Flashcards in Exam 3 - Objectives Deck (78):
1
List the major differences between mucosal immunity and systemic immunity (in the skin, for example)
Mucosal:
Many active immune cells present
No inflammation - inflammation can be a sign of an autoimmune disease
Systemic:
Not many immune cells present
Inflammation can occur - helps to bring immune cells to the infection
2
Describe the basic structure and chemical features of mucin that allow it to protect mucosal tissue
Huge glycoproteins composed of subunits disulfide-bonded together
Has sialic acid as a glycan (sugar)
Polyanionic surface that can bind positively-charged defensins, antimicrobial peptides, and secretory IgA
Have N-terminal globular domains -allows them to disulfide bond together.
3
Describe the organization of Peyer’s patches, being sure to identify abundant cell types within them and the function of the M cells
Peyer's patches are found only in the small intestine.
They vary in size and contain between 5 and 200 lymphoid follicles with germinal centers, interspersed with T cell areas that also include dendritic cells.
M cells within the Peyer's patch brings in antigen from the gut.
There are efferent lymphatics that take the antigens taken in to the mesenteric lymph nodes.
Peyer's patch release CCL21 and CCL19 that bind to CCR7 expressed on naive T and B cells causing them to leave the lymph vessel and enter secondary lymphoid tissue.
4
Associate intraepithelial lymphocytes (IEL) with the gut, and describe what their characteristics are and how abundant they are
IEL are dispersed in the epithelial layer of the gut. They are a type of CD8+ cytotoxic T cells that are activated by antigen and loaded with granules. There is a mix of alpha beta and gamma delta TCR with limited specificity. They express CCR9 and alphaE:beta7 integrin that allows them to bind to E-cadherins of the intestinal epithelial cells. There is one IEL for every 7-10 epithelial cells.
5
Identify chemokine and intgrin receptors expressed differentially on IEL, lamina propria lymphocytes, and skin lymphocytes that are responsible for these cells homing to the correct body site
IEL's express the chemokine receptor CCR9 and alphaE:beta7 integrin that allows them to bind to E-cadherins of the intestinal epithelial cells.
Lamina propria lymphocytes (B and T cells) press CCR9 and alpha4:beta7 inegrin that binds to MAdCAM-1 mucosal addressin.
Skin homing lymphocytes express CCR4 and alpha4beta1 integrin
6
List the four known cytokines that cause plasma cells located in the gut to isotype switch to IgA production
TGF-beta drives isotype-switching to IgA (Treg and TFH).
TGF-beta cooperates with BAFF and IL-10 which are produced by dendritic cells scattered throughout the lamina propria (IgA1).
APRIL, a proliferation-inducing ligand, produced by colon epithelial cells (IgA2) and dendritic cells.
7
Identify the two main functions of dimeric IgA in the mucosa
Neutralization and transport of toxins
8
Describe how the immune system seems to compensate for a lack of IgA in “selective IgA deficiency”
Imune system compensates by over-producing IgM and exporting IgM across mucosa (J-chain via poly-Ig receptor)
9
Describe how Th2 responses in mucosal tissues are specifically effective at ridding the body of helminth infections, including the specific functions of Th2 cytokines Il-4, Il-5, and Il-13
Naive CD4 T cells activated during helminth infection differentiate to become Th1 or Th2 effector cells.
Th2 cells produce IL-13, which increases production of epithelial cells in the infected tissue - increase number of goblet cells produces more mucus and the increase in enterocytes increases their rate of turnover in the epithelium.
Th2 cells produce IL-5 which recruits eosinophils to the infected tissue and activates them - activated eosinophils acquire granules containing MBP and parasite-specific IgE bound to FceRI - this degranulation kills helminths.
Th2 cells produce IL-9 which recruits mast cells to the infected tissue. Mast cells bind parasite-specific Ige - degranulation causes muscle spasms and diarrhea that expels helminths.
10
Define primary immunity and secondary immunity
Primary immune response is the adaptive immune response that follows a first exposure to antigen. This can be slow, but it leads to the generation of memory cells with high specificity to the antigen for future attacks.
Secondary immune response is the adaptive response that occurs the second time a antigen is encountered. This response is quicker because it causes reactivation of memory cells. B and T cells are involved.
