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28 Cards in this Set
- Front
- Back
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immunogen
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a substance that when introduced (i.e. injected) induces an adaptive (specific) immune response
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antigen
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used to detect whether an immune response was induced
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antibody
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an immunoglobulin produced by PLASMA CELLS, part of the adaptive immune response
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cytokines/interleukins
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soluble proteins secreted by active cells that affect other cells and/or the cytokine secreting cells.
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neutrophils
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circulate peripheral circulation syst. w/half-life of 8Hs! prime function=phagocytosis of pathogens.
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other phagocytes besides neutrophils
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macrophages and immature dendritic cells
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development of macrophages in mice and humans
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humans=monocytes in peripheral circulations become activated by infection and their cell-surface proteins (ligands) bind to cell-surface receptors of endothelial cells at the site of infection/tissue damage, where they mature into macrophages
mice=macrophages in their peripheral circulations are always active |
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dendritic cells and macrophages present the phagocytized pathogens--now small peptides--to
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T cells of adaptive immune system
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complement system
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proteins always present in peripheral circulation and always in active state.
-mannose-binding lectin(MBL) -ficolin -alternate -classical The systems primary end product is always C3B! which initiates cascade concluding in the polymerization of C9. |
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complement pathways that DO NOT require antibodies for activation
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MBL, ficolin, alternate complement
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mannose-binding lectin pathway
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MBL lectins bind to carbohydrates containing mannose arranged in unique patterns located on cell surfaces of bacteria and yeasts. Since one MBL molecule contains18 binding sites, large numbers of MBL molecules will coat bacteria. This results in (1) opsinization and promoting phagocytosis (2) activating the C’ sequence resulting in C3b formation concluding in C9 which will “punch” holes in bacterial cell walls!
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alternate pathway activation
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results in DIRECT FORMATION OF C3B, leading to C9 formation.
is activated by infection/cell damage. |
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classical activation sequence!!
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C1, C4, C3, C2.
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classical pathway
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DEPENDENT on specific antibodies binding to pathogens, cells,etc. for activation.
-forms C3B, but allows rest of C' sequence to produce C9 polymerization. -during this opsonization occurs as well as direct destruction of bacteria, cells, etc. |
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opsonization
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the process by which a pathogen in marked for ingestion and destruction by a phagocyte.
-involves binding of opsonin (an antibody) to membranes |
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first response of innate immune system
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inflammation
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complement proteins do what?
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coat (opsonize) bacterial cell-surfaces, facilitating phagocytosis of bacteria by activated dendritic cells, macrophages and neutrophils.
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PAMPS
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pathogen-associated molecular patterns=the result of pathogen metabolism; hence, different than host's metabolism products/cell surface ligands
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Toll-like Receptors (TLRs)
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cell receptor proteins that play major signaling role during infection.
TLR1 - 10 TLRs are encoded in the host germline (genes that do not change) TLRs bind to PAMPs |
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TLRs' intracytoplasmic peptide
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becomes phosphorylated upon TLR activation. TLR's phosphorylated peptide starts a signal cascade that activates genes for expression of proteins that will further activate the INNATE immune system
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use of TLR4 in CD14-LPS activation cascade
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-this is an ex. of how TLRs work.
CD14=LPS(lipopolysaccharide) cellsurface receptor on macrophages/neutrophils. 1. LPS BINDS TO CD14 then the 2. CD14-LPS complex binds to TLR-4 resulting 3. in the activation of NF-κB, Elk-1, AP-1 4. initiates signal sequence producing a transcription peptide 5. activating a gene leads to CELL ACTIVATION |
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What happens to DNA from lysed bacteria?
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they either (1) bind to TLR9 expressed on and within macrophages.This DNA-TLR9 complex is endocytosed by macrophages and facilitates the initiation of specific (Adaptive) immune responses. OR (2) bacterial DNA is released upon phagocytosis and binds to TLR-9 intracellularly. FYI: bacterial DNA consists of CpG motifs. A specific anti-CpG i.e. anti-bacterial DNA, is initiated. The fact that CpG-DNA induces specific immune responses may allow them to be used as vaccines.
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inflammation: the good effects
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clears dead/dying cells and tissues, facilitates repair of damaged tissue and promotes angiogeneis.
necessary for removal of, and resistance to infections! |
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inflammation: the detrimental effects
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exacerbates autoimmune diseases e.g. rheumatoid arthritis, lupus, Crohn’s disease, inflammatory bowel disease.
can induce malignant transformation of cells! |
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the 7 microscopic components of the innate immune system
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-complement system
-natural killer cells -natural killer T cells -neutrophils -macrophages/monocytes -dendritic cells |
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primary and secondary lymphoid tissue
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primary: bone marrow and thymus
secondary: lymph nodes, spleen |
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lymphocytes: b cells
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emerge from bone marrow
and “home” to secondary lymphoid tissue. |
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lymphocytes: t cells
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merge as immature, thymocytes. Thymocytes “home” to the thymus and migrate through the thymus and
become mature T cells! Then, they migrate to secondary lymphoid tissue. |
