83 terms

Anatomy and Physiology Ch. 21 Lymphatic and Immune system Test 2

roles of the lymphatic system
immunity, fluid recovery and lipid absorption
lymphatic vessels
the vessels that carry lymph, which is similar to plasma but less protein; unlike blood vessels have closed loop vessels, closed ends, and epithelial cells
epithelial cells in lymphatic vessel
necessary so flaps can be opened to let in lymph, and allows easier access
course of lymph to the blood stream
lymphatic capillaries>collecting vessels> 6 lymphatic trunks>2 collecting ducts>subclavian vein
right lymphatic duct
drains the head, upper extremeties, and right thoracic
thoracic duct
drains everything that the right lymphatic duct doesnt
natural killer cell
a lymphatic cell that acts a immune surveillance looking for pathogens to kill
T lymphocyte
lymphocyte that is mature in the thymus
B lymphocyte
a lymphocyte that turn into plasma cells when they are activated, they produce antibodies, they are mature in bone marrow
an antigen presenting cell that forms from a monocyte
dentritic cell
an antigen presenting cell that are found in the skin, mucous membrane, and lymphatic organs
primary lymphatic organs
red bone marrow, thymus
secondary lymphatic organs
lymph nodes, tonsils, and spleen
lobules and capsules, trabecule, cortex, medulla and reticular epithelium, which forms the blood thymus barrier and holds back the naive cells; secretes hormones that matue T-cells
lymph node
has capsule and trabecule which divides it; the trabecule filters the lymph and when it does it slows down the lymph; has afferent and efferent vessels
germinal centers
where plasma cells are made from B cells and secreted to produce antibodies
the sight where blood disposes, consist of red and white pulp, which helps with immunity
first line of defense
external barriers like the skin and mucous membranes which are impenetrable to most pathogens
second line of defense
nonspecific defense mechanisms against pathogens that break through first line of defense; leukocytes, macrophages, antimicrobial proteins, immune surveillance, inflammation and fever
third line of defense
the immune system; defeats pathogens adn leaves body with a memory of how to fight pathogens
nonspecific resistance
first and second line of defense because their effectiveness does not depend on prior exposure; present from birth
specific defense
the third line of defense because it results from prior exposure to pathogen
external barriers
the skin because its tough with keratin; acid mantle which is made by sweat which kills the bacteria; mucous membranes because its sticky and the lysozyme in it destroys the bacterial cell walls
phagocytize bacteria, has lysozyme that destroys molecules and breaks them down, creates a killing zone by producing hydrogen peroxide and hypochlorite, unfortunately this also kills the leukocyte
respiratory burst
in a neutrophil when it produces superioxde and reacts with the H+ which produces hydrogen peroxide. another enzyme produces hydrochlorite, the neurophil makes the killing zone and in turn kills itself
involved in allergic reactions, phagocytizes antigen-antibody complexes, fights off parasites, promote action in basophils and mast cells, and secrete enzymes that limit histamine and inflammatory chemicals
secrete heparin, which is an anticoagulant and histamine, which is a vasodilator
becomes a macrophage, which are called microglia in CNS, alveolar macrophages in lung, and hepatic macrophages in liver, the last line of defense against pathogen, have dendritic cells
NK cell, T cell and B cell
interferon protein
secreted by a cell that is virally infected to warn other cells. the infected cell dies activating Nk and macrophages
complement system
complement proteins in the blood that must be activated by pathogens
classical pathway
part of specific immunity and requires antibody
alternate and lectin pathway
part of nonspecific immunity
a defense action that is promoted by C3b opsinization, which is tagging bacterial cells for destruction
immune clearance
a defense action when C3b binds RBCs to Ag-AB complexes, and they go to the liver ans spleen
a defense mechanism when C5 splits and makes C5b bind into C5678 then bind into C9. this creates membrane attack complex and disrupts osmotic gradient shuts down the cell
defense mechanism that limits spread of pathogens, then destroys them, removes debris, and initiates tissue repair
cardinal signs of inflammation
redness, swelling, heat, pain
redness caused by hypernemia
swelling caused by increase in capillary permeability
heat caused by hyperemia
pain caused by inflammatory chemicals like bradykinin and prostagladins that are secreted by damaged cells or from pressure on the nerves from swelling
cellular immunity
specific immunity that is cell mediated
humoral immunity
specific immunity that is antibody mediated
anything that triggers an immune response; complex molecules that consist of proteins, polysaccharides, glycoproteins, and glycolipids
part of the antigen that stimulates an immune response
