Immune system Flashcards
1
Q
What is blood made up of
A
liquid (plasma) and cellular (red and white) component
2
Q
Where does blood come from
A
Blood cells arise from Hematopoietic stems cells in the bone marrow.
Myeloid stems cells and Lymphoid stem cells
3
Q
What are the two types of stem cells
A
Myeloid stem cells and lymphoid stem cells
4
Q
Adaptive immunity
A
Also called acquired or specific immunity
Develops after exposure to pathogens or antigens
Slow and specific response
5
Q
Innate immunity
A
Present in all animals before exposure to pathogens
Involveds FIRST and SECOND lines of defense
Fast and nonspecific response to infection
External barriers, internal cellular, and chemical defenses
6
Q
First line of defense (physical)
A
Skin: Tightly packed cells of outer epidemris (+keratin = tough protein preventing entry of m/o)
Mucous membranes: Lines GI, GU, and resp
Ciliary escalator: trapped and transport microbes away from lungs
Washing action: tears, salvia, urine, and vaginal secretions
7
Q
Chemical factors of first line of defenese
A
Secretions: Skin pH 3-5 (inhibits microbes bc most are neutrophils)
Lysozyme: enzyme in skin, saliva, and tear secretions
Degrade peptidoglycan layer of bacteria making them susceptible to lysis
Fungistatic fatty acid in sebum
Lactic acid in V
Produce lactic acid (acidic pH)
Stomach acid is lethal to most bacteria
Normal microflora: Antoagism/competiic
Some are opportunistic pathogens
8
Q
Lysozyme
A
enzyme in skin, saliva, and tear secretions
Degrade peptidoglycan layer of bacteria making them susceptible to lysis
9
Q
4 second line of defenses
A
Defensive cells
Inflammation
Fever
Antimicrobial substances
10
Q
What are the defense cells of the body
A
WBCs (leukocytes) engulf pathogens via phagocytosis
Phagocytic cells
11
Q
What types of phagolytic cells are there
A
Macrophages: ciricrulating phagocytes
Neutrophils: Stimulate acquired immunity
Dendtricic cells: stimulate acquired immunity
Engulf and destroy pathogens
Act as antigen presenting cells
12
Q
How does phagocytosis occur
A
Chemotaxis and adherence of m/o tophagocyte
Ingestion of m/o to form phagosome
Phagolysome: Fusion b/ww phagosome and lysosome (ingested m/o digested by enzymes)
Residual body containing indigestible material that are discharged as waste to outside
Some m/o pieces presented on surace of APCs
13
Q
Phagosome
A
a vesicle (encolosure surrounded by a membrane)
Pathogen is swallowed an enclosed in a membrane
Recognized by lysosome
14
Q
What do phagocytes use tentacles for
A
To grab on to phagosome
15
Q
How can m/os avoid phagocytosis
A
Capsule preventing adhereance to macrophage
Leukocidins kill macrophage
Lysis of phagolosome
Escape from phagosome
Orevt fusion of phagosome with lysosome
Survive phagolusosome
16
Q
How would a m/o lyse the phagosome
A
An organism like Lysteria: Releases enzymes to destroy phagolysosome complex
17
Q
How does a m/o escape from the phagosome
A
(into the cytoplasm of phagocyte)
i.e Shigella
Begins multiplying inside phagocyte (without worry abt being captured again
18
Q
How do m/o prevent fusion of phagoosome with lysosome
A
HIV and M. TB
Produces chemicals preventing lysosome from fusing (organism cannot be destroyed)
19
Q
How do organisms survive phagolysosome
A
Coxiella bunetti (spore) loves it in the phagolysosome
Uses phagosomatic enzyme to activate multiplication process
Eventually break out via phagolysis
20
Q
Two types of inflammation
A
local
systemic
21
Q
SS of local inflammarion
A
Redness
Pain
Heat
Swelling (edema)
Loss of function
22
Q
Steps of inflammation
A
Injury
Mast cells recognize presence of foreign objects, release histamines in response
Histamines cause vasodialation
Skin appears red with increased bloodflow
Vasodialation also brings neutrophils and other cells
Margination: Neutrophils, macrophages (any cells helping in the process of healing) begin sticking to the walls of capillaries
Vasodialtion cause the capillaries to become leaky (fluids ooze out causing edema/swelling) some cells begin to squeeze out of capillaries = emmigration
Macrophages (phagocytes) in the area where bacteria/pathogens are and they begin phagocytosis
In the process, some macrophages die = pus
Neutrophils (also involved in phagocytosis similar to WBCs)
Histamine: released by mast cells
Tissue repair: Occurs by way of chemicals (platelts ) brought by vasodialaiton
23
Q
Why does warmth occur with inflammation
A
with vasodialtion, as blood brings skin closer to body temperature
24
Q
What causes pain in inflammaiton
A
Swelling pressing against pain receptors
25
What is fever
A systemic response (a kind of systemic inflammation)
Abnormally high body temp
26
What are included in internal antimicrobial substances
COmplement systems
Interferons
Defensisn
27
Complement systmes
special proteins that attack and lyse microbes
28
Interfereons
proteins secreted by virus infected cells that inhibit viral multiplication in response to viral infection
29
Defensins
proteins secretedby activated mactophags to destroy pathogens to start the process of destroying pathogens
30
What part of a bacteria causes fevers?
