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94 Cards in this Set
- Front
- Back
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What are components of innate immunity?
Adaptive? |
mostly fast non specific, dendritic, mast and phagocytes scan extra cellular areas recognize proteins released after infection
- B-cells receptors, Tcells MHC APC's |
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What is the effector region of B-cell?
What are receptor markers for Bcell and Tcell? How do B and Tcells create receptor diversity (3 main steps)? |
Fc
Bcell- CD19 Tcell- CD3 - 1. Somatic Recombination 2. mRNA splicing 3. Junctional Diversity |
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Explain the steps of somatic recombination and what it leads to in BCR and TCR...
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a. Heavy chains 4 gene segments (V,D,J,C), is coded first
b. D and J are chosen then V |
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Explain what happens in mRNA splicing... for BCR and TCR diversity
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C is chosen
RAG1 and RAG2 encode enzymes for process |
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What two conditions do problems with RAGs cause?
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1. Omenn syndrome- partial activation of RAGs... lacking B cells, fewer T cells
2. SCID (sever combined immunity deficeincy) null mutation in RAG1 and RAG2, no B or T cells |
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What happens in junctional diversity?
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a.nucleotide is removed by exonuclease
b. Nucleotide is added by TdT (terminal doxyribonucleotidyl transferase) |
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What two Ags could initially activate B-cells?
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1. TD Ags-
2. TI Ags |
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What role do TD Ags have in Bcell activation?
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activate B-cells with help of Th cells
a. Ag binds to Bcell, TH2 delivers activation signal via CD40L and cytokines b. B-cell proliferates and changes into plasma cells and memory cells (class switching occurs) |
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What role do TI Ag have in Bcell activation?
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a. cross linking, signal transduced by Iga and Igb enzymes bind and lead to cascade of signaling molecules
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How are naive T cells activated and receptors?
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Requires both APC and co-stimulatory signals...
CD28 from T to B7 of APC |
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What is the immunological synapse and its significance?
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It explains all the accessory molecules that line and pair up to ensure that cytokines released by the cell are not affecting bystander cells
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What are the ligand partners for the following things on a receptor? Explain their roles
a. TCR b. CD28 c. CTLA-4 d. LFA-1 c. |
a. MHC peptide pair- TCR Ag recognition
b. B7 co-stimulatory pair c. B7-1/B7-2 negative regulation d. ICAM-1 (intercellular adhesion molecule-1) antigen presenting cells in endothelium |
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Where do B-cells turn into mature cells and what does IgD have role in but where is activation?
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Bcell maturation takes place in bone marrow
Activation in lymph nodes - IgD co-expressed with IgM of naive and mature cells |
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What is negative selection of Bcells?
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Process of teaching Bcell leaves marrow it must develop ability to recognize self as non dangerous.
Has two paths a. B cells attacking self Ags are killed b. Bcells not attacking go through recombination again and express new light change |
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How do T-cells activate B-cells and how is it different than Ag activation of B-cells?
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a. Th2 cells bind to B-cells using CD40L and co-stimulation sent
b. Causes B-cell proliferation Differences: 1) Maturation causes class switching (IgM, IgG, IgE) which increases Affinity of Ab and must decide to be memory or plasma cell |
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What determines which Ig's will be selected after Th2 activates B-cell?
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Depends on cytokines released
1. IFN-g = IgG 2. IL-4 = IgE 3. TGF-B = IgA |
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What is the difference in B-cells becoming plasma vs. memory cell?
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Goal is to be plasma cell
a. Only be plasma cell from TI Ag activation but both from TD and TCR |
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What are 4 facts about TI Ags?
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1. Fast- directly stimulate B-cell through cross linkage
2. Usually lipids 3. Polymeric structure makes hard to degrade 4. Two Types- TI1 and TI2 |
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What are importance of TI1 and TI2?
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Their fast response helps cell avoid wasting time for infection to settle in
TI1- a. polyclonal activators of B-cells b. Ags dont bind to BCR's but bind to molecules on Bcell (cross linkage) TI2- a. Not polyclonal activators b. bind to BCR's c. low affinity d. no memory e. Also activated by PRRs |
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What role does hapten play in B-cells?
