Immunity Flashcards
(139 cards)
1
Q
What percent of success must the immune system function with? Against what types of invaders?
A
100% success
Prions, viruses, bacteria, fungi, protozoans, helmiths, insects
2
Q
What is bacteria differentiated based on? (6) Expand on each
A
Gram stain (positive or negative) Shape (cocci, bacillus, other) Oxygen requirements (aerobic, microaerobic, facultative anaerobic, obligate anaerobic) Toxin Formation (Endo, exo or no toxin) Spore Formation (yes or no) Intracellular (yes or no)
3
Q
Which type of bacteria retains the stain in a gram stain?
A
Gram positive
Gram negative does NOT retain the stain.
4
Q
In the handful that we don’t view as gram positive or gram negative what is one of the most important tests? Why?
A
- Acid-Fast
2. TB
5
Q
Do facultative anaerobs require air?
A
No, they can use air but they can also survive without.
6
Q
As far as oxygen requirements, most bacteria are classified as what?
A
Facultative anaerobs
7
Q
Where do we find the few bacteria that are really obligate aerobics (they need oxygen)?
A
In the lungs.
8
Q
What happens if an obligate anaerobic bacteria see’s atmospheric concentrations of oxygen? Where do we see these?
A
- It dies.
2. Deep penetrating wounds and deep in the GI tract.
9
Q
Why do bacteria form toxins? What are they trying to kill? What are they not trying to kill? What happens to us in the process? Does the majority or the minority of bacteria produce toxins?
A
- If there is food available it is a good environment for other bacteria too, they will multiply rapidly and then try to kill their competition
- Toxins are intended to kill their competition
- They are not trying to kill their host
- We become the collateral damage.
- Minority
10
Q
Most antibiotics come from where? Why?
A
Most of our antibiotics come from microbes because they are intended to kill bacteria.
11
Q
When does a bacteria produce spores? Why are these of concern? What does this mean for the overall survival of the bacteria? Name one.
A
- If the environment is really hostile and the bacteria is about to die.
- They are freaking indestructible
- A spore former can survive anything
- C-diff
12
Q
We are normally carriers for C-Diff (ew). Why do we not normally contract this god awful bacteria?
A
Bacteria in our GI tract keeps it in check (killing it) so we normally see it in patients who are on a ton of immune-suppresents or a lot of antibiotics because we are cleaning out their GI tract and removing the competition.
13
Q
Are most bacteria intracellular or extracellular?
A
Extracellular.
14
Q
Name the six gram positive bacteria from the chart we are supposed to know. Which ones are cocci? Which ones are bacilli?
A
- Staphylococcus-cocci
- Streptococcus-cocci
- Clostridium-bacilli
- Propionibacterium-bacilli
- Bacillus-bacilli
- Listeria-bacilli
Three end in S, two in M and only one in A
15
Q
Name the thirteen gram negative bacteria from the chart we are supposed to know. Which ones are cocci? Which ones are bacilli?
A
- Bacteroides
- Bordetella
- Brucella
- Camplobacter
- Escherichia
- Haemophilus
- Klebsiella
- Legionella
- Neisseria- THE ONLY COCCI (the rest are rods)
- Pseudomonas
- Salmonella
- Shigella
- Vibrio
9 end in A, 3 in S, 1 in O
16
Q
What two things are we supposed to remember about clostridium? Why were here was it gram positive or negative? Cocci or bacillus?
A
- Spore forming and toxin producing
- Positive
- Rod
17
Q
What are the most common bacteria? Second most?
A
Bacteroides are the most common
E-coli is the second most common (when we take antibiotics it wipes these out and then we end up with more C-Diff).
18
Q
Other than C-Diff who else forms spores?
A
Bacillus
19
Q
A gram positive bacterium has a thick layer of what?
A
Peptidoglycan
20
Q
Does the gram negative bacterium have a thick peptidoglycan layer?
A
1 Yes.
21
Q
If the gram negative bacteria has the peptidoglycan layer which is responsible for the positive stain in gram positive bacteria then why do they not stain?
A
They have an outer membrane.
22
Q
Where do most of our antibiotics target?
