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144 Cards in this Set
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adaptive immune system
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develops over time, specific T cells, takes 18-24 hrs to respond, SCID (severe combined immunodeficiency)--lack of adaptive immune system
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hematopoeisis
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development of blood
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the protein on the surface of the pluripotent stem cell
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CD34; should be in the bones; if heavy in the blood = leukemia
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two linneages of the pluripotent stem cell
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monocytic and lymphocytic
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monocytic lineage includes
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innate immunity
--macrophage - --neutrophil - --eosinophils - --basophils - --mast cell-- --NK cells (natural killer) --dendritic cell (most like a macrophage) langerhans cell in skin, cupfer cells in gut |
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mast cells cause
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sneezing and nose running
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little red granules
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eosinophils
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big ugly blue granules
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basophils
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most like a macrophage
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dendritic cell: langerhans cell in skin, kupffer cells in gut
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lymphocytic lineage is adaptive or innate?
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adaptive
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lymphocytic lineage includes
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B and T cells
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B cells start out where and go where
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in the bone marrow and go to the lymph node
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From the lymph node B cells produce
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antibodies; b cells can secrete or have antibodies on their surface; b cells and antibodies should be synonymous with each other
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second name for an antibody
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immunoglobulin
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antibody function
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look like little "y"; grab bacteria
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IgM
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initial response
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IgG
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response to bacteria and viruses
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IgE
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allergies and worms
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IgA
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food; upon repeated exposure the IgA will turn to an IgE and the food will be digestible.
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T cells start where and go to where?
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start in the bone marrow and go to the thymus
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from the thymus T cells differentiate into two different kinds of T cells
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CD4 and CD8
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CD4
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T helper cell, makes cytokines in the lymph node; Th0, Th1, Th2, Th3, Th9 (makes interleukin 9), Th17 (makes interleukin 17)
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CD8
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cytotoxic T cell (also T killer) whole goal is to kill
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NKT cells have the same proteins on their surface as
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NK cells
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Cytokine Th0
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a naive Tcell
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Th1
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bacteria and viruses
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Th2
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worms and allergies
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Th3
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food
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Th9
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asthma
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Th17
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mould
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T cells specialize when they get to the
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lymph node
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Cytokines function
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a small protein that’s released by one cell and causes another cell to do an activity -- it’s a trigger
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to respond to a cytokine you have to have a
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cytokine receptor
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IL-1 (cytokine) Interleukin 1
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triggers a fever
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IFN (interferon
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Interferes with viruses
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TNF - tumor necrosis factor
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in rheumatoid arthritis TNF attacks the joints
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TGF - tumor growth factor
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shuts down the immune system; we need to do this when we eat; if we don't have enough, we will attack our food
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immune system organs
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spleen, thymus, bone marrow, skin, pyers patches in the gut (80% in the gut), sometimes liver
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antigen
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a foreign protein that the body will respond to
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physical barriers = innate or adaptive?
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innate
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physical barriers
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skin, tears, saliva, stomach acid, mucus, surfactants
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defensins
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anti microbial agent on the skin that attacks the lipids of bacteria; we have them on our skin, in our gut, in our mucous membranes
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atopic exema
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caused by lack of defensins; so the body attacks excess bacteria on the skin--this can also happen in the gut--if there's an overgrowth of bacteria that means defensins are too low
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in people who are malnourished
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defensins are too low
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mucus functions to
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cover the receptors so the bacteria can't hold on
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mucins
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proteins on the mucus
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IL-13
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cytokine that produces mucus
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tears and saliva
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can flush out bacteria - they produce lysozyme, which is like a giant trash compactor, a big enzyme that chops up bacteria and virus
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surfactants (in lungs)
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opsinization - coating a bacteria or virus to make macrophages want to eat it
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acute phase proteins (made by the liver)
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kinins
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kinins
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proteins that cause pain and itching to draw attention to the wound, cause smooth muscle contraction and striated muscle relaxation to help with blood flow to the site and cause contraction of vascular endothelial cells to make space for edema; kinins can act as chemokines
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chemokines
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a (protein) cytokine that causes cell movement; works to create a concentration gradient
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kinins will center around
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the injury
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the cell will move toward
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the concentration gradient toward the injurty
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skin is constantly then producing kinins to
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maintain the concentration gradient
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Kinins change the structure of hte vascular endothelium
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to make space for edema
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complement
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pokes holes in the membrane of the bacteria to kill it because the contents escape; the hole poking process is called Big MAC attack (Memory Attack Complex); produced in the liver
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where do T cells differentiate
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thymus
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T cells make cytokines in the
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lymph node
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T cells specialize when they get to the
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lymph node
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complement proteins mediate
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fever, edema
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complements released into the blood stream mediate
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inflammation
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acute phase proteins are
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complements and kinins and CRP
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CRP
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helps mediate inflammation and is important because it's easy to measure
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hsCRP
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high sensitivity test for CRP
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neutrophils hang out
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in blood vessel walls waiting for infection to occur
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neutrophils are attracted to
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concetration gradient created by kinins
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Neutrophils stop because of
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adhesion molecules created by chemokines
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Then they drop thru the blood vessel wall in a process called
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diapedesis
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They roll to the site of infection using
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chemokines adhesion molecules
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neutrophils live
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18-24 hrs
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neutrophils comprise
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pus
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neutrophils are full of toxic granules called
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defensins, lysozymes, and proteases
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If a neutrophil phagocytoses and bacteria
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it can kill it on the spot
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macrophages live
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everywhere
