immune system

natural killer cells

"police" the body in blood and lymph. defensive cells that can lyse and kill cancer and virus infected cells before the adaptive immune system is activated. they are part of a small group of granular lymphocytes. they detect general abnormalities such as the lack of "self cell surface protein called MHC (major histocompatibility complex) kill by apoptosis ( cell death)

complement

a group of bloodborne proteins that lyse microorganisms, enhance phagocytosis by opsonization, and intensify inflammatory responses. 20 plasma proteins that circulate the blood in an inactive state. C1-C9. destroy foreign substances. 3 pathways: classical, lectin, and alternative

self antigens

a huge variety of protein molecules dot the external surface of all our cells. your self antigens are not foreign or antigenic to yo but are strongly antigenic to other individuals. ( transfusions and graft rejections)

phagocytosis

a phagocyte engulf particular matter. flowing cytoplasmic extensions bind to the particle and then pull it inside, enclosed within a membrane-lined vesicle. the resulting phagosome then fuses with a lysosome to form a phagolysosome.

kinins (bradykinin & others)

a plasma protein, kininogen, is cleaved by the enzyme kallikrein found in plasma, urine, saliva, and in lysosomes of neutrophils and other types of cells. promotes vasodilation,increases capillary permeability and promotes formation of exudate. chemotaxis of leukocytes.

reactivity

ability to react with the activated lymphocytes and the antibodies released by immunogenic reactions

vasodilation

accounts for redness and heat of an inflamed region. both due to hyperemia (congestion with blood) that occurs when local arterioles dilate.

classical pathway

activated by antibodies coating target cells. when antibodies bind to pathogens they can also bind complement components this double binding is call complement fixation.

alternative pathwat

activated spontaneously by C3. lack of inhibitors on microorganisms surface allows process to proceed.

humoral immunity

aka antibody mediated immunity- provided by antibodies present in the body's "humors" (fluids). produced by lymphocytes, circulate freely in the blood and lymph where they bind primarily to extracellular targets-bacteria, toxins,viruses, inactivating them temporarily and making them for destruction by phagocytes or complement.

antibodies

aka immunoglobulins, constitute the gamma globulin part of blood proteins. proteins secreted in response to an antigen by effector b cells called plasma cells and the the antibodies bind specifically with that antigen.

innate (nonspecific) defense system

always prepared, responding within minutes to protect the body from all foreign substances. 1st & 2nd line of defense.

interferons

antimicrobial proteins released by virus infected cells and certain lymphocytes that act as chemical messengers to protect uninfected tissue cells from viral takeover. stops the virus from being able to replicate.

cytotoxic t cells

are the only T cells that can directly attack and kill other cells.

adaptive (specific) defense system

attacks particular foreign substances. provides the 3rd line of defense. takes considerably more time to mount than the innate defense respond.

CD8

become cytotoxic T cells that destroy any cells in the body that harbor anything foreign

cell lysis

begins when C3b binds to the target cells surface and triggers the insertion of a group of complement proteins called MAC into the cells membrane. MAC forms and stabilizes a hole in the membrane that allows a massive influx of water, lysis the target cell.

2nd line of defense

called into action whenever the first line has been penetrated, relies on internal defenses such as antimicrobial proteins, phagocytes, and other cells to inhibit the invaders spread throughout the body. INFLAMMATION

t cells

cannot bind to antigens unless the antigens are presented on self-MHC proteins. t cells that are unable to recognize self-MHC proteins are eliminated by apoptosis

pain

caused by edema and from the release of bacterial toxins and the sensitizing effects of released prostaglandins and kinins. aspirin & some anti- inflammatory drugs produce their analgesic effects by inhibiting prostaglandin synthesis.

agglutination

cell-bound antigens are cross-linked and causes clumping of the foreign cells

t cells overview

cellular response, no antibody secretion, targets intracellular pathogens and cancer cells, origin in red bone marrow, matures in the thymus, effects cytotoxic, helper, and regulatory cells and has memory formation

complement fixation

chief antibody defense used against cellular antigens. the complement binding sites on their stem regions alit.

opsonins

complement proteins or antibodies that provide "handles" to which phagocyte receptors can bind. any pathogen can be coated with opsonins, a process called opsonization ( to make tasty) which accelerates phagocytosis of pathogens.