11
Describe the timeline of an adaptive immune response, including the amounts of effector T cells and antibody. Also be able to include the relative timing of first infections, aborted infections, and secondary infections
1 to 2 weeks after first infection, effector T cells and antibody are made. This was able to terminate the first infection. Effector T cells were soon inactive, but antibody remained to protect against further exposure (aborted infections). After about a year, antibody has decreased and an infection could occur again. If a second exposure occurs, the response will be much quicker as the memory cells will quickly respond and produce antibody.
12
Explain three ways that memory is maintained (antibody, T memory, B memory cells) and the cytokines needed for each
Antibody is maintained by plasma cells in bone marrow nursed by stromal cells secreting IL-6.
Memory CD4+ and CD8+ T lymphocytes rely on IL-7 and IL-15 for maintenance.
Memory B cells have isotype-switched high-affinity BCR and express CD27 which distinguishes them from naive and effector B cells.
These cells/molecules will recognize the specific antigen that they were created for quickly and be able to get rid of it before it causes a huge infection.
13
Explain how pre-existing antibody prevents naive B cell activation
In a primary response, antigen will activate a B cell and it will become an antibody-producing plasma cell creating low-affinity IgM antibodies.
In a secondary response, the antigen receptor and the inhibitory Fc receptor FcgRIIIB1 on a naive B cell can be cross-linked by a pathogen coated in IgG that delivers a negative signal that prevents the activation of the cell.
Memory B cells do not express the Fc inhibitory molecule, so they will become activated and make IgG.
14
Explain “original antigenic sin”
An occurrence in which the body will only respond to the original antigens of a pathogen, and has no response mechanism (sinning) to antigens that are rapidly changing. The memory response is to a mutated version of the antigen that no longer exists within the environment due to the pathogen rapidly changing.
15
Describe how RhoGAM protects agains hemolytic disease of the fetus and newborn
When the father is RhD+ and the mother is RhD-, the baby can be born with hemolytic disease.
In a first pregnancy, RhD+ erythrocytes can cross the placenta and stimulate the mother's immune system to create anti-RhD antibodies. These will cause little harm to the fetus as they will be IgM and can't cross the placenta.
In a secondary pregnancy, IgG antibody can be created and transported across the placenta by FcRn and can cause disease in the fetus.
If the mother had not begun created the IgG antibody in the secondary pregnancy, she could get infusions of RhoGAM. This coats fetal erythrocytes with IgG and prevents the mother from making her own that will attack the erythrocytes.
16
Identify the 4 general requirements necessary for a “good” antigen (an antigen that will be immunogenic)
1. Must have a high molecular weight (at least 100,000 daltons)
2. Should have high molecular complexity (like proteins of 20 or more amino acids)
3. Foreignness = taxonomically distant from the host
4. Inflammatory: inducing inflammation by possessing TLR ligand or some other sort of ligand that a pattern recognition receptor in our body induces or also by inducing cell stress that would give a danger signal to our immune system
17
Identify 4 mechanisms that may be responsible for the ability of adjuvants to enhance the immune response to vaccination
1. Complex with the antigen to increase its size
2. Trap the antigen in material that allows it to be relatively indigestible
3. Lipid emulsion - antigen slowly leaks out (causes adaptive immune response rather than innate)
4. Hyper-activate the innate immune cells (like macrophages that will initiate inflammation that will cause adaptive immune cells to be activated)
18
Identify the types of vaccines that are currently in use to immunize individuals against viral infections and bacterial infections
Virus:
Killed/inactivated virus
Live-attenuated virus
Subunit vaccine
Bacteria:
Live-attenuated bacterial vaccines
Subunit (toxoid and purified capsular polysaccharide from different bacterial organisms)
Combination vaccine
19
Describe the process of creating/inducing live-attenuated viral vaccines
1. The pathogenic virus is isolated from a patient and grown in human cultured cells
2. The cultured virus is used to infect monkey cells
3. The virus acquires a variety of mutations that allows it to grow well in monkey cells
4. The virus is not longer grows well in human cells (it is attenuated) and can be used as a vaccine
20
In general, identify how 𝛄δ T cells, NK cells and NKT differ from classic αβ T cells in their antigen recognition
ab T cells recognize peptide in MHC class I or II and use Cd1a,b, and c.
gd T cells recognize a variety of antigens without classical class I or II. Use class-1 like, but can recognize without presentation.