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It is an epitope that processes TI2 antigens to be recognized and made into peptide.
Then MHC is presented on service to attract T-cell |
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Where do T-cells mature?
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Thymus where they differentiate to CD4, CD8
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What role does dendritic cell have as APC to T-cells responses?
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uptake Ag and take it to lymphatic system where it becomes activated and expresses B7 (costimulation receptor)
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Describe the TCR...
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a. alpha and beta receptor- short intracellular
b. CD3 proteins (g, d, e, z) long tails allow for signaling c. CD4, CD8 are coreceptors needed for activation d. Needs co-stimulation (B7-CD28) |
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What are co-stimulatory pairs for T-cell?
Why is there a need for stupid co-stimulation? |
1. Cd28-B7
2. CTLA-4 - B7 3. LFA-1- ICAM-1 4. VLA-4 - VCAM-1 Changes binding confirmation to allow for phosphorylation and therefore is a control mechanism against unwanted activity |
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What determines during restimulation of Th cells in Lymph node tissue is it will become Th1 or Th2?
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Restimulating Th cells releases cytokine and depending on environment and cytokine released determines 1 or 2
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Which cytokines produce TH1 and Th2?
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Th1- IL-12
Th2- IL-4 |
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Which cytokines does TH1 and TH2 produce and roles for them?
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TH1
a. IFG-g and TNF-beta -activates macrophages b. IL-2 proliferation of Tcells TH2 a. IL-4-(anti inflam) B-cell activator, IgE switch, Th2 differentiation b. IL-5 - eosinophil growth c. IL-10 (anti inflam) inhibits macrophages and IL-1 production |
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How do CD8 and CD4 cells interact?
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If there is APC and co-stimulators, CD8 doesnt need help
CD4 is able to enhance ability of APC to stimulate CTL differentiation (CD40L) |
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What kind of receptors do non-traditional T-cells have?
What are uses? |
Gamma and Delta and CD3
most dont have CD4 or CD8 - recognize with APC 1. serve as front line of defense 2. regulatory cell 3. kill stressed cells 4. bridge between innate and adaptive due to duel qualities |
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What are NKTs?
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Natural Killer T-cells, different than Natural killer cells
a. Recognize self and foreign lipids and glycolipids b. Ags present with CD1d, resist TB |
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What does NKTs make? What happens when there is a problem with NKT?
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IFN-gamma, IL-4, and GM-CSF (granulocyte-macrophage colony- stimulating factor)
problems create- Autoimmune disease and Cancer and Asthma |
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What is role of type I IFN.. IFN-a and IFN-b in virus defense?
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Both involved in innate immune response to virus, activate macrophages and NK cells to illicit anti-viral responses and block viral replication
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What is role of Type II IFN in innate virus defense?
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INF II is IFN-g released by NK cells sometimes and activates macrophages
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What is role of NK cells in response to viral infection?
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Until inhibitory receptor engaged between NK and MHCI, they activate and shoot out IFN-g
- NK recognize FcgRII and it will release mediators which cause apoptosis |
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What is adaptive immunity (B-cell and CTLs) role in virus response?
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B cells- Ab located on B-cells neutralize some of the virus
CTLs- susceptibility enhanced by type 1 IFN and allows for killing infected cells |
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What are Innate responders in bacterial infection?
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1. macrophages
2. mast cells 3. b-cells 4. dendritic cells 5. complement system 6. PAMP- pathogen associated molecular patterns on bacteria |
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What are adaptive immune responses to bacterial infection with Th1 and Th2?
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Th1- releases IFG-g, IL-2, TNF-B, which activates macrophages, induces B-cells to produce opsonizing antibody
Th2- releases IL4, IL5, IL10- activates B-cell to make neutralizing Ab, activates eosinophils, and various effects on macrophages |
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What are adaptive immune responses to bacterial infection with CTL?
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a.Recognize Ag with costimulation on APC
bCD4 + Th produce cytokins that stimulate CTL differentiation c. CD4 helper T cells enhance the ability of APCs to stimulate CTL differentiation |
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Which TLR targets LPS, HSPs, and Taxol (Gram -)?
