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51 Cards in this Set

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innate immune system

not specific and there is not memory involved something came into body identifies it as non-self and kills it

innate defenses

1 line: keretinized epithelial cells phsyical barrier, chemical skin vagina stomach acids saliva mucus resp and digestive


2nd line: phagocytes, neutriphils monocytes/macrophages , phagocytosis

macrophages

spit out left over pieces from phagocytosis, pieces released are nuetrilized fragments


macrphages will warn and activate the adaptive immune system

inflammation

part of the innate


leukocytes brought in marginate finally leave the blood and move to tissue via diapedesis then begin cardinal chemical messengers to bring help to the sight

steps of inflammation

1. release of chemicals: histimine basophils complement following phagocytosis


2.vasodilation


3. leakage of fluid w/ clotting factors and ab area


4. phagocyte mobilization

adaptive defenses

react against almost any type of ag,has memory, but must be presented w/ ag

B/T Cells

have a way of remembering what was broken down, the react faster and stronger w/ each exposure cannot be activated until after the innate has been activated





stepwise path

1st line defense, 2nd and then adaptive immune system


keeps the body in check

antigen

is a small piece of the bacteria that the T/B cells act on all non-self


antigeni determinants: portion of ag the ab or lymphocyte binds


MCH

all self cells contain MCH to prove to the immune system that they belong to self all MCH is self to one person no 2 individuals have the same MCH proteins

antigen presenting cells

macrophage and neutriphils


-ag presenting cell after it has engulfed and broken down a bacteria


-comes in contact w/ bacteria bring into cell break it down dump pieces which are now ag


-takes one small piece of the ag and puts it out on a cell surface protein presenting it to B/T Cells

t cell

react to the presented ag all t cells need to have the ag presented

b cells

react to the parts and pieces spit out of the macrophage


-create an army to find bacteria and help phagocyte s destroy it, recognize the ag processed by the phagocyte the proliferates when enough are made bcell changes its form to plasma cell and memory cells (takes days to weeks for trasnformation)



plasma cells

produce ab, ab are specific to the original ag that bonded w/ b cell


overview: b cell recognized something, makes plasma cell and plasma cell makes ab


difference B/T cells

t- help the phagocytes


b- cannot interact in thee same place as the t cells get in the way of each other


common: they both do not do anything with the entire bacteria



antibodies

aka immunoglobulins made by b cells after b cell saw spit out pieces and identified as nonself adn makes the AB,


y shaped 2 heavy 2 light chains help by disulfide bonds


variable region: is specific to only YOU where the ab can bind to ag


constant region: same on each ab


-help other cells in the body kill bacteria


-are proteins

4 primary actions of antibodies

1. neutrilization: ab cover the bacteria so it cannot adhere and hurt the host


2/3agglutination/presipitation: ab clump together from their consant region so bacteria can fall out of solution


4. complement: helps other activities in blood,

memory cells

are made by b cells


1st exposure: do nothing, starts to make MC


1st/2nd steps takes a week to make memory cells


2nd exposure: memory cell proliferates becomes plasma cell to make ab will go back and fight, alot faster b/c memory cells are already made so ab are already there and go staright to killing



cell mediated immunity

t cells are more simple than b cells, made in thymus


when activated make 2 diff t cells


CD4: regulatory and Helper T cells


CD8: cytotoxic t cells


do different things

helper T cells (TH)


CD4

helps everything else


main job is to give permission to the B cell to make the ab then it secretes a chemical telling it yes its bad or no


-tcell first cell to be activated

regulatory T cells (Treg)


CD4

close to t cells, come in and make sure everything is ok


if the tc is starting to work the treg will come and check that the response in appropriate to the invasion

cytotoxic T cells (TC)


CD8

only cell in immune system that can go up to the cell and kill it


-TC works by TH to go to work


-TC will release enzymes that poke a hole in membrane and leak them into the bacteria and kill it


-fast and efficient


-once its dead it will float around blood stream until broken down further doesnt cause harm

overview of all

invades body, gets past skin(1st line of defense),


phagocytes comes(2nd), breaks its down into small pieces puts one piece on the cell surface which are seen by the b cells, b cells turn int plasma cell which makes the ab and b cell also makes memory cells, ab go back and fight original invader, same time tcells are looking for APC is showing, thelpers and tcytotoxic go and kill cells, tc goes into kill mode, th gives permission to b cell to make the antbody

type1: immune response: ALLERGY (IgE)