adaptive systems response

depends on the ability of cells to recognize antigens by binding to them and communicate with one another so that the whole system mounts a response specific to those antigens

direct & indirect effects

direct effect by cell attack, indirect effect by releasing mobilizing chemical and protective antibody molecules

mucin

dissolved in water forms thick, sticky mucus that lines the digestive and respiratory passageways. this mucus traps many microorganism. in contrast, the mucin in watery saliva traps microorganism and washes them out of the mouth into the stomach where they are digested.

antimicrobial proteins

enhance our innate defenses by attacking microorganisms directly or by hindering their ability to reproduce. interferons & complement proteins

1st line of defense

external body membrane- intact skin and mucosae

secondary immune response

faster, more prolonged and more effective bc the immune system has been primed to the antigen and sensitized memory cells are already on alert. these memory cells provide immunological memory

protaglandins

fatty acid molecules produced from arachidonic acid found in all cell membranes, generated by enzymes of neutrophils, basophils, mast cells and other. does the same as histamine and also induces neutrophil chemotaxis and pain.

exudate

fluid containing clotting factors and antibodies seep from the blood into the tissue spaces. this causes local swelling, EDEMA, that presses on adjacent nerve ending causing the sensation of pain.

dendritic cells

found at the bodes frontiers ex.skin, very efficient antigen catchers. once they have internalized antigens by phagocytosis they enter nearby lymphatic to get to a lymph node where they will present the antigens to T cells. most effective antigen presenter known

macrophages

free macrophages: wander throughout the tissue space in search of cellular debris or foreign invaders. fixed macrophages: are permanent residents of particular organs.

histamine

granules of mast cells & basophils released in response to mechanical injury, presence of certain microorganism, and chemicals released by neutrophils. promotes vasodilation of local arterioles. increases permeability of local capillaries, promotion formation of exudate

incomplete

hapten- small molecule

pathogens

harmful or disease causing microorganisms

complete antigens

has immunogenicity and reactivity. proteins are the strongest antigens.

helper t cells

help activate B and T cells and induce B and T cells to proliferate. without the help of t helper cells, there is no adaptive immune response. their cytokines release chemical help needed to recruit other immune cells

C3a

inflammation by stimulation mast cells and basophils to release histamine and by attracting neutorphils and other inflammatory cells to the area.

lectin pathway

involves lectins, water-soluble protein molecules that the innate immune system produces to recognize foreign invaders. activated by lectins binding to specific sugars on microorganisms surface.

inflammatory chemicals

kinins, prostaglandins, and complement. all inflammatory chemicals dilate local arterioles and make local capillaries leakier, and many attract leukocytes to the injured area and some have individual inflammatory roles

cell mediated immunity

lymphocytes themselves rather than antibodies defend the body because living cells provide the protection has cellular targets. act directly by killing the infected cells or indirectly by releasing chemicals that enhance the inflammatory respond or activate other lymphocytes or macrophages

enzymes

lysozyme- found in saliva, respiratory mucus, and lacrimal fluid of the eye destroy bacteria. proteins- digesting enzymes in the stomach kill many different microorganisms.

MHC proteins

major histocompatibility complex. among the cells surface proteins that identify a cell as self is a group of glycoproteins. genes of the MHC code for the proteins.

defensins

mucous membranes and skin secrete small amounts of broad-spectrum antimicrobial peptides called defensins. their output increases in response to inflammation when surface barrios are breached.

mucous membranes 1st LOD

mucous membranes line all body cavities that open to the exterior : digestive, respiratory,urinary, and reproductive tracts.

antigen antibody complex

neutralization, agglutination, precipitation, and complement

phagocytes- innate 2nd LOD

neutrophils become phagocytic on encountering infectious material in the tissues. the most voracious phagocytes are MACROPHAGES ( big eaters) which derive from monocytes that leave the bloodstream, enter the tissues, and develop into macrophages.

opsonization

not all phagocytic attempts are successful. in order for a phagocyte to ingest a pathogen, the phagocyte must first adhere to the pathogen. this is done by recognizing the pathogens carbohydrate signature. many bacterial have capsules that hide their carbohydrate signature. our bodied get around this by coating pathogens with opsonins.

