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Chapter17MicroFinal
Specific Immunity
Question | Answer |
---|---|
Immunity results | from production of Anitbodies and specialized lymphocytes |
4 Types of Acquired Immunity | Naturally Acquired Active and Passive Immunity Artificially Acquired Active and Passive Immunity |
Naturally Acquired ACTIVE Immunity | Immunity resulting from infection and may be long lasting |
Naturally Acquired PASSIVE Immunity | Antibodies transferred from mother to fetus |
Artificially Acquired ACTIVE Immunity | From vaccination, may be long lasting |
Artificially Acquired PASSIVE Immunity | Humoral antibodies, like an antiserum for a snake bite, may last a few weeks. |
For every antigen there is only | one antibody |
Antibodies are very | Anitgen specific |
Antigens may have multiple | determinant groups |
Five antibodies | IgG, IgM, IgA, IgD, IgE |
IgG | Monomer, #1, located in blood/lymph intestines, stimulates phogocytosis, neutralize toxins and virus's, and protect fetus |
IgM | Pentamer, #3, located Blood/Lymph, B cell surface (monomer), 1st Antibody produced |
IgA | Dimer, #2, located in body secretions, protect mucosa, initial line of defense |
IgD | Monomer, located in B cell surface and initiates immune response. |
IgE | Monomer, lease common, located Mast and basophil surface, reacts to allergies and parasites |
1st Antibody produced at the first exposure of the antigen is | IgM |
Initial line of defense among subsequents exposures is | IgA |
Most common and crosses the placenta | IgG |
Benefit of IgM | Pentamer allows for more binding (agglutination) |
Humoral Immunity | antibodies produced by B Cells, |
B cells come from | Bone marrow stem cells that migrate to lymphoid organs |
Apoptosis | programmed cell death, machinery is turned off before it is phagocytised. not releasing toxin |
Activation of Antibody-Producing Cells | B cell activated when antigen rx's with antigen receptor on B cell, B cell produces a clone of plasma & memory cells |
Plasma cells secrete | antibodies and divide until pathogen is destroyed |
Memory cells can | recognize pathogens from previous encounters |
Memory B Cells result | in a faster and effecient immune response the 2nd time around |
Primary response = | 1st exposure ever, IgM followed by IgG |
Secondary, anamnestic, or memory response | results in a high anitbody titer, primarily IgG antibody is involved. |
Antibody titer | amount of antibody in a serum |
End of Humoral Immunity | Begin T cell and Cell-Mediated immunity |
Cell mediated immunity involves | lymphocytes called T cells that respond to intracellular antigens |
Helper T Cells | Release cytokines to activate macrophages, NK cells, and CT T-cells. |
Helper T Cells control | and coordinate the immune response |
T-cells respond to | cells with antigenic changes |
Cytoxic T-cells | release perforin to destroy cell |
Regulatory T-cell | suppress other T cells, allows control of immune response |
Types of Cytokines | Interleukins, Interferons, and Chemokines |
Interleukins | Cytokines that serve as communicators between leukocytes |
Interferons | Cytokines that protect against viruses = Alpha, Beta, Gamma |
IL-1 | Stimulates helper t cells, attracts phagocytosis |
IL-2 | proliferation of T and B cells |
IL-8 | initiates positive chemotaxis to site |
IL-12 | Stimulates differentiation of T-cells |
Alpha and Beta Interferons | antiviral, halts protein synthesis in infected cells |
Gamma Interferon | Activates macrophages = increased phagocytosis |
Tumor Necrosis Factor | Cytotoxic to tumor cells, increase phagocytosis |
Helper T cell = | #1 production of cytokines |
Opsonization | coating an antigen with antibodies to flad it and start phagocytosis |
Helper T cells = Effector Cells | has no direct role in immunity- it directs other cells on what to do. |
Helper T cells activate | B cells |
NK (Natural Killer Cells) | lyse viral-infected and tumor cells |
T cells mature | and differentiate in the thymus gland |