NK cells activating or inhibitory ligands. Lack of MHC class I will cause them to kill.
NKT cells can recognize class-1 like molecules such as CD1d. These present lipids.
21
Specifically identify the antigen that V𝛄9:Vδ2 T cells bind, where these T cell populations are located in the body, and what their general effects function is once activated
V𝛄9:Vδ2 T cells: dominants adult human blood 𝛄δ T cells.
Contain the same V gene segments and variable D and J gene segments
Respond to a range of pathogens
Antigen recognized is NOT peptides, but phosphoantigen
Most (80%) can't enter secondary lymphoid tissues and instead home to inflamed/infected site by using CCR5
Act as cytotoxic T cells to kill infected cells
Highly activated:
Capable of antigen presentation
Begin expressing MHC class II, B7, and CD40L
Increase MHC class I expression
Gain CCR7 expression to allow migration to lymph nodes and there present antigen to alpha beta T cells
22
Identify the CD protein expressed on the surface of all human NK cells
Mononuclear cells that lack CD3, but express CD16 and CD56 on their cell surface
Some will lack CD16, but all will have CD56
23
Compare and contrast NK and Tc target cell recognition and killing mechanisms
NK and Tc cells kill in a similar manner.
NK cells use inhibitory and activating receptors to find target infected cells or tumor cells that need to be killed. They lack CD3 and TCR proteins. They are an innate immune cell. They detect the loss of MHC class I on the infected cell. Can kill by signaling through activating receptors that detect stress ligands. All NK cells express NKG2D and CD56.
24
Describe the “ligand” for NK cell receptors (in general) and how the signals through these receptors are interpreted by the NK cell
HLA-E inhibitory ligand whose presence depends upon HLA-A,B, and C.
"Self-MHC class I"
25
Identify the specific ligand for the NKG2D receptor, whether it is an activating or inhibitory receptor, and what the NK cell will do if it encounters this ligand
NKG2D is an activating receptor.
It gets a signal from MIC stress receptors expressed on the target cell.
NK cells also need another signal such as 2B4 getting a signal from CD48 from the target cell.
Once the NK cell is activated, it will release its cytolytic granules on the target cells surface and induce apoptosis,
26
Describe how HLA-E is involved in preventing NK cell killing of healthy self cells
HLA-E is invariant; it can only be expressed on the cell surface and fold properly if it is containing nonamer peptides derived from the leader sequence of HLA-A, HLA-B, and HLA-C
HLA-E on the target cell will signal CD94:NKG2A on the NK cell to say that it is healthy and not to kill it
Lack of HLA-E targets a cell for killing (no inhibitory signal will occur)
27
Describe the role of fetal HLA-E and HLA-G in creating the maternal blood supply to a developing placenta, and the immune cell involved in this process
Fetal extravillous trophoblast cells invade maternal tissue in order to develop placental blow supply. They do not express classical MHC class I, they express low levels of HLA-C, and high levels of HLA-E, HLA-F, and HLA-G which interact with the NK cells from the mother.
HLA-E and HLA-G inhibit the NK cells from the mother from attacking the developing trophoblast and then the placenta and the developing fetus.
Soluble HLA-G activates NK cells to secrete cytokines and vascular growth factors to create the blood supply for the placenta.
28
Compare and contrast αβ and 𝛄δ T cells in regard to expression of CD3, CD4, and CD8, type of antigen and antigen-presenting molecule each TCR binds to, the amount of TCR diversity, their abundance in blood/lymph circulation, and their overall functions
1
29
Identify what kind of antigen is presented by CD1a, CD1b, and CD1c molecules and what cell they present this unique antigen to
These are considered "class-1 like" and associated with B2-microglobulin.
They present lipid antigen.
Expressed on dendritic cells, activated macrophages, and double positive cortical thymocytes of developing T cells.
The lipid sits in a hydrophobic channel with the hydrophilic head group sticking out for TCR recognition.
30
Identify the class-I like molecule that presents antigen to NKT cells, where NKT cells are located in the body, and what they do in response to antigen presentation that can influence a subsequent adaptive immune response
CD1d is the class-1 like molecule that presents antigen to NKT cells. CD1d is expressed on epithelial cells present within the intestine, liver, pancreas, uterus, thymus, and tonsils.