Endotoxins
31
3 ways that complement proteins are involved in the immune response
Opsinization
Cytolisis
Activation inflammation
32
Opsinization
Bacteria are marked to be easily reconizable to macrophages (complement protein attached to pathogen)
33
Cytolisis
Breaking up of the bacteria cell (complement proteins have invaded into the membrane of the pathogen)
34
How do complement proteins aid in the activitation of inflammation
Complement protein that attaches to the mast cell that stimulates the mast cell to release histamines that lead to vasodialtion
Aid the body to stimulate inflammation (especially local)
35
Margination
Phagocytes sticking to the walls of blood vessels is a condition known as _________________.
36
Diapedesis or emigration
Fluid and cells leaving the capillaries
37
Opsinization increases a phagoycites
Adherence
38
Which cell is inbolbed in producing cytokines to activate other immune system cells
T cells
39
leukocidins
Molecules that are capable of destroying phagocytes
40
Measles viruses are capable of inactivating host defenses by
suppressing the immune system.
via suppressing activity of cytokines or reproducing within T cells
41
How are complement proteins labelled
With a C and a number 1-9
42
What are the general requirements for any organism to cause a disease within a host
Gaining access to host (portal of entry)
Evasion of host defenses
Adherence to host tissues
43
Why does V. chloreae have such a high ID50 (10 to the 8)?
To cause infection, V. cholerae must survive immune responses AND acidic environment of stomach
44
What are the properties of exotoxins
Target speciic cellular structures or molecules
Protein molecules
Very small amount of exotoxin is lethal
45
Why are antibiotics alone not ideal treatment for V. cholerae
Antibiotic therapy addresses only the growth of V. cholerae; it doesn’t address the extreme dehydration suffered by a person infected with V. cholerae.
46
What are toxoids?
Bacterial exotoxins can be altered to create toxoids, which can be used to produce protective immunity in a host.
47
Must all pathogens penetrate the body to cause disease?
No
48
Properties of exotoxins
Produced and secreted by active/growing cells
Usually inactivated by cooking
Host responds with specific antibodies called antitoxins
49
Antitoxin
Host responds to the production of exotoxins with specific antibodies called antitoxins
50
Are exo or endotoxins more toxic in smaller doses?
Exo
51
What type of toxins can BOTH G+ and G- produce?
Exotoxins
52
Examples of exotoxins
Tetanus toxin
Cholera toxin
Staphylococcal enterotoxin
53
Properties of endotoxins
Produced by Gram-
Released upon phagocytosis/death of cell
May survive sterilization and contaminate medical devices/medications even if completely free of bacteria
54
Examples of endotoxin using diseasse
Salmonella typhi (causing typhoid fever)
Neisseria meningitdis
55
Do viruses produce endo or exotoxins
No
56
Steps of the A-B exotoxin
57
How can action of A-B Toxin be blocked?
