Unit 1 Flashcards
1
Q
Pathogens enters on what side to what side?
A
Afferent lymphatic vessel to the efferent lymphatic vessel
2
Q
Why do lymph nodes swell?
A
B cells and T cells are replicating their other lymph cells
3
Q
Steps of when someone gets a cut
A
1- Macrophages come and eat large pathogens
2-Dendrites eat smaller pathogens
3- They travel down the lymph ducts
4- into the lymph nodes and look for matching T cells and B cells.
If not found,
5- They keep moving along the line until they find the right lymph node
4
Q
What does the spleen filter?
A
Blood. Removes blood Bourne pathogens, damaged or dead red blood cells
5
Q
Cells that stimulate B and T cells arriving in the spleen
A
Splenic macrophages and dentritic cells
6
Q
Asplenia
A
People born without spleens. They are very susceptible to infections
7
Q
Pulp where RBC are monitored and removed
A
Red pulp
8
Q
Pulp in spleen where WBC gather
A
White pulp
9
Q
Most extensive mucosal surface of the body
A
Gut
10
Q
Gut associated lymphoid tissues (GALT)
A
Tonsils, adenoids, appendix, peyer’s patches
11
Q
Function of the GALTS, BALTs, and MALTs
A
Filter out pathogens to activate lymphocytes. M cells deliver pathogens across the mucosa for delivery to lymphocytes to be activated.
12
Q
Physical and chemical barriers
A
Skin
Mucosal epithelium
13
Q
Baby’s have no _____ in utero until birth
A
Flora, or anything in the gut
14
Q
Commensalism microorganisms function
A
Colonize the skin and mucosa
15
Q
Optimal commensalism action because of the reliable food source
A
Gut
16
Q
2 categories of infection
A
Intracellular infections and extracellular infections
17
Q
Most bacteria is this type of infection, as well as fungi and parasites
A
Extracellular
18
Q
Infection subject to soluble secreted molecules of the immune system
A
Extracellular infection
19
Q
Infection inside the cell. Once the cell is infected, the whole cell has to die. Typical viral infections
A
Intracellular infections.
20
Q
First defense mechanism
A soluble protein
A
Complement
21
Q
Where are complements present and where are they made?
A
Made in the liver
Present in lymphatics and blood
22
Q
Actions of complements
A
They coat the surface of bacteria/virus to make them easier or tastier to phagocytise
Some complement proteins are proteases
23
Q
Key to complement cascade
A
C3
24
Q
Upping activation, what happens to C3?
A
C3 is cleaved into C3a (the smaller molecule) and C3b (The larger molecule)
25
Inactive form of complements
Zymogens
26
What C3 binds to the pathogen surface? What is this called?
C3b
| Compliment fixation
27
Which C3 calls for help, and who do they call?
C3a, calls macrophages
28
Why does C3b bind to pathogens?
It has a high-energy thioester bond in the glycoprotein. This is targeted by water to allow tight fixation to any pathogen surface
29
3 pathways of complement activation
1- Alternative pathway
2- Lectin pathway
3- Classical pathway (discovered first, but last pathway)
30
Pathway that works at the start of infection
Alternative pathway
31
Pathway induced by infection but takes time
Lectin
32
Pathway that required binding of an antibody or specialized protein (C-reactiv protein) to pathogen surface?
Classical pathway
33
First step of alternative complement pathway
Hydrolysis of C3 by water or pathogen surfaces
| Makes iC3 or C3(H2O)
34
In alternative complement pathway, C3b molecules:
attach to molecules on the pathogen’s surface
35
What does C3 convertase do?
