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bolus of immunoglobulins injected from healthy source |
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response to antigen by mast cells which recruit more WBC's and increase dilation of vessels |
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mast cells - mnediators in preformed granules and de novo mediators IgE from B cells and T cells allergens |
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leave blood, enter lymph nodes, join efferent lymph, return to blood, cycle |
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transported to lymph node, activate immune response |
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spread of infection into blood activates macrophages in spleen and liver (increase TNF-alpha -> systemic vasodilation) disseminated intravascular coagulation (uses up clotting factors, leakage and clotting in capillary beds) vital organ failure (due to blocked capillary beds) |
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small amphipathic molecules, secreted by epithelial cells alpha and beta calsses constitutively maintained, increase when pathogen present mechanism: invade membrane of cell and form pore in pathogen makes it hard to survive and gives more time for rest of immune system to react |
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formation of WBCs for innate and adaptive neutrophils, eosinophils, basophils, dendritic cells, macrophages, and mast cells |
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form WBCs that are mainly adaptive B cells, T cells, plasma cells, effector T cells and NK cells (only innate cell from this processes) |
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from common lymphoid progenitor requires IL7 and IL15 large lymphocyte major role in viral elimination |
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derived from common myeloid progenitor and unknown precursor cell requires IL3 and MCSF circulating cell, longer life than PMNs tissue specific differentiation to macrophage activated by chemokines and integrins at infection site |
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common myeloid -> unknonw precursor -> monocyte -> tissue specification requires IL3 and MCSF tissue located cell recognize, phagocytize, release cytokines and recruit neutrophils, also APC |
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macrophage surface molecule recognizes fungal infections by glucan on wall form of direct pathogen recognition |
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macrophage surface molecule recognizes by-products of inflammation form and mannose on pathogens form of direct pathogen recognition |
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macrophage surface molecule recognizes bacteral cell wall by the lipids and other components form of direction pathogen recognition |
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macrophage surface moleulce recognizes marked bacteria form of indirect pathogen recognition |
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macrophage surface molecule recognizes fMet-Leu-Phe that is only found from prokaryotes GPCR type activattion caues monocyte and PMN recruitment and increased antimicrobial activity (e.g. NADPH oxidase assembly) |
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toll-like receptors expressed on macrophages and other cells recognize patterns associated with pathogens (PAMPs) activation causes cytokine production and secretion, amplification of immune response and elimination of pathogen internally activates NFKB, activates cytokine gene program and AP1 |
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external receptor organisms: mycobacteria, T. cruzi, yeast |
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internal receptor responds to dsRNA important for viruses |
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external receptor recognizes Gram-negative and Gram-positive bacteria |
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external receptor recognize flagella |
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internal receptor recognizes inappropro ssRNA important for viruses |
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external receptor recognizes G-rich oligonucleotides |
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internal receptor recognizes unmethylated CpG DNA important for intracellular bacterial infections |
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cytokine from macrophage causes systemic fever, acute-phase protein production in hepatoctytes appears 6-12 hrs after initial recognition |
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macrophage-released cytokine Local: activates vascular endothelium and increases vascular permeability, localized blood clotting, integrin expression systemic: fever, mobilization of metabolites, shock (6-12 hours after recognition) |
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macrophage-released cytokine Local: activates vascular epithelium, activates lymphocytes, local tissue destruction, increases access of effector cells Systemic: fever, IL-6 production, appears 6-12 hrs after initial recognition |
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cytokine released by macrophage, fibroblasts, epithelial and endothelial cells bind to CXCR1 and CXCR2 Local: chemoattractant, recruits neutrophils and basophils, activates cells to release granules |
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macrophage-released cytokine Local: activates NK cells, viral elimination |
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released by monocytes, macrophages, fibroblasts and kertinocytes Local: recruits monocytes to site of infection |
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common myeloid -> unknown precursor requires IL3 found in all CT major role: release histamines and leukotrienes causes redness and swelling, allergic response role |
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common myeloid -> common granulocyte requires IL3, GMCSF, GCSF and IL5 circulating cell 1-2 day half-life active phagocytes 30-reservoir in marrow, band forms eliminate bacteria recruited by CXCL8, fMLP, and C5a (integrins and cytokines) dies after phagocytosis of pathogen |
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common myeloid -> common granuloctye requires IL3, GMCSF, GCSF, IL5 circulating cell parasites and worms |
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common myeloid -> common granulocyte requires: IL3, GMCSF, GCSF, IL5 circulating cell parasites and worms |
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pathogen or plant derived, artificial to body recognized by macrophage, dendritic cell or B cell |
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synthesized by normal cell machinery, like in virus infected cell recognized by NK and T cells |
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movement of leukocytes into infected area |
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acidification toxic oxygen-derived products toxic nitrogen-derived products (rare) antimicrobial peptides enzymes competitors |
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used by macrophages and neutrohils to kill pathogens produces toxic oxygen-derived products |
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used by macrophages and neutrophils to kill pathogens make holes in pathogens for access |
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type of enzyme used to kill pathogen digests cell walls of some Gram-positive bacteria |
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enzymes used to kill pathogens break down ingested microbes |
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method used by PMNs to kill pathogens i.e. lactoferrin, vit b12-binding protein prevent effective growth of pathogen |
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IL1, IL6 TNFalpha increase body temperature to decrease replication rate of pathogen |
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systemic effects of inflammatory cytokines pyrogen activation and liver activation to produce acute-phase proteins increased erythrocyte sedimentation rate due to increased blood viscosity |
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compliment activation fibrinogen -> make clots, control pathogen mannose-binding lectin -> activates complement system C-reactive protein -> activates complement system |