Blocking binding sites on B portion of toxin
Inhibiting secretion of proteins from bacterial cell
Blocking receptor mediated endocytosis in cells targeted by A-B toxin
Block host cell receptors to which toxin binds
Block separation of A and B components of toxin
58
Strategies to block/reduce effects of superantigen toxins
Block secretion of proteins by bacterial cells
Block release of cytokines from T cells
Block molecular determinants on superantigens that interact with T cells
Neutralize circulating cytokines
59
Methods that toxin likely disrupts [plasma membrane of host cell
Insertion of protein channel
Disruption of phospholipid bilayer
60
Possible symptoms of endotoxins
Fever, chillls, weakness, fatigue
May worsen after treatment of G- infection
Causing life-threating drop in BP called endotoxin shock
61
Pyrogenic response
Fever
62
How does G- bacteria cause fever
First, a gram-negative microbe is phagocytized and digested. In the process, endotoxin is released within the phagocytes;
the phagocyte responds by releasing cytokines,
These cytokines are distributed throughout the body by the circulatory system.
When they reach the brain, the hypothalamus responds by releasing prostaglandins, which ultimately raises the body’s temperature and causes a fever.
63
Is a parental route a portal of entry or exit?
Both
64
Injections, surgery and deep wounds are examples of what kind of portal of entry?
Parental route
65
What kind of anthrax infection is the easiest to acquire
Cutaneous antrhax
66
Antigenetic variation
process allows pathogens to alter their surface antigens to avoid attack by antibodies produced by the immune system.
67
Invasins
These microbial surface proteins rearrange the host cell's actin filaments, allowing pathogens to enter and move in and between cells.
68
Siderophores
proteins that extract iron from host proteins; the bacteria obtain the iron by retrieving these proteins.
By tightly binding iron, removing it from host proteins.
69
nutrient depletion, accumulation of waste products, pathogen entry and exit, and ruptured host cells are examples of what kind of damage?
Direct
70
Cytopathic effects
These describe the visible effects of viral infections that results in host cell damage.
71
Why does S. aureus need iron
Without iron, S. aureus cannot generate energy via the electron-transport chain.
72
the name for a protein that can lyse red blood cells?
Hemolysin
73
Which of the following features of Salmonella prevent it from being phagocytosed?
Flagella
74
Where do Salmonella pathogens grow and replicate in the infected host?
Inside phagocytes
75
How are immune cells able to detect foreign pathogens?
They are able to detect structures on the surfaces of foreign cells that are not found in the host.
76
How does a capsule help certain bacteria evade detection by the immune system?
The capsule is composed of polysaccharides that are similar to those found in the host; thus, the immune system does not recognize it as foreign.
77
TB bacterium grows where
Inside macrophage
78
How does the protozoan Trypanosoma evade detection by the immune system?
It can change the surface antigens frequently, preventing the immune system from tracking it.
79
An exotoxin that has the ability to kill or damage host cells is referred to as a(n)
Cytotoxin
80
Which domain of the A-B toxin binds to cell surface receptors on the host cell?
B Domain
81
How are superantigens different from other types of exotoxins?
Superantigens must be endocytosed into a target cell before becoming active.
82
leukocidins
Molecules that are capable of destroying phagocytes
83
How do superantigens enable pathogens to hide from the immune system if they actually stimulate the immune system?
They cause the immune system to produce an exaggerated response, distracting it from the actual pathogen.
84
How can capsules enable bacteria to evade the immune system?
Capsules block the complement biding sites on the surface of the pathogen.
85
Certain traits that allow pathogens to create infection and cause disease are termed
VIrulence factors
86
Which of the following enzymes breaks down the "glue" that holds cells together?
Hyaluronidase
87
How do fibrinolysins enhance a pathogen's virulence?
They break down fibrin proteins that are involved in clot formation, allowing the cells to penetrate deep into damaged skin.
88
Fever and NK cells are part of what line of defense
Second
89
T and B lymphocytes are part of what line of defence?
Third
90
Eosinophils phagocytic?