Which TLR targets fungi? Which TLRs target virus (ssRNA) Which TLRs target virus dsDNA? |
TLR 4
TLR 6 TLR 7,8 TLR- 3 |
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1. Which cytokines are anti-inflammatory properties?
2. Which are pro? |
1. IL-4, IL-10, IL-13, TGF-B
2. IL-1, IL-6, IL-8, IL-12, IL-18, INFg, IFNa/b, TNF-a |
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What are the four major types of tissue grafts (organ transplanting)? and describe each
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1. autograft- one part of body to another
2. isograft- different people same genes (identical twins) 3. allograft- different people 4. xenograft- different species |
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What two main factors determine success of transplant?
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1. condition of allograft- if bad condition sends signals to host to attack (Danger signals)
2. donor-host antigen disparity- body may naturally recognize it as non-self... everyone has MHC Ags |
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What are HLA's?
What types are there? |
Human luekocyte Antigen complexes... are the MHC Ags
a. HLA1 (a,b) b. HLA2 (DR,DP,DQ) |
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What is a test done with HLA1's to determine if host/graft are match?
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HLA1 microtoxicity test- take lymphocytes from spleen and find out if match
a. HLA added to donor and recipient and compliment added b. If donor/recipients dont have Ags then they will be lysed by compliment c. Cells are dyed if they have Ag then dye shows up d. When serums mixed they will show same Ags |
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What test is done with HLAII's to determine if host/graft are match?
What are stimulator and responder cells? |
Mixed Lymphocyte Response- If match no proliferation of cells
a. Mix leukocytes of donor/host b. one group is irradiated (stimulator cells) and non-radiated are responder cells c. Tritiated Thymidine is added to measure if responder cells proliferated |
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What are often causes and examples of GVH response/ aspects?
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a. mostly in immuno compromised
b, against minor H Ags c. ex. (small bowel, lung, or liver) d. Chronic vs. acute |
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What are the two types of allorecognition of T-cells in a HVGD?
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a. direct- primary response, TCR directly recognize MHC molecules (tissue damage)
b. indirect- TCR recognize after APC processing |
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What are the four types of HVGD rejection reactions and what causes them?
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a. hyperacute- very fast and caused by blood type or previous recognition recently
b. Accelerated- takes days reaction to something previous but long time ago c. Acute- days to weeks causes parenchymal damage and interstinal damage d. Chronic- months to years sometimes nothing to do with immune response 1. both indirect and doesnt respond to immunosuppresents |
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What are 3 forms of parasites?
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1. endo- within body
2. ecto- live external surface 3. meso- penetrates external |
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What are the types of parasites?
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1. zoonosis- disease of animal that can be transmitted to human
2. vector- living carrier that transmits a pathogenic organism (mosquito-malaria) 3. Carrier- person who harbors parasite with no symptoms |
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What are the subkingdoms of parasites?
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All eukaryotic
a. protozoa- unicellular (malaria, falciparum b. metazoa- multicellular (worms, ticks, arthropod) |
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What causes malaria?
What are clinical presentations and effects? What are clinical treatments? |
Infection from vector (mosquito)
a. Plasmodium falciparum- causes neuro problems, coma, CNS hemorrage b. presents with high fever c. Chloroquine, and larium (causes night terrors) |
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What is the difference between host and definitive host in parasites?
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Host- harbors parasite and gives it nourishment
Definitive host- where parasite undergoes its sexual reproduction |
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What usual techniques for diagnosis for parasites?
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1. Knowing area and symptoms shown
2.Microscope examination (O&P)/ blood exam for Abs 3. Detection of parasite Ag by ELISA 4. PCR for parasite genes |
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What is toxoplasmosis and what clinical effects does it have on humans? Why do women have to be careful when eating meat?
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Parasite that uses Cats as definitive host cats shit out oocytes and infects things that associate with cat poop (cat litter cleaning)
Clinical Findings- a. Headaches- (more for immuno compromised and AIDS patients b. TORCH syndrome- can make a baby mentally retarded or blind 2.Can infect through raw meat |
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What protozoa causes retinochoroiditis and encephalitis?