NKT cells recognize lipid antigens and respond rapidly to infection, but do not generate memory because they are not classical T cells.
NKT cells develop in the thymus and when mature are distributed throughout the tissues. They make up less than 1% T cells in the blood and do not recirculate like classic T cells do.
31
Define the acronym SCID. List the currently known mutations that can lead to SCID, and the consequences of SCID in regards to infectious disease susceptibility (e.d. is SCID associated with bacterial infections, fungal infections, viral infections, or all of the above?)
SCID = severe combined immune deficiency
Absence of both B and T lymphocyte function
General susceptibility to all infectious agents.
Recurrent infections begin appearing when a child is only a couple months old when the mother's passive IgG becomes depleted.
Genetic cause is sometimes X-linked
32
Describe the basis of DiGeorge Syndrome and the immune cell population that is defective as a result. Explain why DiGeorge Syndrome can have variable levels of severity associated with it
Causes variable decrease in T lymphocytes (both CD4+ and CD8+) due to thymic chromosomal aboration
Loss of a portion of chromosome 22
Depending on how much information is lost in the chromosome depends on how much the thymus will develop
Symptoms: immune deficient, mental retardation, cardiac abnormalities, and abnormal facial development
33
Identify what two primary immune deficiencies lead to selective susceptibility to viral infections, and for each, whether the patent is susceptible to all virus infections or just certain types of viruses
MHC class I deficiency:
Lacks of CD8+ T lymphocytes
Susceptible to all viral infections
NK
Susceptible to only herpes infections
34
Explain why MHC class II deficiency causes infectious disease susceptibility similar to SCID
Loss of transcriptional regulators of MHC class II leads to an absence of CD4+ T cells due to a lack of positive selection in the thymus
Susceptible to all infectious agents because CD4+ cells are necessary for activating cytotoxic T cells to kill
Technically not SCID because B cells are there, they just can't function properly
35
Compare and contrast X-linked agammaglobulinemia and X-linked Hyper-IgM syndrome,, specifically listing whether B cells are present in circulation, and whether IgG, IgA, and IgM are absent or produced as reduced, normal, or excessive levels, and the type of infection susceptibly associated with the diseases
X-linked agammaglobulinemia:
Absence of B lymphocytes du rot Btk deficiency (Pre-B cells die in bone marrow - never released)
Seen in males
Can make no Ig
Selective susceptibility to pyogenic extracellular bacterial infections
X-linked hyper-IgM syndrome:
Lack of isotyoe switching because of CD40-L deficiency
B lymphocytes are there but not effective because interaction with T lymphocytes is not occurring because of the lack of CD40L
B cells can only make T-independent IgM - no memory response created
Can only make IgM
Selective susceptibility to extracellular bacterial infections because IgM is not generally allowed into interstitial tissues
36
Identify why complement deficiencies are associated with increased susceptibility to extracellular pyogenic bacterial infections (be sure to define pyogenic)
pyogenic = pus causing.
Complement deficiencies would cause bacteria to not be opsonized so not phagocytosis would occur.
37
Identify whether deficiencies of early components of the classical complement pathway, the alternative complement pathway, or the lectin complement pathway can cause a risk for systemic lupus autoimmunity, and why this risk develops
Classical pathway. The way remove immune complexes from the blood using C1q.
Immune complexes will start participate out - not able to clear them. Make too much antibody.
38
For the primary phagocyte deficiencies (CGD, Chediak-Higashi syndrome, G6PD or Myeloperoxidase deficiency, and LAD), identify the type of infectious disease susceptibility seen in patients, and whether the infections respond to antibiotic treatment or not, and why some do not respond to antibiotics
Chronic granulomatous disease (CGD):
Lack a subunit of NADPH oxidase and can't activate granule proteases
Patients do not have effective respiratory burst
Can't kill the pathogen they ingest, causes macrophages to fuse together and form a granuloma
Can treat with antibiotics because the cells are able to leave the bloodstream because inflammation will occur.