Yes, they are phagocytes
91
Steps of phagocytosis
Chemostaxis
Adherence
Pseudopods engulf and internalize microbe forming phagosome
Lysosome and phagosome fuse and form phagolysosome
Digestion of microbe
Discharge of excess material
92
How do microfilaments play a role in chemotaxis
Chemotaxis is brought about by the binding of various chemoattractant substances (microbial components, complement components, cytokines) to receptors on the surface of phagocytes. This triggers cell movement toward higher concentrations of the attractant. The interaction of actin microfilaments and myosin (cytoskeletal elements) within the phagocyte makes this movement possible.
93
Strategies microbes use to avoid [hagocytosis
Produce leukocidin
Capsule
Preventfusion of phagosome with lysosome
Escape phagosome
94
What does the plasma membrane of a phagocyte attach to on a microorganism?
Glycoproteins
95
What is the role of opsonins?
They create "handles" that make it easier for the pseudopods of phagocytes to attach to the microbe invader.
96
How is Streptococcus pneumoniae able to avoid destruction by a phagocyte?
Their capsules make them "slippery" to phagocytes.
97
Which of the following microorganisms use M protein to avoid destruction of a phagocyte?
Streptococcus pyogenes
98
If a new bacterial pathogen entered a human body through an accidental needle stick, the first cell that would try to kill the pathogen would likely be
a phagocyte.
99
When does maturation occur in phagocytosis
After ingestion, before killing
100
why the lectin or alternative pathway would stimulate a more immediate response than the classical pathway.
Neither pathway relies on antibodies.
101
What direct effect do histamines and leukotrienes have on capillaries?
They allow capillary walls to open and become leaky.
102
Cells from damaged tissues and the complement pathway both release
Histamenes
102
Emigration is
the migration of phagocytes through blood vessels to the site of tissue damage.
103
5 classes of antibodies
IgG
IgM
IgA
IgD*
IgE
104
IgG
Produced as monomer
80% of all antibodies
Enhances phagocytosis (opsinization)
23 day life
105
Most antibodies are
IgG
106
IgM
Pentamer (5 antibodies held together into this large structure)
First antibodies produces in initial response to infection
Antigen binding sites are on outside, therefore this molecule can bind many antigens and can bring about agglutination of antigens (several antigens clumped together) and phagocytes easily able to grab onto these structures
5 day life
107
IgA
Two antibodies joined together (dimer)
Found in secretions (mucous, saliva, milk, tears)
Provide localized protection in these specific areas
6 day life
108
Which antibody is a pentamer
IgM
109
IgE
Can bind to mast cells (histamine granules) causing release of histamines and basophils cells (responsible for meany allergic reactions)
Responsible for lysing large parasites (parastic worms)
2 day life
110
How does pathogen recognition occur
When you encounter pathogen to thefirst time, pieces of the pathogen are take nto the lymphoma, and there they are tested against different T cells and B cells, and those that respond proliferate (clones) and each one that responds will now be ready if they encounter the pathogen again
They differentiate into long lived memory cells and short lived plasma cells
111
Which antibody aids in opsinization
IgG
112
Antibody titer
the amount of Ab in the serum
Two immonlogical responses
113
When do IgM and IgG begin production after exposure to pathogen?
2-4 days
114
When does IgM peak in primary encounter
10 days
115
When does IgG peak in primary encounter
14 days
116
What is the difference in curves in IgM and IgG
In primary encounter, IgM is produced quicker, but all is destroyed after encounter, and is replicated in second encounter
IgG Produced slower in intial encounter, but does not drop down to 0, therefore, secondary encounter the IgG antibodies remeber the antigen or a quicker stronger secondary response
117
How many days untl IgG increases considerably in second encounter
5 days
118
Do IgM and IgG recognize different antigens?
Both IgM and IgG recognize similar structures on antigens
119
What would a third encounter immune response look like
Third time exposure results in a very similar response
120
Agglutination
Antigen binds to multiples antibodies to cause it to be easier to spot by phagoccytes
Reduces number of antigens to be dealt with
121
Opsinization
Complement proteins bind to pathogens helping phagocytes recognize antigens much better
Adherence of pathogen to phagocyte much greater (Handles)
122
Neutralization
Bc toxins need to get INTO body to causes damage, but the presence of antibodies that bind to the toxins do not allow it to enter the cell
Bacteria and viruses normally need to interact with host cell to cause damage, coating them in antibodies prevent them from interacting with the cell
Blocks adhesion of bacteria and viruses to mucosa
123
Activation of complement:
Two antibodies bind to pathogen. Complement protein binds to athe antibodies and becomes activiated, in doing this it attracts other complement proteins to the pathogen, and they start forming holes in the pathogen to cause lysis.