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Toxoplasmosis
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Whats the difference between active and passive vaccination?
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Active- stays active for long time due to immune building memory cells ready to act when it sees antigens again (uses antigens)
Passive- short lived due to use of serum based Abs used for those with B-cell deficeincy lasts 6 weeks |
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What is the difference between prophylactic vs therapeutic vaccine?
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Pro- to prevent disease (passive)
Therapeutic- to treat current disease (i.e. person bit by rabid dog, or Herpes 2... point is to get more Abs in before damage of virus is done) active |
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Give information about and side effects of Live attenuated microorganistic vaccine
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Used for measles, mumps, rubells, (BCG for TB), yellow fever
Made of: - germs that have been weakened by constant reproduction in labs |
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What are killed microorganism vaccines?
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killed germs introduced and still develop immunity for them
flue, poliomyelitis (Salk) |
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What are anti-toxin vaccines (give an example of something they are used against?
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Formalin inhibits Ags from releasing toxins and allows immunity to create response
Diphtheria, tetanus |
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What vaccine would you use for a. diphtheria? b. Flu?
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a. Anti-toxin
b. killed micro organisms |
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What are subunit type vaccinations and what are they used for?
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Only part of microorganisms (unable to infect system) placed in body and body developes Ab for it. (Hep A, B) pertusis
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Which vaccine would you use for pertusis?
New experimental vaccines for AIDS and HIV are known as what? (2 kinds) |
Subunit
a. Vectored vaccines b. Naked DNA |
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What are adjuvants and roles in vaccines?
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they help elicit a more powerful immune response
ex. Heat-killed bacteria are commonly used |
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What is aluminum hydroxide gel used for in vaccinations?
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As an adjuvant to elicit a more powerful B-cell response
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What are some immunization approaches to cancer? What type of therapy is this? What is current state of vaccines against tumors?
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1. Isolating T-cells from lymph nodes and mixed with cell lines of tumor and hopefully make closes of those T-cells
2. Immunotherapy that targets tumor with antibodies and T- cell 3. Each type of actual vaccine has been used to try to target tumors and most have been tried on melanoma |
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What are common oncogenetic strains of cervical cancer? What is the idea behind the current therapy/vaccines?
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1. HPV 16 and 17
2. genes are E6 and E7 Expression of E6 and E7 is required for growth of cancer cells, so if can train immunity to respond to E6 and E7 could prevent tumors caused by HPV |
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How do tumor cells evade immune response?
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Sneaky and are able to lost expression of antigens by altering MHC molecules and producing suppressive cytokines
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What types of labeling do current labs use?
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FITC and PE
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What is agglutination used for and how does it work?
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Used for Blood typing... recognizes Ab-Ag reaction that results in precipitate different techniques
1. Use of Precipitin 2. Diffusion 3. Immunoelectrophoresis 4. |
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What is flurescent Ab technique and what is it used for?
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Dyes are attached to Ab and made visible by UV light and visualized reaction to Ag
1. Direct reaction- Ab interacts directly with Ag 2. Indirect reaction- Ag attached to slide and blood is added and washed... then dyed. To see interaction |
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What is Western Blotting used for?
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To test if positive immunological screens is false or true. Usually used after ELISA positive test.
a. HIV proteins separated electrophoretically showing descrete bands b. Pt's serum added, if Abs present they bind to proteins, and then add antibody to IgG labeled with radioactively or with horseradish peroxidase |
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What is Flow cytometry used for?-
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To measure # of various types of immunologically active blood cells by dying protein cells will bind to and counted by a sorter
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What is ELISA used for?
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ELISA- Enzyme linked immunosorbent Assay-- quantitation of either antigens or antibodies on patient specimens.
a. enzyme activity measure by adding substrate and estimating color reaction. |
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What are the markers here to identify?