A
The cell wall.
23
Q
Plasmids are equivalent to what in bacteria? Why? Where is this most useful for bacteria? Is it useful for humans? Why? Give an example.
A
- Superpowers
- Bacteria can make a copy of it’s DNA and give it to its neighbor in the form of the plasmid.
- Resistance
- Yes. Say we have a peptide or a protein that we want made in big gallon drums. We put the DNA on a plasmid, stick it into the bacteria, convince them that it is really useful and then the bacteria makes a ton of copies of it. Then we kill the bacteria and harvest what we want.
- This is how we make insulin. Once we have the DNA for insulin we can change it and make it last longer, shorter or whatever.
24
Q
A virus particle is called a? What does it consist of?
A
- Virion
2. Some kind of a capsule and genetic material, has a minimum of 3 genes, does not have ribosomes.
25
What does the virus do on their own?
Nothing. They have to infect a host cell in order to do anything.
26
What are virus particles looking for when searching for a host cell? What does this make them? Give an example.
1. Looking for a cell surface protein only cells with a cell surface protein close enough to what that virus is looking for will work.
2. Not just species specific but cell type specific as well.
3. HIV going after T-helper, Hepatitis goes after the liver, Herpes goes after neurons
27
When can a virus switch species?
Only if the second species has a cell surface protein close enough.
28
How does a virus infect a host cell?
1. It's capsule binds with our plasma membrane and fuses, penetrates and un-coats itself releasing it's genetic material. It's genetic material can go into the nucleus and get inserted into our DNA so now we have a little piece of viral DNA in our DNA. We make it's proteins. We copy it's DNA. It's DNA goes out and combines with proteins and forms new virus proteins and takes a piece of our plasma membrane and away it goes as more virus particles.
29
What are the three most medically relevant Fungi?
1. Candida albicans (normal gut flora, causes opportunistic infections)
2. Aspergillus spp. (highly aerobic, respiratory infections)
3. "tinea" (not a specific fungus, but rather a general term for skin fungus "dermatophytes"
tinea capitis- head
tinea cruris- groin (jock itch)
tinea pedis-feet (athletes foot)
30
Name the 5 types of Hematopoietic cells that come from the bone marrow.
1. RBCs
2. Megakaryocytes-platelets
3. Mononuclear phagocytic system
4. Polymorphonuclear leukocytes/granulocytes
5. Lymphocytes
31
What kind of a role do megakarocytes have in the immune system?
Responsible for platelets so they do form clot. Clotting is one of the first things that happens after an injury.
32
What are the three major families of immune cells?
1. Mononuclear phagocytic system
2. Polymorphonuclear leukocytes/granulocytes
3. Lymphocytes
33
What does the mononuclear phagocytic system give rise to? Then what do these cells do? So what part of this family does stuff? What do they do?
1. Monocytes
2. Monocytes do not do anything but they do become macrophages.
3. The macrophages do stuff
4. Macrophages typically camp out in a particular place in the body for a long time.
34
What kind of a life span do macrophages have?
Long-lived.
35
What are macrophages named for? Name the type of macrophages in the liver, brain and lungs? Which one is not an immune cell?
1. Named for the location they inhabit
2. Liver-Kupffer cell, brain-microglia, lungs-dust cell, bone-osteoclast
3. Osteoclast is not an immune cell,
36
If an osteoclast is not an immune cell what is it responsible for?
They are macrophages of the bone. They chew up the bone.
37
What do we call a cluster of macrophages with immune roles?
Multinuclear giant cell
38
What type of cell is normally confused with macrophages? Give an example. What is it's life span?
1. Dendritic cells
2. Langerhans cell-skin
3. They hang out for a long time
39
Name the three types of the mononuclear phagocytic system.
1. Monocyte
2. Macrophage
3. Dendritic cell
40
What is the job of the polymorphonuclear leukocytes/granulocytes family? What is the most common cell type of this family?
1. They have granules. There job is to find something and go de-granulate it.
2. Neutrophils are the most common.
41
When you have a problem who shows up first and what do they do?
1. Neutrophils are the first responder. They degranulate and destroy the area.
42
What is the order of frequency of the immune cells?