124
Antibody-dependent cell-mediated cytotoxicity
Antibody that bind s to large parasite, attract WBCs, becomes activated to produces enzymes that damage the parstite membrane
125
Two different chains on T cell receptors
Alpha and beta
126
3 regions of an antibody
Constant, variable, and transmembrane regions
127
What region of antibody provides specificty
Varibale region provide antigen specificity
128
How does age affect a persons ability to make t cells?
Decrease with age
129
Infected cell:
Factory for creating more viruses/pathogens
130
Affected cell
Going crazy like cancer cells
131
How do T cells act in an autoimmune disorder
When T cells cannot recognize affect/infected cells accurately, they can destroy healthy cells (auto immune disorder)
132
MHC
Major histocompatibility complex (MHC) are genes that code for MHC proteins found on cell surface. Two major classes of MHC proteins
133
Class 1 MHC
Found on all nucleated cells in the body (of infected cells - declare that they are infected
Identify self
They display peptide antigens TO cytotoxic T-cells - these T cells destory the infected cell
134
Class II MHC
Proteins located on Antigen presenting cells
Dendtric cells, macrophages, and B-cells
Display antigens to Helper T cells and Cytotoxic T cells
135
APCs
Digest and process cells and then display a mark on the surface of them so that other cells can recognize them
136
How are T cells distinguished
Distutished by proteins on cell surface called “clusters of differentionaton (CD) antigens
137
Helper T-cell
CD4 Cells
65% of mature lymphocytes
Bind to MHC class II on APCs to activate B and T cells
HIV attacks/destroy CD4 cells
138
Cytotoxic T-cells
CD8 Cells
35% of mature T lymphocytes
Binds to MHC class 1 on infected self cells (being displayed by MHC class 1 proteins on the surface of infected cell) to activate cell apoptosis (programmed cell death)
139
How do MHC 1 cells behave when infected
they take bits and pieces of antigen and display them on there MHC class 1 proteins
140
What is the double recognition of T cells
Bind to antigen receptor and reconize how the cell should look
Recognize MHC 1 or 2
141
What occurs if infected cell displays antigen of MHC 1 protein
If there is an antigen being displayed, the antigen receptor will see it and generate the reaction (cell aptosisis)
Cytoxic T cells go around checking cells, regardless if they are infected or not
142
What do Helper T cells do
After Dendritic Cell engulfs pathogen it displays antigen fragments on MHC class 2 on their surface
Helper T binds with MHC, the recognition of antigen fragments causes secretion of cytokines by APC cell
Helper T cell proliferates, all with receptors for MHC antigen fragment complex
H T cells secrete cytokines activating B cells and cytotoxic T cells
B cells differentiate to remember antigen for future and C T cells destroy infected cell
143
How does a helper T cell act on a B cell
B cell internalizes antien, displays antigen fragment on MHC 2
Helper T cell with specific receptors for fragement binds and activates B cell
B cell proliferates and differentiates into memory B cells and antibody secreting plasma cells
Antibodies produced are specific to for the antigen that started the response
Without helper T cell, B-cell would do this process on it’s own, but helper T cell comes in to help it to the job better
144
How are affected cells dealt with
Cytotoxic T cells would recognize them by abnormal structures (antigens) being displayed on the MHC class 1, therefore these cells are also destroyed
Cells that are going crazy all the time, but we don’t notice
145
Why are transplants problematic
All cells in the body with a nucleus have MHC class 1 proteins
These are the proteins the distinguish all your cells from someone elses
This is the problem with transplants
Immunosuppressants act to try and reduce the recognition of new cells by Cytotoxic T cells (double recognition)
146
How do C T cells kill
Recognize infected cells and secrete proteins (perforins) that form holes in infected cells- destroying infected cells
147