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one of acute phase proteins binds to mannose produced on exterior or pathogen activates complement system |
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acute of actue phase proteins binds phosphocholine on bacterial surfaces activates complement system |
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recognition: macrophages amplification: cytokine secretion (band recruitment) elimination: phagocytosis |
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recognition: TLRs amplification: interferons from cells elimination: NK cell cytotoxic granules |
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activates oligoadenylate synthase -> endoribonuclease -> degradation of viral RNA activates PKR -> phosphorylates EIF-2 -> inhibits protein synthesis activates IFN-alpha -> IRF7 -> amplifies IFN response |
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natural interferon producing cell dendritic like cells in peripheral blood produce huge amounts of IFN when TLR7 and TLR9 activated (viral recognition) migrate from infection site to lymph node to help with switch to adaptive |
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Definition
activated by IFNs, IL-12, and TNF-alpha can recognized MHC on cells recognize abnormal MHC, MIC-A/MIC-B and other stress-induced surface markers on cells secrete cytotoxic granules to kill infected cell expressing weird surface markers |
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CD56 (high = immature, low = mature) NDG2d for all immunogloublin-like and lectin-like |
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receptor expressed on all NK cells has internal DAP10 for signaling activates PI3 kinase, promotes survival and inhibits NK granule release |
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internal component of some NK cell receptors activates granule release |
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internal component of some NK cell receptors inhibits granule release |
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granzymes = serine proteases, activate apoptotic response in infected cells perforin = similar to C9, creates pore intracelluarly, assists in killing of infected cells IFN-gamma = activates macrophages |
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six alleles: A, B, C, E, G, F expressed on all cells except RBCs req. peptide to migrate to PM |
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five alleles: DR, DQ, DP, DM, DO expressed on APCs from immune system req. peptide to migrate to PM |
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large number of proteins in blood, lymph and other fluids produced by Kuppfer cells in liver bind to surface and signal for phagocytosis and perforation of pathogen, also activates inflammation |
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pathogen surface creates local environment conducive to complement activation C3 tickover (constitutive baseline activity) requires: C3, B, and D |
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mannose-binding lectin binds to pathogen surface and activates complement system requires: MBL/ficolin, MASP-2, C4 and C2 |
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C-reactive protein or antibody binds to specific antigen on pathogen surface and activates complement system requires: C1a, C1r, C1s, C4 and C2 |
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alternative: iC3Bb, C3bBb classical: C4b2a lectin: C4b2a |
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classical and lectin: C2a4b3b alternative: C3bBbC3b |
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C5a>C3a>>>C4a increase vascular permeability increase adhesion molecules on vascular endothelial cells (recruit more phagocytes) activate mast cells to amplify response recruit antibodies, complements and PMNs to infection site signal pathogen bearing DCs to mirgrate |
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complement fixation results |
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Definition
no RBC lysis -> complement was fixed -> PT has antibodies
RBC lysis -> complement was not fixed yet -> PT did not have Abs |
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adaptive response characteristics |
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Definition
interaction of APCs and T cells activates of B cells interaction of B and T cells effector lymphocytes leave lymphoid tissues effector cells and antibodies eliminate pathogen memory |
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interaction of APC and T cells |
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Definition
recognition - adehsion - co-stimulation - T cell diff and prolif reacts within hours, lasts for days |
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interaction of T and B cells |
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Definition
formation of germinal centers formation of effector and memory B cells production of antibody response within days, lasts for weeks |
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involves maintenance of memory B and T cells show high serium or mucosal antibody levels protects against reinfection response within days to weeks, can last lifelong |
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common lymphoid requires: IL7 leaves marrow as almost mature form can recognize angtigens migrate and reside in lymph nodes |
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Definition
= immunoglobulin = BCR maintained on PM of B cell produce more in response to activation by antigen recognizes Ag of pathogen directly help by binding or neutralizing pathogens |
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Definition
activated B cell produces and releases antibodies |
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Definition
small molecule that are usually too small to be recognized themselves but can alter proteins on surface of cell and create an antigen antigen can be recognized by B cell |
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property of an antigen that allows for it to induce specific immune response |
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common lymphoid requiers IL7 leave marrow as immature (capable of B or macrophage still) enters thymus for final development require APC for antigen recognition migrate to and reside in lymph nodes |
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Definition
highly specific recognize processed antigens in complex with MHC proteins |
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MHC-2 interaction with T cell |
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Definition
expressed on B cells and macrophages recognized by CD4 T cells |
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macrphage: signals T cell to make IFN-gamma T cell: signals macrophage to produce TNF-alpha and activates it further |
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B cell: signals T cell to produce cytokines and switch isotope of Igs T cell: signals B cell to secrete antibodies, attach pathogen and create memory cells |
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MHC-1 interaction with T cell |
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Definition
expressed by all cells recognized by cytotoxic T cell (CD8) activates T cell, which kill the infected cell that is presenting the antigen |
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dendritic cell development |
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Definition
common myeloid -> unknown -> monocyte -> DC requires IL3, MCSF tissue located cell found in CT and lymphoid tissue major role: movement of antigens to secondary lymph tissue from infection site antigen processing and presentation to T cell |
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recognition: macrophage and dendritic cells movment: DCs 2* recognition: T cells (random interact with DCs) and B cells amplification: lymphocytes prolif and migrate to infection site elimination: T cells and B cells memory: B and T cells |
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Definition
recognition: MHC-I comlex with viral peptide and T cell interact (or) B cell elmination: cytotoxic T cell (or) B cell makes neutralizing Abs that bind viral particle |
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