macrophages- adaptive system

often present antigens to t cells for another reason- to be activated themselves. certain effector t bells release chemicals theta prod macrophages to become activated

C3b

opsonization

lymphocyte development

originate in red bone marrow from hematopoietic stem cells. immunocompetence & self tolerance.

passive humoral immunity

ready made antibodies are introduced into your body, as a results, your b cells are not challenged by antigens, immunological memory does not occur and the protection provided by the 'borrowed' antibodies ends when they naturally degrade in the body. naturally- mother passing to a fetus. artificially administering exogenous antibodies

4 cardinal sings of acute inflammation

redness, heat, swelling, and pain.

mast cells

release histamines (potent inflammatory chemical)

immunity

resistance to disease

neutralization

simplest defensive mechanism occurs when antibodies block specific site on viruses or bacterial exotoxins

chemicals produced by 1st LOD

skin and mucous membranes produces many protective chemicals: acid, enzymes, mucin, defensins, and other chemicals

skin 1st line of defense

skin is heavily keratinized epithelial tissue.keratin is resistant to most weak acid and bases and to bacterial enzymes and toxins.

precipitation

soluble molecules instead of cells are cross-liked into large complexes that settle out of solution.

antigens

substances that can mobilize the adaptive defenses and provoke an immune respond. they are the ultimate targets of all adaptive immune responses. can be complete or incomplete

fever

systemic response initiated by pyrogens, high body temp inhibits microbes from multiplying and enhances body repair processes. pyrogens are released when leukocytes and macrophages are exposed to foreign substances. causes the liver & spleen to sequester iron and zinc and increases metabolic rate of tissue cells

primary lymphoid organs

t cells- thymus b cells- bone marrow

antigenic determinants

the ability of a molecule to act as an antigen depends on its size and complexity. only certain parts of an antigen are immunogenic.

immunogenicity

the ability to stimulate specific lymphocytes to multiply

acid

the acidity of skin, vaginal, and stomach secretions inhibits bacterial growth

adaptive defenses

the adaptive system must "meet" an initial exposure to a specific foreign substance to be able to protect the body against the substance. it is specific, it is systemic, it has memory.

t cell activation

1. antigen binding, t cell antigen receptors bind to an antigen-MHC complex on the surface of an APC. 2. co-stimulation, t cell must bind one or more co-stimulatory signals which are other molecules that appear on the surfaces of APCs in tissues that are damaged or invaded by pathogens.

innate defenses

1st LOD:SURFACE BARRIERS: skin & mucous membranes 2nd LOD: INTERNAL DEFENSES: phagocytes, natural killer cell, inflammation, antimicrobial proteins, and fever.

adaptive defense

3rd LOD: Humoral immunity : B cells Cellular immunity: T cells

3 cell types of the adaptive system

B lymphocytes (b cells) oversee humoral immunity T lymphocytes (t cells) are non-antibody -producing lymphocytes that constitute the cellular arm of adaptive immunity APCs do not respond to specific antigens as lymphocytes do but the play essential auxiliary roles

primary immune response

the first exposure to a particular antigen. has a lag period of 3-6 days after the antigen encounter

MAC membrane attack complex

the three pathways converge at C3,which cleaves into C3a and C3b. this event initiates a common terminal pathways that enhances inflammation, promotes phagocytes, and can cause cell lysis.

B lymphocytes

they present antigens to certain kinds of t cells called helper t cells in order to obtain help in their own activation. response if humoral, antibody secretion, effects plasma cells, has memory cell formation

inflammatory response

triggered whenever body tissues are injured by physical trauma, intense heat, irritating chemicals, or infections by viruses, fungi, or bacteria. prevents the spread of damaging agents to nearby tissues, disposes of cell debris & pathogens, alerts the adaptive immune system, and sets the stage for repair.

CD4

usually become helper T cells that help activate B cells, other T cells, and macrophages, and direct the adaptive immune response. Some become regulatory cells which moderate the immune response

active humoral immunity

when your B cells encounter antigens and produce antibodies against them, can be naturally acquired when you get a bacterial or viral infection or artificially acquired when you receive vaccines