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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

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