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macrophages can't kill unless
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commanded to
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macrophages are of the
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myeloid linneage
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macrophages in blood
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monocytes
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macrophages in tissue
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macrophages
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dendritic cells are more phagocytic than
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macrophages
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they live 24 to
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48 hrs
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dendritic cells are really good at
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antigen presentation
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antigen presentation means
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macrophages and dendritic cells carry antigens to the nearest lymph node--this causes lymph node swelling --so that as T and B cells circulate they just have to go lymph node to lymph node
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PRR (pathogen recognition receptor) =
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receptors on the surface of macrophages, dentritic cells, and neutrophils that recognize and bind to different parts of a pathogen
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TLR (=PRR)
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the signal my cell gets that it’s infected-the danger signal - tell immune system that you have an infection
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TLR's can be
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inside or outside the cell
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If a bacteria binds to a TLR it sends a message to the nucleus that
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there is danger, produce immunity
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phagosome
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the compartment in which the bacteria ends up when a macrophage invaginates and takes it that bacteria in
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the phagosome fuses with a lysosome to produce
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a phagolysosome
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a phagolysosome
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is very acidic and chops up the unfriendly bacteria
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the bacteria wind up in an
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MHC (the hot dog bun on the surface of the cell)
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Processed bacteria will bind to an
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MHC
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whole bacteria will bind to
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TLR
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when a TLR triggers danger the cell produces
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lipid mediators, cytokines, chemokines, costimulatory molecules, reactive oxygen species
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lipid mediators are
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prostaglandins, platelet activating factor, leukotryeens (sp?) - lipids that are going to go throughout the body and help trigger events, such as fever, redness, heat, pain, swelling
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Inflammatory cytokines are
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IL1, IL6, TNFalpha
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IL1, IL6, and TNFalpha
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mediate inflammation by fever and trigger acute phase proteins
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IL1 causes
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depression
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IL6 causes
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anxiety
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TNFalpha causes
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hostility
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chemokines
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they help cells move
based on a protein that’s going to bind to a receptor for that protein, and that receptor is gonna be on the surface of some cell Most chemokines have a cytine in them --an amino acid (c) |
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costimulatory molecules
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proteins on the surface of an infected cell that help stimulate a T cell --only on macrophages, dendritic cells, and B cells - how the T cell is going to tell whether or not danger has been signaled -- CD86
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T cell asks, R U me? It is looking at
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the MHC and the peptide bound to the surface of the cell
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T cell asks, R U danger it is looking at
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CD86 molecule - a costimulatory molecule
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reactive oxygen species =
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free radicals; Oxygen molecules that are charged; they can kill bacteria
they are secreted to try to kill some of the bacteria surrounding that macrophage they attack the membrane--But free radicals also kill your own cells. So we take antioxidents to reduce free radicals. Antioxidents: vit E, A, corotenoids, glutathione |
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phases of immune response
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acute phase,
innate phase specific phase memory phase |
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NK cells kill by
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poking holes: There are two proteins involved: perforin(hole poking protein), granzymes--once the perforin pokes holes, granzymes go in and chop up everything inside
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NK cells can kill
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a variety of different cells (as opposed to CD8, which are specific)
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MHC-1 on the surface of a cell
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deactivates NK cells, MHC-1 makes you you; this is a problem in transplants
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when T cells are activated in the lymph node this =
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the activation of the specific immune response and the end of the innate response
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B cells are
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lymphocytic
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B cells make
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antibodies
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One antibody can bind to how many antigens?
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two
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The FC region binds to
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a cell
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The FAB region binds to
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antigen
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How many specificities can one B cell make?
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one
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How do we get the specificities
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gene recombination
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What part of the antibody are we rearranging?
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The FAB
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allelic exclusion
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you can only rearrange one antibody gene at a time
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receptor editing
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when a B cell binds to self, it can rearrange its other gene--two chances
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If antibodies bind really well, what occurs
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opsinization
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B cells can take the antibody on the surface and make little point mutations in the FAB region to make the antibody bind tighter, to increaes its affinity. By the time we see the flu again and again and again, we should have antibodies that bind really tightly. This process is called what?
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Somatic Hypermutation
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In Multiple Sclerosis
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B cells bind to Myelin Basic protein (it lines the spinal cord)
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The FC part of the antibody can change but once it's changed it can't go back to the class it was before (MDGEA). This is called
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Class switching
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is made first in an immune response--can indicate initial exposure to a bacteria or virus and that they’re very early in the immune response
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IgM
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IgM is pentameric, which means
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it will bind to around 5 antigens
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IgM lives for about
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2 weeks
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We need IgM around until
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We can make more specific antigens and our T cells get activated
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CD4 T cells make cytokines that help B cells do what
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class switch to another type of antibody (once it's made IgM)
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If someone has a bacterial infection which class of antibody will be at the top of the serum
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IgG
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We associate IgG with what kinds of T cell response?
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Th1
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Can IgG cross the placenta?
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yes
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what is the half life of IgG?
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23 days (so baby has protection from mom after birth for about a month without breast milk to help)
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IgE =
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monomeric, allergies and worms, half life of two days, Th2 response
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IgA =
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monomeric or dimeric, tolerance to food and infectious material, esp found in mucous membranes in the gut, we make it in our microflora, its found in secretions: tears, mucus, saliva, breast milk, vaginal secretions, secretions from the gut, sweat
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In this whole process, what is telling the T cell what to make to initiate a class switch for the antibody?
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dendritic cells and macrophages
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the antibody involved in allergies
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IgE
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the antibody that can be pentameric
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IgM
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response to bacteria and virus
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IgG
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food intolerance
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IgA
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this antibody binds to the FCespsilon receptor
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IgE
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this antibody can make mast cells degranulate
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IgE
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this antibody has the longest half life in the blood
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IgG
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If you have high levels of this antibody, you recently got an infection to a microbe you haven’t seen before.
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IgM
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