Cleaves C3 to make C3a and C3b
36
Process of C3 converts to C3bBb
C3b binds
B sits on top of C3b. Now C3bB
D comes and sits on tip then breaks B into B.B. and Ba
Bb stays so now is C3bBb
This now goes to cleave other C3s
This is a self-perpetuating process
37
C3bBb is also knows as:
Alternative C3 convertase
38
Complement control proteins regulate:
Plasma proteins that interact with C3b on human and microbial cell surfaces which include:
Properdin (factor p)
Factor H
Factor I
Membrane proteins on humans cells that prevent complement fixation on human cells
39
Properdin action:
Comes along and binds to C3 convertase and improves the entire response. Increases power, speed and efficiency
40
Factor H
Acts opposite of Properdin. Binds to C3b and promotes cleavage of it by factor I so that is becomes iC3b
41
Factor I action
Works with Factor H. Decreases C3 convertase molecules on the pathogen surface
42
What happens when there is no factor I?
C3bBb is unchecked, so all complements are burned through quickly. Causes increases amount of illnesses
43
Membrane proteins that interfere with complement activation at human cell surfaces
Decay-accelerating factor (DAF)
Membrane cofactors protein (MCP)
44
DAF action
Binds to C3b and renders it inactive
45
MCP action
Makes C3b more susceptible to cleavage and inactivation by factor I
46
Monocytes mature into:
Macrophages
47
Cell that serves as a part of innate and adaptive immunity
Macrophages
48
Location of macrophages
On mucosal surfaces and in the lives (Kupffer cells)
49
Macrophages can phagocytose ____ (nonspecifically/specifically)
Both
50
What does complement receptor 1 (CR1) do?
Enhances phagocytosis
51
What bind to iC3b on microbial surfaces to enhance phagocytosis
Complement receptors, CR3 and CR4
52
All of the CR’s work together to:
Promote effective phagocytosis of complement-coated pathogens
53
Other complement components: (5) other than binding
1-C3b binds to alternative C3 convertase (produces an enzyme- alternative C5 convertase- acts on C5 component)
2- Alternative C5 convertase- composed of B.B. and 2 C3b fragments. Designated C3b2Bb
3- C5 is cleaved into C5a and C5b fragments -
C5b forms a membrane-attack complex (MAC attack) which breaches pathogen membranes by making holes into the membranes- C5b binds to C6 and C7 and these I sent into the lipid bilayer
4- C8 binds to C5b and inserts into the membrane to initiate polymerization of C9 to help form transmembrane pores
5
54
Terminal complement components are regulated by:
Soluble and surface associated proteins
55
Purpose of soluble proteins
Prevent pores from forming in the host cells-
S protein
Clusterin
Factor J
56
Purpose of Cell surface proteins
Homologous restriction factor
57
CD59 prevents:
C9 from being called by the C5b, C6, C7, C8
58
What complement peptides have larger effector functions?
C3b and C5b
59
What complements cause inflammation and what do they call
C3a and C5a- calls phagocytes, endothelium cells and mast cells
60
What acts on neutrophils and monocytes to increase their adherence to blood vessel walls? Acts as a chemoattractant to call cells to the side of inflammation
C5a
61
Plasma enzymes that induce blood clotting
Coagulation system
62
Functions of complement ****IMPORTANT*****
1- Opsomization- binds to pathogens to make tasty
2- Causes inflammation (chemoattractants- chemical components that call all to the site)
3- MAC Attack
63
What happens in a blood clot
Microorganisms are trapped and blood and fluid loss is decreased. Platelets release substances that cause inflammation and trigger wound healing I
64
Enzymatic cascade triggered by tissue damage to cause vasodilation
Kininsystem
65
Pathogens make ______ to damage host tissues
Proteases
66
What lure proteases which are attracted by the thioactive region to envelope and sequester the proteases?
Alpha 2-macroglobulins
67
Produced by neutrophils
| Penetrate microbial membranes to disrupt the integrity of bacteria, enveloped viruses and fungi
Defensive
68
Antimicrobial peptides
Defensins
Specialized defensins
Pentraxins
69
Assist with phagocytosis by binding bacterial membranes to phagocytic cells
Pentraxins
70
How can innate immunity be induced?.