```
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
```
Never Let Monkeys Eat Bananas
43
Where are macrophages, dendritic cells and mast cells normally found?
Primarily in the tissue. Not in the blood.
44
Name the four subtypes of the polymorphonuclear leukocytes/granulocytes.
1. Neutrophils
2. Basophils
3. Eosinophils
4. Mast cells.
45
How many flavors do lymphocytes come in? Name them.
1. Three
| 2. B-cells, T-cells and NK cells
46
What can B-cells differentiate into? What is each cell type responsible for?
Plasma Cells which only make a lot of antibody.
| Memory cells which camp our waiting for that particular disease to come back when they will spring into action.
47
What are the three types of T-cells?
1. Cytotoxic T cells
2. Helper T cells
3. Memory cells
48
Why is the immune system complicated?
It has a lot of different parts that interact.
49
As far as the immune system, when we are thinking about "fluid" such as ECF, blood, synovial fluid, the gunk in our intestines and all of the stuff outside of the cells what part of the immune system are we considering?
Humoral
50
As far as the immune system, when we are thinking about the intracellular environment where it is much harder to get something inside, where we would think about viruses, what part of the immune system are we considering?
Cell Mediated
51
The part of our immune system that doesn't change. It is what we were born with and it's what we're going to wake up with each day. What is it called?
Innate
52
Which part of our immune system changes specifically in response to diseases we have experienced? What happens if we haven't experienced it?
1. Adaptive
| 2. If we haven't experienced it then we haven't adapted to it.
53
So our Humoral-Innate immune system contains what kind of cells? What are they and what are they looking for?
Myeloid cells like neutrophils and macrophages that are looking for non-host epitopes.
54
What is an epitope?
Something that the immune system can grab on to.
55
Our Adaptive-Humoral immunity includes what kind of cells? What do they do?
1. B-cells
| 2. They produce antibody.
56
In general where is antibody going to bind?
To stuff outside our cells.
57
What kind of response do we see by our Innate-cell mediated immune system?
In response to intracellular problems like viruses the NK cell is going to look at MHC existence.
58
Our Adaptive Cell Mediated immune response includes what? That do what?
Cytotoxic T cells that kill cells. If we want to get rid of something inside the cell, we have to kill it. The host cell has to die.
59
The cells of the innate immunity include?
Everyone but the lymphocytes. So macrophages, dendritic cells, neutrophils, eosinophils, basophil and mast cells.
60
What are the three activated functions of a macrophage?
1. Phagocytosis
2. Activation of bactericidal mechanisms
3. Antigen presentation
61
What are the two activated functions of a dendritic cell?
1. Antigen uptake in peripheral sites
| 2. Antigen presentation in lymph nodes.
62
What are the two activated functions of a neutrophil?
1. Phagocytosis
| 2. Activation of bactericidal mechanisms
63
What is the activated function of an eosinophil?
Killing of antibody-coated parasites
64
What is the activated function of a basophil?
Unknown
65
What is the activated function of a mast cell?
Release of granules containing histamine other active agents.
66
When there is an injury what do we typically see happen first with the innate immunity?
Bacteria trigger macrophages to release cytokines and chemokines. Cytokines are the signaling molecules that the immune system uses.
67
Cytokines/chemokines signal that the problem is here and then who responds first?
The neutrophil will leave the blood vessel following the chemokines and more towards the macrophage.
68
What is the life-span of a neutrophil?
Short lived. Leave, fight and die.
69
Vasodilation and increased vascular permeability cause what?
Redness, heat and swelling.
70
Inflammatory cells migrate into the tissue releasing what?
Inflammatory mediators that cause pain
71
After macrophages have seen the damage, released cytokines which get to the blood vessel capillary the endothelial cell will extravagate allowing fluid to leak out, what important thing is leaked out? What is the result?
1. Plasma proteins
2. We lost the oncotic pressure that is normally responsible for drawing that fluid back in and now we have local edema and lots of it.
72
What are the five events in the sequence of inflammation?
1. Vasodilation
2. Vascular permeability
3. Cellular infiltration (pus)
4. Thrombosis
5. Stimulation of nerve endings
73
Mast cells are responsible for what two processes? What do we consider it our cell of?
