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47 Cards in this Set
- Front
- Back
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Phagocytosis Sequence of Events:
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1. Chemotaxis: movement of phagocytes in response to chemotactic factors
2. Adherence: attachment of phagocyte to pathogen 3. Ingestion: by formation vesicle and after ingestion called phagosome 4. Digestion: IN phagolysosome 5. Formation of residual body: 6. Discharge of waste material: ( CAIDFD) |
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1. Humoral immune response from cell mediated immune response:
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Humoral is the response against antigen circulating in body fluids.
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Cell Mediated
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Is effective against intracellular pathogens and tumor cells, using mainly T lymphocytes
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3. Characteristics of Antigens?
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Protein, glycoproteins, polysaccharides, nucleic acid nature. Cell wall components, flagella, fimbrae, of bacteria, spikes or protein coat of viruses, pollens, fungal spores, metals, certain food items, drugs are examples.
4. Antibodies: proteins produced by B lymphocytes in response to a specific antigen is an antibody. Examples: IgG, IgM, IgA, IgE, IgD |
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5. What 5 types of antibodies and important features of each one of them?
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• IgG: Monomer
80% of serum antibodies fix complement-activates complement system Crosses placenta to protect the fetus Enhances phagocytosis; neutralizes toxins and viruses; and protects fetus & new born via opsonization • IgM: Pentamer: 5 “Y shaped” monomers formed together Can bind to 10 antigens Fix complement Agglutinates microbes; It’s the first Ab produced in response to infection IgM levels increase with infection • IgA: Dimer, Located in the GI tract Main Ab in secretions such as SALIVA and MUCOUS Provides mucosal protection • IgE: Monomer 0.002% of serum Ab present on mast cells and basophils in blood allergic reactions, lysis of parasitic worms • IgD Exact function in blood is unknown On b cells, initiate immune response |
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6. Results of antigen antibody interactions:
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Agglutination: enhances phagocytosis and reduces number of infectious units to be dealt with
Opsonization: Coating Ag with Ab enhances phagocytosis Neutralization: blocks adhesion of bacteria and viruses to mucosa Activation of Complement: Activatoin of C3 Inflammation: disruption of cell by complement/reactive protein attracts phagocytic and other defensive immune system cells Ab dependent Cell Mediated cytotoxicity: Ab attached to target cell cause destruction by non-specific immune system cells. |
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7. Neutralization reaction:
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blocks adhesion of bacteria and viruses to mucosa, IgG Ab inactivate viruses by blocking their attachment ot host cells, and they neutralize toxins in a similar manner.
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The basic mechanism of antibody dependent cell mediated cytotoxicity:
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stimulates Natural Killer cells and cells of innate defense system to kill targeted
phagocytized can be attacked by immune system cells. |
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8. Antibody Structure:
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a protein produced by B lymphocytes in response to a specific antigen is an antibody. IgG, IgA, etc…
Monomer Has 4 protein chains; two identical light chains and 2 identical heavy chains. Joined with a disulfide links to form a y shaped molecule. Flexible y shape can look like a T Variable region binds to epitopes Specific to the two ag binding sites found on each ab monomer. Stem of Y shape is called Fc region that binds Ab |
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9. 4 types of acquired immunity and examples:
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Naturally acquired
ACTIVE: ag enter the body naturally; body produces Ab and specialized lymphocytes PASSIVE: Ab pass from mother to fetus via placenta or infant in the mother’s milk Artificially Acquired: ACTIVE: Ag are intorducedin vaccines; body produces Ab’s and speicialized lymphocytes PASSIVE: performed Abs in immune serum introduced into body by injection. |
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10. Components of cell mediated immune response:
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1. A t cell binds to mhc-antigen complexes on the surface of the infected cell, activating the T cell with it’s cytokine receptors.
2. activation of macrophages…enhance3d phagocytic activity. 3. CD8 T cell becomes cytotoxic T lymphocyte able to induce apoptosis of target cell. (programmed cell death). |
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11. APC ‘s are:
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1. B lymphocytes
2. dendritic cells 3. activated macrophages. Dendretic cells and macrophages release ang by phagocytosis and ag fragments bind with MHCII molecule sin APC’s and then the Ag-MHC complex is presented on the surface of these APCs 4. any nucleated cells of body that are infected with pathogens 5. tumor and cancer cells. |
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12. Memory B Cells:
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responsible live a long time and are responsible for enhanced secondary response to an Ag.
Plasma Cell: Produce Antibodies Helper T Cell: have CD 4 type of glycoprotein on the surface. Activated T cells release cytokines that stimulate differentiation of B lymphocytes into memory cells and plasma cells. *it also stimulates macrophages and CD8 T cells to perform their function more efficiently. |
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Cytotoxic T cells:
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have CD8 glycoproteins on surface
Upon activation, it is differentiated into an effector cell called cytotoxic T lymphocyte (CTL) CTLs are able to destroy cells infected with viruses or other parasites, and are also albe to destroy any nucleated ell of the body that has trnaformed (like tumor or cancel cells), and can also destroy transplanted foreign tissue. |
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13. MHC II:
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present exogenous Ags on the surface of APC (b lymphocytes, macrophages, dendritic cells)
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MHC I:
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present on all nucleated cells of the body and present endogenous antigens on infected cells and on tumor cells.
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14. Helper T cells initiate immune response:
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: cooperate with b cells int the production of ab, mainly through cytokine signaling.