By the invading pathogen
| Delay of 4 days
71
Properties of innate immunity receptors
Expressed by innate cells like macrophages, NK cells
| Specific for microbial carbohydrates, lipids and proteins
72
Innate immunity receptors allow the cells to distinguish:
Self from non-self
73
Antigens recognized by the innate cell receptors are:
General, shared components
74
In a cell becomes infected by a pathogen, what happens to the cell?
It HAS to die
75
Macrophages receptors recognize:
The cells-surface carbohydrates of bacterial cells, but NOT those of human cells
76
Natural killer cell receptors recognize:
Changes at the surface of human cells that are caused by viral infection
77
Macrophages in tissues are ready to:
Attack pathogens and unauthorized commensalism
78
Phagocytic receptors are specific for:
Bacterial carbohydrates and lipids
79
Recoeptors that recognize bacterial carbohydrates
Lectins
80
Lectins include:
Mannose receptor and dentin-1
81
C-type Lectin
Ricin
82
Macrophages receptors that recognize negatively charges microbial ligand
Scavenger receptors
83
SR that protects the macrophage and assists with phagocytosis. Collagenous structure
Marco
84
Receptors recognize ligands like LPS, hemagglutinin, Luca NS
Complement receptors CR3 and CR4
85
After macrophage receptors are boundL
Receptor mediated endocytosis occurs
86
Phagosomes fuse with lysosomes to form:
Phagolysosomes- enzymes in the lysosomes destroy the microbe
87
Signal macrophages that recruit additional cells
Toll-like receptors (TLR)
88
Inflammatory cytokines include:
Interleuken-1beta
IL-6
IL-12
CXCL8
Tumor necrosis factor alpha
89
Action of CXCL8
Calls neutrophils, macrophages and NK cells toward damaged or infected areas
90
IL-6 action:
Acts upon muscle cells and fat cells. Causes them to generate heat.
91
Short lived killers
| Circulate in blood in tremendous numbers- polymorphonuclear cells
Neutrophils
92
What handed when neutrophils die?
They form pus
93
Neutrophil extracellular traps (NETs) continue killing pathogens
Netosis
94
Antibodies are secreted by:
B cells, or plasma cells
95
Antibodies action:
They clear the blood and tissue of invading pathogens and their toxins
96
Antibodies are specific for
any number of pathogens that can enter the body
97
Antibodies Binding to a specific pathogen results in
B cell proliferation
98
Colonial selection
Large amounts of antibodies are produced specifically for a single pathogen
99
Lack of game globulin in plasma
Agammaglobulemia
100
Antibodies recognize and bind to:
Antigen
101
Variable part of the antibody is based on
Amino acids on the ends of the Y structure
102
Differences in types (or isotopes) are in the ______ region and they :
Constant
They confer functional differences
103
Polypeptide chains of antibody structure (4)
2 identical heavy chains- H chains
2 identical smaller light chains (L chains)
104
Antibody variable region
Forms the antigen-binding site
105
Antibody Constant Region
No variation in amino acid sequence
106
Hinge region in antibodies
Region in the middle with flexibility
107
FAB in antibodies
Fragment antigen binding region- bind antigen
108
Fc in antibodies
Mediates the effector functions
109
Ig types
IgG IgM IgD IgA IgE
Think MADGE
110
Loops that create differences in the binding sites
Hypervariable regions
111
regions that bind to the antigens complementarily
Complementarity-determining regions (CDR1-3)
112
Part of the antigen that binds to the antibody
Antigenic determinant (epitope)
113
Antigen that contains more than one epitope or copy of the epitope
Multivalent antigen.
114
Differences in epitope
Linear epitopes- successive amino acids
| Discontinuous epitopes- amino acids brought together because of folding
115
Bonding strength of the antibody to antigen
Affinities
116
What can be used to make antibodies
Animal vaccinations
117
What is produced specific for immunizing antigens
Anti sera
118
Making immortal B cells
Hybridoma production
119
B cells fused with a tumor cell form a _____
Hybridoma
120
Detecting antibody producing B cells- exposure to a laser and separating by antibody
Flow cytometry