1. Immediate degranulation (fast mediator)
2. Long term synthesis of other molecules (slow mediator)
Our cell of allergic rhinitis
74
The granules that fill mast cells contain (three)? Which have what kind of effect?
1. Histamine which increases vascular permeability causing the runny nose.
2. Neutrophil chemotactic factor which attracts neutrophils to the area
3. Eosinophil chemotactic facter which attracts neutrophils to the area.
75
What do mast cells synthesize?
Progstaglandin (vascular effects and pain., leukotrienes (vascular effects) and Platelet activating factor (vascular effects and platelet activation).
76
Why can't our mast cells synthesize cosinoids in advance? What medication works here to block prostaglandins? What medication works here to block the synthesis of phospholipase A2?
1. They are highly liophilic and would just leak out.
2. Cox-inhibitors, NSAIDs
3. Steriods
77
If you have a heart attack that triggers an inflammatory response what is the first thing that is going to happen? Where? Then what?
1. Edema
2. In the wounded tissue (not the entire heart)
3. Increased vascular permeability, fluid moving in, neutrophils moving into the area, plasma proteins leaking out of the blood vessel, neutrophils clean up and debride the area and macrophages oversea the reconstruction. In the heart reconstruction is just going to be scar tissue.
78
When a monocyte leaves the blood it becomes what? When is it activated?
1. An inactivated macrophage
| 2. Activated when something happens
79
Phagocytosis is completed by which two cell types?
Macrophages or neutrophils
80
What are neutrophils looking for on the surface of the bacteria? What happens when they find it? What happens if the neutrophil sees antibody stuck to something?
1. Non-host epitope. Something that could never occur on a human
2. Grab a hold of it and starts eating it.
3. It immediately knows that it is good to eat (opsonization). It's like the bacteria covered in chocolate. They will have 1000x more affinity for chocolate covered bacteria.
81
Chemokines direct the neutrophil to?
Where the problem is.
82
Antibody increases the rate at which?
Something is phagocytosed.
83
Once we phagocytose a bacteria what must we be able to do to it? What happens if this doesn't happen?
1. Destroy it.
| 2. Then we just have live bacteria in our neutrophil or macrophage.
84
What is PAMP? How many of these do bacteria want to have? Why?
1. Pathogen associated molecular pattern. It is something on the bacteria that looks nothing like our cells.
2. Bacteria want to have as few as possible.
3. We can bind antibody here and it is much easier for the phagocyte to detect that it needs to destroy it.
85
Opsonization greatly increases?
efficiency.
86
What are cytokines responsible for in the initiate response of inflammation? What is the time frame here?
1. Cytokines induce vessel leakage and endothelial adherence molecules (integrins and selectins)
2. Seconds
87
What are cytokines responsible when recruiting cells to the inflammation? Time frame?
1. Cytokines induce adherence molecules, chemotaxis, and leukocyte growth and proliferation.
2. Minutes to hours.
88
How are cytokines responsible in the removal of debris? Time frame?
1. They activate leukocytes, lymphocyte growth and antibody synthesis
2. Half an hour.
89
How are cytokines responsible for promoting repair and regeneration?
They induce fibroblast and collagen production.
90
Which cytokines communicate between cells?
ILs
91
Most of the time that you have acute inflammation you are going to have what?
Resolution. You are going to end up with something that is pretty much as good as what you started with.
92
What does resolution include? (4).
Clearance of injurious stimuli
Clearance of mediators and acute inflammatory cells
Replacement of injured cells
Normal function
93
Occasionally, you end up with a pus formation or abscess. Hopefully you can clear and cure it. When you heal the abscess what replaces it?
Scar tissue.
| Healed and repair could mean loss of function.
94
What is going on with chronic inflammation? When do we see it? When does the insult stop?
1. Recurrent injury that never stops.
2. Chronic diseases
3. It never stops
95
Our adaptive immunity includes what type of cells?
Lymphocytes.
96
Are NK cells part of our adaptive immunity? Are NK cells lymphocytes?
