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56 Cards in this Set
- Front
- Back
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Innate immunity |
defenses against any pathogen (not pathogen-specific) |
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Adaptive immunity |
induced resistance to a specific pathogen |
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Primary lymphoid tissues |
generate lymphocytes (bonemarrow, thymus) |
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Secondary lymphoid |
tissues maintain mature lymphocytes and help to initiate immune responses (e.g.lymph nodes, spleen |
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Humoral immunity |
◦Dueto antibodies ◦Controlof extracellular pathogens ◦B cellsmature in the bonemarrow |
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Cellular immunity |
◦Dueto T cells ◦Controlof intracellular pathogens by killing infected cells ◦Activatemacrophages ◦Providinghelp to B cells (T cell-dependent B cell responses) ◦T cellsmature in the thymus |
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Antigen |
a substance that causes the body to produce specific antibodies or sensitized Tcells |
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Antibodies (Ab) interact with |
epitopes,or antigenic determinants |
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Hapten |
antigen only generates an antibodyresponse when combined with carrier molecules |
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B cells interact with intact antigens in their native conformation via their |
Bcell receptors (BCR) |
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T cells respond to Ag by |
T-cellreceptors (TCRs) and can only see antigen as a peptide on MHC ( CLASS 1or 2) |
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MHC |
Major histocompatibility complex |
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Major histocompatibility complex |
expressed onmost mammalian cells ◦MHCclass I (MHC-I) ◦MHCclass II (MHC-II) |
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MHC molecules present |
peptides,not whole proteins |
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MHC-I |
Present endogenous antigens (from within the cell) |
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MHC-II |
Present exogenous antigens (from outside the cell) |
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Activation of B Cells ( T-dependent antigens ) steps |
◦Bcell recognizes Ag ◦Agis taken up, processed and presented by B cells on MHC-11 to THcell ◦THcell recognizes the peptide-MHC-II complex and produces cytokines that activatethe B cell ◦TDresponses occur in secondary lymphoid tissues |
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Activation of B Cells ( T-independent antigens ) steps |
◦Stimulatethe B cell to make antibodies by bypassing the need for T cell help ◦Antigensthat are repetitive in structure and/or arrangement ◦Rememberpolysaccharides (capsules) ◦PrimarilyIgM response |
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once B-cells are activated what happens |
Antigen-specificB cells undergo clonal expansion, to increase the number of antigen-specific Bcells Bcells differentiate into: ◦Antibody-producingplasma cells ◦Memory cells |
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Antibodies |
has immunoglobulins The number of antigen-bindingsites determines valence |
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immunoglobulins |
Globular proteins |
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IgM Antibodies |
◦Pentamer ◦5–10%of serum antibodies ◦FixcomplementInblood, in lymph, and on B cells ◦Agglutinatemicrobes; first Ab produced in response to infection ◦Half-lifein serum = 5 days |
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IgG Antibodies |
◦Monomer ◦80%of serum antibodies ◦Fixcomplement ◦Inblood, lymph, and tissues ◦Crossplacenta ◦Enhancephagocytosis; neutralize toxins and ◦viruses; protect fetus and newborn ◦Half-lifein serum= 23 days |
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IgA Antibodies |
◦Dimer (in secretions) ◦10–15%of serum antibodies (as monomer) ◦InsecretionsMucosalprotection, intestinal protection for nursing infants ◦Half-lifein serum= 6 days |
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IgD Antibodies |
◦Monomer ◦0.2%of serum antibodies ◦Primarilyon B cells ◦OnB cells, initiate immune response ◦Half-lifein serum= 3 days |
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IgE Antibodies |
◦Monomer ◦0.002%of serum antibodies ◦Onmast cells, on basophils, and in blood ◦Allergicreactions; lysis/expulsion of parasitic worms ◦Half-lifein serum = 2 days |
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what are some Antigen–Antibody Binding mechanisms |
Agglutination Neutralization Opsonization Activationof complement Antibody-dependentcell-mediated cytotoxicity |
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Agglutination |
Reduces the number of infectious units to be dealt with by clumping the pathogenstogether |
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Neutralization |
◦Antibody binds strongly to active sites and prevents viral or toxin entry into cells. ex ◦Influenza virus, Bacterial toxins (such as tetanus toxin), and snake venoms |
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Opsonization |
-Enhance phagocytosis (opsonophagocytosis) via receptors that bind to complement components or the antibodies themselves (Fc receptors) |
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Activation of complement |
C1can bind to antibodies bound to their target antigens and becomes activated,which causes lysis of apathogen or assisting in phagocytosis. 2or more IgG molecules are needed to be bound to the same target antigen. Showsthat IgG can work to activate complement |
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Antibody-dependent cell-mediated cytotoxicity |
Antibodies attached to target cell cause destruction by macrophages, eosinophils, and NK cells |
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T cells |
maturein the thymus Thymic selection eliminates many immature T cells that could be autoreactive |
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APC's |
Digestantigen Ag fragments on APC surface with MHC-II |
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APCs include |
◦B cells ◦Dendritic cells ◦Activated macrophages |
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T Helper Cells |
CD4+ or TH cells |
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CD4+ or TH cells |
◦recognize Agsand MHC II (together) on APC ◦TLRsarea costimulatory signal on APC and TH ◦THcells produce cytokines and differentiate |
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TH cells produce cytokines and differentiate into: |
TH1cells TH2cells TH17cells Memorycells |
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TH1 |
cell-mediated immunity |
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TH2 |
activate eosinophils and B cells toproduce neutralizing antibody humoralimmunity |
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TH17 |
key in autoimmunity |
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Cytotoxic Tlymphocytes |
◦CD8+ or TC cells
◦CTLsrecognize Ag + MHC I ◦Induceapoptosisin target cell ◦ perforinandgranzymes |
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Target cells are self-cellscarrying WHAT
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endogenous antigens |
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T Regulatory Cells |
CD4 and CD25 on surface Helpstoshut off immune responses |
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Natural Killer (NK) Cells
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Granularleukocytes destroy cells that don’t express MHC I
Killvirus-infected and tumor cells Attackparasites (ADCC) |
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Cytokines
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Chemical messengers Responsiblefor many of the symptoms of being sick i.e ◦Fever ◦GeneralmalaiseOverproductionleads to cytokinestorm |
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Antibody titer |
is the amount of Ab in serum |
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Primary response |
occurs after initial contact with Ag |
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Secondary (memory or anamnestic) response |
occurs after second exposure
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Types of Adaptive Immunity
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Naturally acquired
Artificially acquired |
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Naturally acquired active immunity
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◦Resulting from infection |
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Naturally acquired passive immunity |
◦Transplacentalor via colostrum |
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Artificially acquired active immunity |
◦Injection of Ag (vaccination) |
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Artificially acquired passive immunity |
◦Injection of Ab |
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M cells
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on the mucosal surface helps immune system sense whats going on on the other side |
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Pathogens entering the gastrointestinal or respiratory tracts pass through
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M (microfold) cells Peyer’s patches (whichcontain APCs) |