Chediak-Higashi syndrome:
Endosomes and lysosomes will not fuse together
Can develop granulomas
Can be treated with antibiotics
G6PD or Myeloperoxidase enzyme deficiency:
Defective respiratory burst - impairs killing of ingested bacteria or fungi
Mores susceptible to fungal infections
Can be treated with antibiotics
Leukocyte adhesion deficiency (LAD):
Loss of CD18
Leads to defective neutrophil and macrophage migration into infected tissue and an inability to phagocytose opsonized pathogens
Respond poorly to antibiotics because the cells are not able to leave the bloodstream
39
Identify the infectious disease susceptibility that results from defects in the IL-12 or IFN-𝛄 receptors, and the immunological basis for this susceptibility
See a defect in cell-mediated immunity to particularly resistant or resilient organisms.
Leads to tuberculosis from M. avian and M. bovine vaccine.
Defects in innate and adaptive immunity.
IL-12 that is secreted from macrophages can't activate NK cells since its deficient.
IFN-𝛄 from NK can't activate macrophage production of inflammatory cytokines.
40
List 2 routine laboratory tests that can be performed using patient blood samples (serum or cells) which are useful in evaluating possible primary immune defects in humoral immunity
First test would be a CBC with WBC differential. This will tell you if the innate and adaptive cell components are present.
Can quantify the B cells using CD19 or CD20 surface marker by flow-cytometry. If B cells are there, can look for their activity state by looking for IgA, IgD, IgM, and IgD
Can quantify the amount of total soluble IgG, IgM, and IgA present in patient serum.
41
Describe the steps of a complement activation enzyme (CAE or CH50) immunoassay (specifically identifying what is coated onto the assay EIA plastic plate wells, the patient sample used, the detection reagent used, and how results are reported) and what pathway of complement is being assayed
CAE immunoassay is EIA that detects C9 bound to IgM-coated micrometer wells.
CH50 liposomal lysis assay replaced traditional hemolytic titration assay. Measures the classical complement pathway ability to lyse antibody-sensitized membranes.
42
Explain the flow cytometry technique, including the reagents that are used, the patient sample utilized, and how that label is detected. List what information can be collected on each cell analyzed, and how that information is interpreted
A cell mixture is labeled with fluorescent-tagged monoclonal antibodies specific for cell marker of interest (sample is whole blood).
Cells are suspended in saline and run through a flow cytometer. This separates the cells into a single-cell stream and activates the fluorochrome labels with a laser light. It will deter the fluorescent emission with detectors.
43
Identify whether AIDS (Acquired Immunodeficiency syndrome) due to HIV infection is a primary or secondary immunodeficiency
Secondary
44
Identify whether HIV-1 or HIV-2 is more common in the U.S.
HIV-1 is the principle cause of AIDS in most countries.
HIV-2 is endemic in West Africa, widely seen in Asia, and occurs in small but significant numbers in all countries (including the US).
HIV-1 causes more aggressive disease than HIV-2.
45
State whether the number of people infected with HIV worldwide has leveled off, declined, or is still increasing
Still increasing
46
Identify the function of gp120 and gp41 in the interaction with host cell membranes and eventual infection of host cells
HIV gp120 proteins forms knobs that protrude from the viral envelope and bind CD4 and a chemokine receptor.
gp120 and gp41 are virally encoded envelope glycoproteins that form the viral spike.
gp120 binds tightly to human CD4 and that allows gp41 to be released which will allow the fusion of the plasma membrane and then allow the RNA to be released into the host cell.
47
Explain the difference between macrophage-tropic and lymphocyte-tropic HIV strains, and how they can change over time during HIV infection of an individual
Macrophage-tropic HIV strains generally initiate infection at mucosal sites of entry by binding to CCR5, and preferentially infect macrophages and dendritic cells as well as CD4+ T cells.
Lymphocyte-tropic HIV strains preferentially bind CXCR4 and preferentially infect CD4+ T lymphocytes (later in infection, hastens progression to AIDS)
48
Explain the function and importance of “reverse transcriptase” and integrase” HIV enzymes in creating a permanent stable infection of a host cell
Reverse transcriptase converts the viral RNA into cDNA
Integrase splices it into the host DNA - the virus is now part of our DNA and is permanent.
49
Explain when the Acute HIV syndrome occurs following exposure to HIV and identify the symptoms of this syndrome. Is the infected individual infectious to others at this time? Do all patients develop these symptoms?