1. No.They are part of the innate. They look just like T cells but hey are not specific in their killing.
2. Yes
97
Immature lymphoid cells can go to the bone marrow, secondary lymph organs, thymus or bone marrow. If they go to the Thymus what will they become? Which will become what?
T- lymphoctyes which will differentiate into Helper T cells or Cytotoxic T Cells.
98
Immature lymphoid cells are made into B cells where?
The bone marrow and secondary lymphoid organs.
99
Immature lymphoid cells are made into NK cells where?
Bone marrow
100
Cytotoxic T cells an kill what kind of cells? What type of immunity are they part of?
1. Cells that are infected by a virus.
| 2. Adaptive immune system
101
After being matured in the thymus the T cell leaves as an? What does this mean?
1. Immunocompetent naive T-cell.
| 2. They are ready to go but have not found their antigen yet. They have to go look for it.
102
After being matured in the bone marrow B cells leave a an? What does this mean?
1. Immunocompetent naive B-cell
| 2. They have not found their antigen.
103
What happens when a immunocompetent naive B cell finds it's antigen? What about immunocompetent naive T cells?
1. The B-cells will replicate, undergo proliferation and make lots of copies. Some will become plasma cells that will produce a lot of antibody. Some will become memory cells and will be ready incase this pathogen ever comes back.
2. They also undergo proliferation and make lots of copies and then do what they are supposed to do
104
When immunocompetent naive cells find their antigen they become?
Active.
105
Name the two primary lymphoid organs.
Bone Marrow and thymus
106
Name the seven secondary lymphoid organs.
1. lymph nodes
2. spleen
3. peyers patches
4. Tonsils
5. Gut associated lymphoid tract
6. bronchiole associated lymphoid tissue
7. Mucosal associated lymphoid tissue
107
Where do we want to catch problems?
Where they are. Secondary immune places are where the cells are going to find their antigen.
108
Antigen is going to cause a response in what kind of cell?
Lymphoid cell.
109
What is an epitope? How many does a cell have?
1. Something that the immune system can grab on to it is a specific part of a protein to recognize whether this is self of non-self.
2. Could have many. Think of it as a bolder. Could have all different kinds of shapes but parts of the immune system are looking for specific ones.
110
Most of our antigens are going to be?
Proteins but some could be a polysaccharide or DNA.
Triggers an immune response
111
In order for a molecule to be an antigen it has to be so specifically complex that?
We can recognize it as not self.
112
How many classes of antibody do we have? What are they?
1. 5.
| 2. M, D, G, E and A
113
What does the antibody D do?
We have no idea so we ignore it.
114
We always start with? G is the antibody of? A is the antibody we are going to? E is where?
1. M and then we can switch to G, E or A
2. Our blood
3. Secrete (into GI tract, bronchi, vaj) into place outside of our body proper but still inside of our body that we would like to protect.
4. In peripheral tissues sinuses and skin
115
What part of an antibody binds to an antigen? What part of the antigen is the antibody binding to?
1. The variable region.
| 2. Antigenic determinant.
116
How many antibodies can we make?
Almost an infinite number.
117
How do we make a new antibody?
We start with a stem sell progenitor cell that gives rise to a lymphocyte. We randomly mutate the DNA for the binding domain to then make random new B cells.
118
Once we have a random B cell (with mutated DNA for the binding domain and the rest normal DNA) what do we do with it?
We have to check our protein against it. We throw antigen at it.
119
What happens if this newly made B cell (with DNA mutated for the binding domain) likes our protein? What happens if it does not like our protein?
1. We kill it because it would be self reactive. We kill it by apoptosis.
2. If they do not like our protein it becomes part of our pool of mature immunocompetent naive B cells and we release them into the blood to look for it's antigen (bar hopping)
Clarification: immune cells are only immature before they go to a primary lymphoid organ to be made into T, B or NK cells. One the cell has been made into one of these cells it becomes mature but is still immunocompetent and naive because it has not found it's antigen.
120
What happens if a newly made B cell, released as an mature immunocompetent naive B cell into the blood, goes too long without finding it's antigen? What happens if it finds it's antigen?
1. It dies of boredom.
| 2. Makes a gazillion copies of itself.