molecules too small to be antigenic, but stimulate immune response by binding to a macromolecule and creating a unique complex that the body thinks is foreign; for ex. penicilin
T cells
born in red bone marrow,, must show that they can bind to reticular epithelial cell when they are in the thymus , and they must show that they wont react so they wont damge tissue
clonal deletion
if a T cell does not pass their 2 test in the thymus then they get deleted; ends up in about 90% of all cells
clonal expansion
if the T cell passes the 2 test in the thymus they go through this; this is when they are able to bind to MHC proteins on reticular epithelium and not react to itself antigen
if the T cell does not pass its tests then it becomes an inactive state of self-tolerance
naive lymphocyte pool
cells that have not encountered the enemy and leave the thymus to disperse everywhere
antigen-presenting cell APC
an antigen that helps T cells to recognize foreign antigens; they use MHC to stick epitope onto our cells to help us identify what is ours; B cells or macrophage will display antigens on T cell
cytoxic T cell
the class of T cell that destroys cell and attacks virally infected cell
helper T cell
the class of T cell that helps promote Tc cell and B cell action and nonspecific defense mechanism
memory T cell
the class of T cell that provides immunity from future exposure to antigen
Tc cell recognition
binds to MHC-I proteins to present the antigen which are found in all nucleated body cells
Tc cell activation
when Tc cell binds to abnormal peptides on MHC-I, costimulation via a cytokine. this triggers clonal selection
Th cell recognition
binds to MHC-II proteins, which is found only in antigen presenting cell
Th cell activation
when Th cell binds to epitope displayed on MHC-II of APC, costimulation via a cytokine. this triggers clonal selection
attack phase of a helper T cell
it binds to Ag-MHCP to attack, then it secretes interleukins that attract lymphocyte, stimulate phagocytosis, and stimulate T and B cell mitosis and maturation
attack phase of a cytoxic cell
the only T cells that directly attack enemy cells, by this they use lethal hit mechanism by docking on cell with Ag-MHC-I protein complex and releasing chemicals
perforins and granzyme
lethal hit chemical released by T cell and eat stuff up
lethal hit chemical released by T cell that tell healthy cells to gear up for possible viral attack
tumor necrosis factor
lethal hit chemical released by T cell that aids macrophage in killing cancer cell
cellular immunity
a cell is infected with a virus, the virus(antigen) binds to MHC-I protein and is exposed out the cell, a helper T cell and a cytoxic T cell that have antibodies to fit the antigen
are found and bind to antigen, the Tc cell and Th cell cosstimulate eachother with cytokines, the costimuation make the Tc cell goes through clonal expansion, those Th cells kill the infected cell, mean while memory cells hang out and wait for that same virus to come again and kill it fast than before.
humoral immunity
bacteria is engulfed by a macrophage, bacteria bind to MHC-II protein and is exposed outside the cell, a Th and a B cell(plasma cell) is found that fit on the exposed bacteria, the B cell and Th cell costimulate each other through cytokines, this makes the plasma B cell go through clonal expansion to produce more antibodies to attack the bacteria, meanwhile the memory T cell hang out, so next time you get the bacteria you know how to fight it off
has 2 heavy chains and 2 light chains, these all have variable regions, which make antibody unique and the rest of the chain is the constant region, which is the same in all antibodies; the binding sight of these have 1 heavy and 1 light chain
the antibody class that has the strongest effect in bodily secretions; monomer in plasma, dimer in mucus, saliva, tears, milk, intestinal secretions; passive immunity through breast milk
a monomer in plasma, activates B cells by antigen
found on basophil and mast cell, attract eosinophils,involved in immediate hypersensitivity reactions
monomer; 80% of them are circulating, crosses placenta, involved in complement fixation
pentaner, make up 10% of plasma, involved in agglutination and complement fixation
antibodies mask pathogenic region of antigen
complement fixation
antigen binds to IgM or IgG, antibody changes shape and intiates complement binding
antibody has 2-10 landing sites, it binds to multiple enemy cells immobilizing them
antibody binds antigen molecules and creates Ag-Ab complex that precipitates, these are phagocytized by eosinophils
excessive immune reaction against an antigen that most people tolerate
environmental Ag rxns
type I
antibody mediated (IgE), acute reaction and has immediate effect, anaphylaxis
type II
antibody mediatied, cytoxic reaction and can take a few hours; responsible for mismatched blood transfusions
type III
antibody mediated, IgG adn IgM form Ag-Ab complexes, this triggers inflammation; occurs in lupus and glomerulonephritits
type IV
cell mediated, has a 12-72 hour delay,APCs in lymph nodes display antigens to Th cells which activate Tc cells and macropahges; haptens, TB, type I diabetes, graft rejection