Acute HIV syndrome occurs at around 4-8 weeks. Flu like symptoms occur within this syndrome. This individual is highly infectious to others at the time. Not all patients develop these symptoms.
50
Explain why CD4+ T cell numbers temporarily plummet during the end of the acute infection stage of HIV, and then rebound at least partially
They plummet because T cells kill all the CD4 cells. B cells are making antibodies that neutralize gp120 that binds to CD4. After the immune system gets ramped up, CD4 T cell count rises
51
Define the acronym HAART and explain why HAART drug treatment is used in fighting HIV infection instead of single drug therapy
HAART = highly active antiretroviral therapy.
Single drug therapy will combat one mechanism of action, whereas HAART is a combination drug therapy of 1 drug from 2 or 3 classes with different mechanisms of action.
52
List the characteristics of HIV that make it very difficult to create an effective vaccine against HIV
Hight mutation rate
Must target both CD8+ T cell response and mucosal antibody response
HIV remains latent as provirus integrated into host genome and can reactivate at a later date.
53
Identify the two main analyses that can be measured in serological tests for infectious disease
Pathogen antigen and host antibody
54
Describe the testing algorithm that should be followed for diagnosis of HIV infection in a high risk adult. Interpret possible HIV screening and confirmatory test results using the CDC testing algorithm for HIV diagnosis. For example, if the screening test is negative, the interpretation would be that the patient does not have HIV infection
Screen:
HIV-1/HIV-2 antibody and antigen combination assay. Detects patient Ab to HIV-1 or HIV-2 or circulating antigen HIV-1. Any of these will cause a positive test result.
Confirmatory:
HIV-1/HIV-2 differentiation immunoassay. Works with antibody only. Will determine if positive for HIV-1 and/or HIV-2. Can also be negative for both.
If negative for both, then do nucleic acid test to look for HIV RNA.
55
Explain the EIA treating for detection of either patient antibody, or antigen in patient serum
Take solid antigen (HIV viral antigen) and place it in the well and wash out excess.
Add patient serum (antibodies) that will stick to the viral antigen, wash away excess.
Add an anti-human anti globulin conjugate that reacts against the heavy chain of the antibody. An enzyme is attached to the anti-human conjugate which seeks out its conjugate antigen (the human antibody) and sticks, forming a "sandwich" complex. Wash away.
Add a clear substrate specific to the enzyme. If the Ab-Ag complex formed, you will get a color change reaction.
If there is no color change, there were no antibodies in the patient serum, therefore the conjugate had nothing to stick to.
The less color you see, the fewer number of the complexes that formed and caused a color change. This is used as a semi-qualitivative measures of how much antibody is there.
56
List the drawbacks of the early generation EIA tests for HIV diagnosis, and how the “fourth generation” EIA test has limited these
Fourth generation decreases the window period of a false negative to 14-21 days instead of 45.
Now can detect both HIV1 and HIV2 using recombinant proteins in a sandwich EIA format.
It can detect p24 antigen from HIV-1.
Still many false positives in low risk populations due to history of multiple pregnancies, auto-antibodies, severe liver disease, recent vaccinations, certain malignancies, repeated freezing/thawing of specimen.
Earlier generation tests couldn't detect HIV-2 infections or patient antibody to HIV-2
57
Identify the confirmatory tests available for HIV diagnosis in adults (assuming the screening test is positive)
HIV1/HIV-2 antibody differentiation immunoassay.
58
Identify the preferred methodology for detecting HIV infections in newborn infants, and why the usual screening test for HIV cannot be used to diagnose HIV infections in infants
Can't test baby's serum because of mother's passive IgG antibody can result in false positive in children up to 18 months.
Baby's IgM antibody to HIV lacks specificity and is not adequate for testing.
Best method for babies is viral nucleic acid when baby is >1 month old. This is qualitative PCR for HIV cDNA provirus in baby's mononuclear cells.
59
Correlate an increase or decrease in HIV viral load to the success of drug therapy in the patient. Identify specifically what “HIV viral load” is measuring and the patient sample used
Viral load testing is quantitive HIV viral RNA.
Successful drug therapy results in drop in viral load level.
Drug resistance results in increased viral load.
60
Identify the laboratory test used in monitoring patient progression from HIV+ to AIDS
Monitored by CD4 T cell counts and HIV RNA vial load with repeat testing every 3-6 months
61
Define antigen.