2. CD19 3. CD 14 or CD68 4. CD45 5. CD45RO 6. CD45RA 7. CD5 |
2. B cells
3. Monocytoes 4. All leukocytes 5. Antigen-experienced Memory T cells 6. Naive T cells 7. T-cells, B-cells, Chronic lymphocytic leukaemia |
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What types of labeling do current labs use?
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FITC and PE
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What is agglutination used for and how does it work?
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Used for Blood typing... recognizes Ab-Ag reaction that results in precipitate different techniques
1. Use of Precipitin 2. Diffusion 3. Immunoelectrophoresis 4. |
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What is flurescent Ab technique and what is it used for?
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Dyes are attached to Ab and made visible by UV light and visualized reaction to Ag
1. Direct reaction- Ab interacts directly with Ag 2. Indirect reaction- Ag attached to slide and blood is added and washed... then dyed. To see interaction |
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What is Western Blotting used for?
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To test if positive immunological screens is false or true. Usually used after ELISA positive test.
a. HIV proteins separated electrophoretically showing descrete bands b. Pt's serum added, if Abs present they bind to proteins, and then add antibody to IgG labeled with radioactively or with horseradish peroxidase |
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What is Flow cytometry used for?-
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To measure # of various types of immunologically active blood cells by dying protein cells will bind to and counted by a sorter
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What is ELISA used for?
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ELISA- Enzyme linked immunosorbent Assay-- quantitation of either antigens or antibodies on patient specimens.
a. enzyme activity measure by adding substrate and estimating color reaction. |
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What are the markers here to identify?
2. CD19 3. CD 14 or CD68 4. CD45 5. CD45RO 6. CD45RA 7. CD5 |
2. B cells
3. Monocytoes 4. All leukocytes 5. Antigen-experienced Memory T cells 6. Naive T cells 7. T-cells, B-cells, Chronic lymphocytic leukaemia |
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What is role and explain purpose of granzymes and perforin
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both releases from activated CD8 ctyo toxic lymphocytes
- enter cell through receptor mediator pathway - enter cytopolasm through help of perforin and activate apoptotic pathway |
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What is role of ITAM in immunological synapse?
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causes confirmation change and activation to begin is regulatory role
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What microbes are sense by these receptors?
1. C type Lectin [Mannose Receptor] 2. Scavenger receptor [SRA1, SRA2, MARCO!] 3. Gram + |
1. terminole manose
2. anionic polymers 3. TLR-2 |
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What are roles of cytokines...
1. IL-1B 2. TNF-a 3. IL-6 4. IL-8 5. IL-12 6. INF-a,b |
1. local tissue destruction and fever
2. TNF-a - increased vascular permeability, fever shock, fluid drainage to lymph 3. Local Effects- lymphocyte activator, 4. IL- 8 - Chemotactic factor recruits all to site of infection 5. IL-12 activates NK cells and makes CD4 differentiate to Th1 6. INF-a-b- viral resistance |
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Describe complement activation...
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1. after initial Ab binding C3b binds to surface components
2. recrutiment of inflammatory cells 3. Opsonization 4. Perforation of membrane 5. Death of pathogen |
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Describe Lectin Pathway activation
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- activated early
Mannose binding lectin binds to mannose residue on glycoproteins or carbs on surface of micro organism |
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Describe alternative pathway activation
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Activated first
- usually recognizes patterns in cell wall/envelope - requires no Ab activation - Requires large bacteria |
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Spell out 3rd part of Complement...
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2. Formation of C5 convertase and MAC
a. C5 convertase cleaves C5a and C5b b. C5b makes self assembly of MAC 3. C5a becomes anaphyltoxin 4. MAC is huge and starts lysing |
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Spell out 1st part of Complement...
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1. Formation of C3convertase
a. C1 binds to IgG b. C1 cleaves to C2 and C4 c. C4b can attach microbials and phagocytize d. C2a binds to surface attached C4b and C3 convertase if formed |
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Spell out 2nd part of Complement...
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2. C5 convertase formation
a. cleaving of C3a to C3b b. C3b- opsonin tagged increases phagocytosis combines with C3convertage to give C5 convertase |
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What carries (transports) proteins to MHC1 groove from proteosome produced peptides?
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TAP1-2
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