell vesicle trafficking, escape endosome in cytoplasm
75
How pathogens avoid being killed once in the cell
Modify endosome for survial
Escape endosome and replicate
Block endosome-lysosome fusion
76
How can a pathogen avoid phagocytosis by a macrophage and PMN
Capsule that interferes with complement deposition on bacteria
77
How a capsule aids in avoiding innate host defense
Binds factor H present in serum-degrades complement protein C3b preventing it's deposition on bacterial cell surface
78
How a pathogen will avoid contact with phagocytes
Invade location not surveilled phagocytes
avoid inducing inflammation
Inhibit phagocyte chemotaxis
Bind host molecules to hide antigenic surface
79
How can a pathogen Inhibit phagocytosis
```
Polysaccharide Capsule
M protein and fimbriae
O Polysaccharide
K Antigen
Cell-bound Protein A
```
80
How Cell-bound Protein A inhibits phagocytosis
Binds to Fc region of IgG and blocks Ab binding(prevents opsonization)
81
How can a pathogen munipulat PAMPS and AMPS
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
What does Varying surface antigens on pathogens do
Prevent PAMPS from being recognized
83
Why pathogens would kill host cells
Decrease number of defenders and prevent the alarm bells from sounding
84
Roll of strptolysin and Leukocidin
Target neutrophils to release lysozomal content into cytoplasm
85
Roll of Exotoxin A
Targets and kills Macrophages
86
Ways baceria can injur host
Exotoxin, endotoxin, hydrolytic enzymes, superantigen exotoxins
Inflammation
87
Bacterial secreted proteins
Exotoxins
88
Lipid A portion of LPS of Gram-negative bacteria that stimulates cytokine release(inflammation)
Endotoxin
89
Facilitate tissue invasion
Hydrolytic enzymes
90
Stimulate massive sytokine secretion (toxic shock)
superantigen exotoxins
91
Prolonged immune response to bacteria can damage host tissues
Inflammation
92
What can be exotins
Local or Systemic if in blood
93
What can exotoxins bind to
Host cell specific-bind to specific cell receptors
94
Effect of Exotoins
Depends on target but may inhibit, stimulate, or kill
95
A- B exotoxin parts
B=bind to host cell surface receptor glycoproteins or glycolipids
A=transported by direct fusion or endocytosis into host to act on target
96
Create pores in host cell membrane(DAMPS)
Membrane active exotoxins
97
Lipid A portion of LPS
Endotoxin
98
How endotoxin induces fever
macrophages release IL-1 and TNF
99
Useing antibiotics on Endotoxin
Makes it worse because Lipid A is released
100
Binds to MHC II, activating T cell non specifically, causing them to release Cytokines IL-1 and TNF to cause shock/inflammation
Superantigen
101
Chronic infection can cause
delayed type hypersensitivity reaction