-making of the anitbody

1. initial encounter- sensitizing dose


2. second encounter- memory cells and immunoglobins (antibodies)


are ready to react

mast cells and basophils

bind to IgE during sensitization , contain active cytokines-tagret organs&allergic symptoms, degranulate, principal chemical mediators production

histamine

stiumlatees smooth muscle, glands, eosinophils- whal and flare reaction w/ pruritis(itching) and headache


-non-specific



serotonin

complements histamine

leukotriene

induces gradual contraction of smooth muscle

platelet-activating factor

lipids w/ similar effects as histimine

prostaglandins

inflamm agents responsible for Vasdilation


-increases pain

bradykinin

prolonged smooth-muscle contraction of branchioles, dilation of peripheral arteries, increase mucus secretion


-account for the wide range of allergic symptoms

specific desease w/ IgE


mast-cell mediated allergy

hay fever, allergic asthma(dust animal dander), food allergy, drug allergy, eczena, anaphylaxis(massive release of histamine)

Diagnosis of Allergy

-virtro: elevated levels in blood, blood count, histamine release test


-skin: injected w/ pure allergen extract on back will wheal if allergic



treatment for allergen

avoid allergen , meds that blovk action of lymphocyte, mast cells or chemical mediators, desensitization therapy

type 2: reactions that Lyse Foreign cells


(IgG)


-t cells go out and find the antigen

group of syndromes that involve complement-assisted lysis of cells by IgG and IgM directly on antigens

include

1. transfusion reactions


2. autoimmunity- acitvates t-cells when it shouldnt adn kills self cells


-ABO blood groups

blood types

A, B, AB , O




-ABO anitgen markers on RBCs are genetically determined and made of glycoproteins


-named for dominant antigen

RBC

-in type O person has an antigens bt not A and B antigens



tissues other than RBC

carry A and B antigens

universal transfusions

type O is- universal donor


type AB+- universal recipient

transfusion reaction

given the wrong blood type


-massive hemolysis leading to systemic shock and kidney failure


-s/s: fever, anemia, jaundice


-tx: stop transfusion, meds to remove hemoglobin from wrong blood, begin infusing right blood

Rh Factor(D antigen)

+ is dominant over -


1. inherit one Rh gene is Rh +


2. inherit 2 recessive genes of Rh+


-antibodies against this factor are thru placental sensitization or transfusion of other RBC antigens


positive can get + and -


negative can only get neg-

blood types w/ anitgens

A+: ANTI B, can get: A+, A-, O-


A-: ANTI B can get: A-, O-


B+: ANTI A can get: B+, B-, O-


B-: ANTI B can get: B-, O-


AB+: ANTI A AND B, can get: ALL universal recipient


AB-: ANTI A AND B can get: AB-, O-


O+: no antigens, can get: O-, O+


O-: no antigens, universal donor, can only get: O-

type 3: Hypersensitivity


immune complex reactions


-cause tissue damage

-reaction of soluble antigen w/ anitbody and depostionof the resulting complexes in basement memebranes of epithelial tissue simular to type2


-produce IgG and IgM afte repeated exposure to antigens the activation of complement differes from type 1, antigens not attached but free-floating deposited in tissue causing an immune complex reaction



differ from anaphylaxis b/c..

they depend of IGG, IGM, IGA rather than IGE


-require large dose od antigen, symptoms delayed

step by step reaction

1. more anitgens then anitbodies free flowing in blood, smakk immune complexes formed


2. large immune complexrs form that fix complement and are cleared from circulation, antigen and antibody even


3. large amounts of antibody then antigen, medium size immune complex form fix complement and cleared from circulation

type 4: cell mediated(delayed)


-cause tissue damage

involve t-cells, result when t-cells repsond to ag dislayed on SELF tissue or transplanted foreign cells


dx: infectious allergy, contact derm, exposure t resins in poison

t cells in organ transplantation

donor tissue displayed on surface molecules of a different MHC class, the t cell will of recipient will recognize it as foreign and react to it

immunodeficiency disease

lower immunity: get sick alot


-primary- congenital(at birth) lack b/t cells or absence or immature thymus gland


-secondary: after birth caused yb natural or artificial agents


caused by: infection, organic disease, hemotherapy, radiation, AIDS

identifying bacteria

phenotypic, genotypic, specimen collection


-cell shape and size, colony appearance, speed of growth, patterns of growth, physio/bio chem iD, presence of specific enzymes, gram stain reaction

tube agglutination test

-last resort if others dont work


-equal amount of ag-ab w/ pts serum


-wait fro which tube has agglutination


-precipitation- antigen is a soluble molecule