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64 Cards in this Set
- Front
- Back
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Why doesn't the adaptive immune system normally attack your own body tissues?
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It has created safe guards to make sure that antibodies aren't made that will attack self cells, etc.
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Differentiate innate from adaptive immunity
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innate is very general, adaptive is incredibly specific
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differentiate humoral from cellular immunity
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humoral involves antibodies and cellular involves T-cells
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where do matured B and T cells migrate to?
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Lymphoid tissue such as spleen, but especially lymph nodes
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Humoral immunity involves what cells? What provides humoral immunity?
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B cells; antibodies
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Cellular immunity involves what cells?
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T cells
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Antigen:
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a substance that causes the body to produce specific antibodies or sensitized T cells
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epitope/antigenic deteriminant sites
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Ab interact w/these; can be parts of proteins, RNA, DNA, or other macromolecules; the structural feature recognized by the antibody!
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immunoglobulins (Ig) |
antibodies; globular proteins |
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what determines valence for Ab?
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the number of epitopes
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V=?
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the variable part of the aby
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C=?
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the constant part of the aby
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Characteristics of IgG Antibodies:
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-Monomer
-80% of serum Abs -Fix Complement -In blood, lymph and intestine -cross placenta -enhance phagocytosis: neutralize toxins and viruses; protects fetus and newborn -half-life = 23 days! -valence = 2 |
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Characteristics of IgM antibodies:
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-Pentamer
-5-10% of serum Abs -Fix complement -In blood, lymph, and on B cells -Agglutinate microbes; first Ab produced in response to infection -half-life = 5 days -valence = 10 |
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Characteristics of IgA antibodies:
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-Dimer
-10-15% of serum Abs -In secretions -Mucosal protection -half-life = 6 days -valence = 4 |
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Characteristics of IgD antibodies
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-monomer
-0.2% of serum Abs -In blood, in lymph, and on B cells -On B cells, initiates immune response -half-life = 3 days - valence = 2 |
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Characteristics of IgE antibodies:
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-monomer
-0.002% of serum Abs -On mast cells, basophils and in blood -Allergic rxns; lysis of parasitic worms -half-life = 2 days -valence = 2 |
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serology
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the study of rxns b/n antibodies & antigens
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antiserum
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the generic term for serum b/c it contains Ab (part of serum)
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Globulins
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serum proteins
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immunoglobulins
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Antibodies (proteins)
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Gamma globulin
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serum fraction containing Ab (part of antiserum)
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Major Histocompatibility Complex (MHC)
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expressed on mammalian cells; keeps us from damaging our own cells
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T-dependent antigens
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-Ag presented w/self MHC to T helper cell
-T helper cell produces cytokines that activate the B cell to produce antibodie -Reads degraded products from microorganisms being spit out by macrophages |
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T-independent antigens
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-stimulate B cell to make Abs immediately
-reads epitopes |
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Clonal Selection
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-The selection of Abs that can interact with a specific antigen to produce more antibodies
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plasma cells
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B cells that make antibodies
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memory cells
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B cells that live forever (could) and cause secondary immune response
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clonal deletion
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eliminates harmful B cells
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What are the 5 results of Ag-Ab binding?
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1. Agglutination
2. Opsonization 3. Complement Fixation 4. Antibody-Dependent Cell-Mediated Cytoxicity 5. Neutralization |
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Agglutination
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-reduces #s of infectious units to be dealt with
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opsonization
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-coating antigen w/antibody enhances phagocytosis
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Complement Fixation
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-causes inflammation and cell lysis
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Antibody-dependent cell-mediated cytoxicity
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-Antibodies attached to target cell cause destruction by macrophages, eoinophis (secrete perforin and lytic enzymes) and NK cells
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Neutralization
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-blocks adhesion of bacteria & viruses to mucosa
-Blocks attachment of toxins to mucosa |
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T-cell receptors (TCRs)
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how t cells respond to Ag
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antigen-presenting cells (APCs)
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required by t cells to recognize antigens
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what 2 things can pathogens entering GI or respiratory tracts pass thru?
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M (microfold) cells or Peyer's patches
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T helper 1 cells make? what do those products do?
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IFN-gamma, activating cells related to cell-mediated immunity, macrophages, and Abs (useful against viruses and other intracellular pathogens)
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T helper 2 cells activate what to produce what?
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activate eosinophils and B cells to produce IgE
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T Cytotoxic Cells (CD8+/ Tc cells)
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target cells that are self-carrying endogenous antigens (e.g., virus-infected cells)
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what are Tc cell activated into? What do they then perform?
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Cytotoxic T lymphocytes; CTLs; recognize Ag + MHC I; induce apoptosis in target cell
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what do CTLs release?
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perforin and granzymes
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antigen-presenting cells
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digest antigen by digesting a microbe & present parts of this microbe on their surface
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what are the 3 Ag fragments on APC surface w/MHC?
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1. B cells
2. Dendritic cells 3. Activated macrophages |
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Natural Killer Cells
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granular leukocytes that destroy cells that don't express MHC I
-kill virus-infected and tumor cells -attack parasites |
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What does over-production lead to?
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cytokine storm
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IL-1
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stimulates T helper cells in presence of antigens; attracts phagocytes
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IL-2
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proliferation of antigen-stimulated CD4+ T helper cells, proliferation and differentiation of B cells ;activation of CD8+ T cells and NK cells
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IL-4 & IL-5
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activate eosinophils, good against parasites (but also cause allergies)
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chemokines
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induce the migration of leukocytes
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TNF-alpha
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-by T helper 1 cells
-promotes inflammation |
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hematopoietic cytokines
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influence differentiation of blood stem cells
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IFN-alpha and IFN-beta
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response to viral infection; interfere w/protein synthesis
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IFN-gamma
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by T helper 1 cells
-stimulates macrophage activity (good for cells that have been invaded by e.g., Salmonella, Shigella) |
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antibody titer
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the amt. of Ab in serum
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Primary response
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occurs after initial contact w/Ag
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Secondary (memory) response
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occurs after 2nd exposure
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passive immunity
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immediate (Abs present) but doesn't last
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Active immunity
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takes time to develop but lasts longer
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Naturally acquired active immunity
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resulting from infection
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naturally acquired passive immunity
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transplacental or via colostrum (breastmilk)
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artificially acquired active immunity
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injection of Ag (vaccination)
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artificially acquired passive immunity
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injection of Ab (e.g., used to neutralize snake venoms)
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