Antigen is a substance that reacts with antibody (BCR) or T lymphocytes and their TCR
62
Define immunogen.
Immunogen implies that the antigen evokes a protective adaptive immune response and usually this equates with the fact that there is some component in the immune system that causes inflammation by activating a pattern recognition receptor, the most well-known as the TLRs
63
Define hapten
Small molecules (even a chemical side chain) that can become immunogenic when complexed to larger molecules (like proteins), even though by themselves are not immunogenic
Responsible for latex allergies, drug allergies, and poison ivy
64
Define adjuvant
A substance administered with (physically mixed with) an antigen to enhance its immunogenicity
By itself, the antigen might be ignored, but if it is mixed with the adjuvant, it now becomes an immunogen
Examples: aluminum hydroxide, aluminum phosphate, or potassium aluminum sulfate
65
Define vaccination
Any deliberate immunization intended to induce immunity against disease
66
Define herd immunity
The ability to prevent epidemics of dangerous infections when the vast majority of the population (>95%) are immune by vaccination.
Individuals who are not immune or cannot be vaccinated are protected because the organism cannot spread in the highly immune population
See outbreaks of disease when immunity reaches 85%
67
Pros and cons of live attenuated virus vaccine
Pro: induces both cytotoxic T cells which can rapidly go out and kill cells infected by the virus and it also induces neutralizing antibody to protect against further infections
More potent than killed vaccines because it replicates in the human cell and mimic real diseases
Cons: can cause disease in individuals who have cell-mediated immune deficiency that either could be induced by drugs from treatment for cancer for instance, or that might have an underling immunodeficiency we did not know about
Can revert back to pathogenic strain and then cause disease
68
Pros and cons of killed/inactivated viral vaccines
Pro: safe for those who might have underlying immunodeficiency
Con: manufacture large amounts of live virus in the manufacturing facility that is dangerous to the workers
Activates neutralizing antibody but does not activate cytotoxic T cells
69
Pros and cons of subunit viral vaccines
Pros: induces neutralizing antibody
Can be produced without live virus - protects manufacture personnel
Con: only effective in 85% of the population
70
Pros and cons of live-attenuated bacterial vaccines
Pros: induces a very strong cell-mediated immunity and neutralizing antibody at the same time
Cons: can be dangerous and cause disease in someone with an underlying immune deficiency
71
Pros and cons of bacterial subunit toxoid vaccines
Toxoids are inactivated forms of bacterial toxins
Goal: induce high titer of neutralizing antibody in the individual
Cons: Toxoids by itself does not induce T cell help or protective antibody, so it must be combined with another vaccine (whole killed bacteria) to be effective
72
Pros and cons of bacterial subunit purified capsular polysaccharide vaccines
Bacteria can coat themselves with polysaccharide that inhibits the innate immune complement from binding to it.
Goal: Create opsonizing antibody that can allow for phagocytic disposal of these extracellular bacteria
Con: Only induces protective T-independent antibody responses in healthy adults
73
Identify where V𝛄4:Vδ5 T cells cells bind, where these T cell populations are located in the body, and what their general effects function is once activated
Respond to tumor cells and cells with CMV infection
Interacts with conserved epitope of ligand expressed on tumor cells and CMV-infected cells = EPCR (Endothelial protein C receptor)
Phosphoantigen is in groove of EPCR - helps it fold properly in the ER and be transported to the cell surface where it provides the activating signal to kill
CMV= cytomegalovirus (herpes that infects myeloid lineage cells: monocytes and macrophages)
74
Identify where V𝛄:Vδ1 T cells bind, where these T cell populations are located in the body, and what their general effects function is once activated
Abundant in the fetus and neonate
In adulthood, these cells move from the blood and become confined to mucosa and spleen
Kill damaged or infected gut epithelial cells, leading to eventual repair of injured mucosa by removing damaged cells and allowing new cells to replace them
Target lipid antigens that are presented in MHC class-1-like molecules called CD1d
75
Define serology
Study of non-cellular components in the blood
76
Define window period
Time between potential exposure to HIV infection and the point when the test will give an accurate result. During the window period a person can be infected with HIV and infections but have a negative HIV test.
77
Define false positive:
A test result that indicates a person does not have a disease or condition when the person actually does have it
78