121
When an mature immunocompetent naive B cell first finds it's antigen and makes a gazillion copies of itself, what do the copies look like? What does this process result in?
1. With each cell division it is going to mutate the DNA so that the binding domain is a little bit (one base pair change) different. Some of the daughter copies will bind a little bit better. Some will not. The ones that bind better we keep and they keep replicating. The ones that are worse we get rid of.
2. After a couple generations we have B cells that are very (very!) specific to the antigen.
122
The process of killing antibodies that bind to self protein is technically termed?
Clonal deletion.
123
As a part of IgE mediated destruction of a parasite, what originally binds to the parasite? What happens next?
A naive B cell binds to it and replicates a million times.
124
When a naive B cell replicates a million times in response to binding with a parasite what will it produce?
1. Some of the B cells will become plasma cells that start producing IgE.
125
When plasma B cells produce IgE in response to a parasite what binds to the IgE? What happens if a second parasite comes along expressing the same protein?
1. A mast cell.
| 2. These antigens will bind to the mast cell.
126
What happens when a mast cell degranulates?
It produces things like histamine which increase vascular permeability and eosinophil chemotactic factor which attracts eosinophils.
127
When eosinophils are attracted by eosinophil chemotactic factor to the site of a mast cell degranulating after being bound to a parasite what do they do? What does this cause?
1. They cross over from the blood stream and release IgE.
2. The IgE binds to the mast cell and releases more histamine and ECF-A which is a chemotactic factor that attracts more eosinophils. More eosinophils dump more IgE. The worm is coated with IgE. The eosinophis see the IgE and degranulate and kill the worm.
128
Eosinophils are the immune cell against?
Huge parasites.
129
Antigen responses are dominated by which to classes of antibody? Which predominates upon initial exposure to the antigen in the primary response? Which shows up later?
1. IgM and IgG.
2. IgM
3. IgG
130
After the host's immune system is primed, another challenge by the same antigen induces the secondary response in which what are made?
Small amounts of IgM and larger amounts of IgG.
131
During a first response, how long does it take to really produce a significant response? Why?
1. About a week.
2. There is a delay because we do not have any memory cells for it. We are randomly throwing naive B cells at it hoping that one will be right. This is such a random process that it is super amazing that it actually works.
132
As part of the peyers patches (gut associated lymphoid tissue) in response to there being things we should not have eaten in the lumen what do we secrete? What do the M cells do? If a B cell sees an antigen that it likes what will happen?
1. IgA.
2. Antigen is sampled through the M cells that reach out. They preform transcytosis and antigens will be carried across from underneath the epithelial cells where there are dendritic cells, B-cells and Helper cells.
3. The B cell will become active, produce plasma cells which will produce IgA which will bind to the antigens in the lumen of the GI tract to prevent that problem from infecting you.
133
The antibody of our blood is? Can it cross the placenta? What does this mean?
1. IgG
2. Yes.
3. The fetus does not have an adaptive immune system (only innate) so it needs antibodies to help it along. It gets those antibodies from mom. Moms IgG will cross into the fetal circulation and then bind to whatever bad there is out there. Fetus can then use this innate the same way we use opsonization. Anything that the mom is exposed to the fetus is exposed to . Moms immune systme is going to raise all the antibodies the fetus would need.
134
Moms secrete which antibodies in the breast milk?
IgE and IgA
135
What two antibodies can the fetal immune system produce before birth in small amounts?
IgA and IgM.
136
The human placenta is covered with a specialized multinucleate cell called a?
Syncytiotrophoblast.
137
What kind of process is the transport of maternal IgG across the syncytiotrophoblast into the fetal circulation?
An active process.
138
What must maternal IgG bind to on the surface of the syncytiotrophoblast? What happens after it binds?
1. Fc receptors.
| 2. It is internalized by the process of endocytosis.
139
Are Fc receptors specific to IgG? What is the interaction of IgG with Fc receptors protective against? How is it released to the fetal circulation?
1. Yes.
2. Protects the antibody from lysosomal digestion during transport of the vacuole across the cell (transcytosis).
3. Through exocytosis