Recognize an ag on the surface of a macrophage and activate the macrophage, making it more effective in phgocytosis and ag presentation. Secretes cytokines And differentiates into populations of Th1 and Th2 A. antigen presentation B. activation of helper t cell C. proliferation and differentiation of helper t cell D. function of effector helper t cell |
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15. Cytotoxic t cells:
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• .antigen presentation
• cytotoxic t cell activation • Tc cell proliferation and differentiation • Destruction of infected cell by effector 1)Virus infected cells, tumor cells, grafter foreign tissue Apc’s would display endogenous ag MAC I proteins combine w/antigenic gragment and MHC I-Ag complex is then display on APC |
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Cytotoxic T cells continued...
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2)Tc binds to MHC I Ag w/ TCR and CD8 receptors
further develop receptors for cytokines (Il- & gamm interferon) Tc cells are activated when cytokines released by active helper t cells, bind to cytokine receptor on Tc cell 3) clones of activated Tc cells are formed some of thesecells become memory t cells some become effector Tc cells or cytotoxic T lymphocytes (CTL) 4) Destruction of virus infected cell Effector Tc cell releases perforin that forms pores in the infected cell. Granzyme released by Tc cell enters into infected cell through the pores. Cell structure are digested that resuls in cell death (apoptosis) The dead infected cell is ingested by phgocycte (macrophages). |
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Vaccines:
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a suspension of microorganism or components of microorganisms that induce immune response
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Adjuvants:
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agents when combined with antigen increase the effectiveness of an antigen. Ie. Aluminum phosphate
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Types of Vaccines:
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Attenuated whole agent vaccine:
uses living weak microbe that is able to induce immune response, but are not able to cause disease in host It provides life long immunity Examples: MMR, polio(sabin vaccine) There is a chance of backmutation Inactivated whole-agent vaccine Uses microbes that have been killed usually by formalin or phenol Example: inactivated viral vaccine: rabbies, influenza, polio(salk) Inactivated bacterial vaccine: pneumococcal peumonia and cholera. |
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Toxoids
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Inactivated toxins used against toxins produced by pathogens. Ex. Tetanus and diptheria toxoid.
Needs series of injections for full immunity Requires boosters every 10 years |
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Subunit Vaccine:
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Uses only those antigenic fragments of a microorganism that best stimulate an immune response.
Ex. Recombinant vaccine against Hep B |
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Conjugated Vaccine:
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Antigen is combined with some proteins to initiate immune response.
Ex. Capsular polysaccharide are combined with protein such as diptheria toxoid other wise they do not initiate immune response in children. |
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Nucleic Acid Vaccine:
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Under research dna injected into muscle
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Monoclonal Antibodies:
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Minimize graft or organ transplant rejection.
Treatment of illness: for some forms of leukemia, Crohn’s disease and rheumatoid arthritis, non-hodgkin’s lymphoma. As immunotoxins or conjugated monoclonal antibodies: kill specifically cancer cells. |
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Hybridoma Cells:
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A cell made by fusing an antibody-producing b cell with a cancer cell.
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Properties of Monoclonoal Antibodies:
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They are uniform,
Highly specific Can be produced readily in large quantities |
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Differences of agglutination and precipitation:
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Precipitation: antigens and antibodies rabpidly form small ag-ab complexes.
Soluable antigens with IgG or IgM ab form large interlocking lattices. Interaction occurs in seconds Occurs when ratio is optimal Agglutination: Particulate antigens or soluble antigens adhering to particles Sensitive tests and are easy to read. Classified as direct or indirect |
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Hemagglutination:
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Clumping of red blood cells.
Blood typing- RBC Ag’s bind to anti A/b and RH ab |
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Neutrlization reactions?
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To detect ab to specific virus or detects antitoxin in serum
Ex. Flu, MMR. |
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Applications of Direct ELISA and In-direct ELISA(the order of added ingredients)
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Direct: used for drug testing
Home pregnancy test Indirect: detect antibodies to HIV, Hep A, B, Rubella |
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Direct:
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1. Antibody in well
2. patient sample is added; complementary antigend binds to ab 3. enzyme-linked ab specific for test antigend is add and binds to antigen forming sandwich 4. enzyme’s substrate is added and reaction produced a produce that causes a visible color. |
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Indirect
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1. Antigen is in well
2. patient antiserum is added; complementary ab binds to ag 3. enzyme-linked anti HISG is added to bind ab 4. Enzymes substrated is added and reaction produceds a rpduct that causes visible color change. |
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What is the complement system?
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consists of goup of proteins (C1-C9, B,P,D) They are produced by liver cells and secreted in blood where they are present in INACTIVE form.
Inactive complement: C1, C2 Active Components: C3a, C3b |
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Classical Pathway?
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Activating complement system through Ab. Ab recognize protein and polysaccharide antigens.
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MAC
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membrane attack complex
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Cytolysis
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by formation of MAC in plasma of membrane of bacteria
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Inflammation
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chemotaxis: by c3a & c5a attracting phagycytes c5a component binds to mast cells activating them and thus they release histamine.
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Opsonization
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coating of pathogens w/ specific molecules. phagocytes will recognize pathogens easily.
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3 results of complement C3 activation
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1. Opsonization
2. Inflammation 3. Cytolysis |
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Sequence of events during Inflammation
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1. tissue damage
2.release of acute phase proteins 3. vsaodilation 4.phagocytic migration 5. phagocytic margination 6. phagocytic emigration 7. phagocytosis 8. tissue repair |
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Phagocytic Migration
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movment of phagocytes in response to chemcials to the site of infection
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Phagocytic margination
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attachment of phagocytes to the inner lining of blood vessels(endothelium)
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Emigration
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release of phagocytes from teh space between endothelial cells.
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Interferons
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proteins produced in response to viral infections
-virus infected cells and some blood cells(lymphocytes) and fibroblasts produce interferons |
