The Immune System ***

Question 1

leukocyte

Answer 1

only formed element that are complete cells
1% of blood volume
protection against bacteria, viruses, parasites, toxins, tumour cells

Question 2

travel in blood

Answer 2

made in red bone marrow,
get to where they’re needed through blood stream
can leave for immune/inflamm. response
to survey or attack toxins

Question 3

leukocytosis

Answer 3

bodies response to bacterial/viral invasion
number inc rapidly, 2x in hours

Question 4

2 types

Answer 4

granulocyte and agranulocyte
separated based on how granular their cytoplasm are
if many vescivels are present

Question 5

descending order of prominence in blood

Answer 5

never let monkeys eat bananas

neutrophils lymphocytes monocytes eosinophils basophils

Question 6

granulocytes

Answer 6

spherical and larger than RBC
has granules

neutrophils
eosinophils
basophils

Question 7

neutrophils

Answer 7

most prominent
2 types of granules
have hydrolytic/digestive enzymes and some antibiotic-like proteins (defensins)

polymorphic leukocytes = nucleus has many diff shapes

numbers are incccccc if have acute infections since are phagocytes = ingest and destroy bacteria

Question 8

eonsinophils

Answer 8

nucleus w 2 lobes
coarse granules

mostly modulate immune response to asthma and allergies

also surround parasitic worms and attack w digestive enzyme to chew it up, bc can’t
bc of size, need more than 1

Question 9

basophils

Answer 9

rarest WBC
granules contain histamines
big vasodilator makes blood vessels leaky and attract other WBC
easier for cells to leave and do their jobs in surr tissues

not attacking cells, more behind the scenes

Question 10

Agranulocytes

Answer 10

lymphocytes and monocytes
no granules, spherical or kidney shaped nuclei

Question 11

lymphocytes

Answer 11

2nd most common
some in blood stream, most in lymphoid tissue

large nucleus w a rim of cytoplasm

waiting to be notified if pathogen has invaded so can inc #s to fight that micro orgs
T cells = act directly agsint infected or tutor cells = soldiers

B cells = give rise to plasma cells that produce antibideos

Question 12

monocytes

Answer 12

largest leukocytes
U or kidney shaped nucleus
differentiate into macrophages

exist in circ sys as a sphere to move around better , move ot infected tissue, diff in to macrophages.

phagocytic in chronic infections + against some virus some bacteria

Question 13

leukopoiesis

Answer 13

production of WBC
prod isn’t equal for all types, inc based on demands of body

Question 14

production pathway

Answer 14

hemocytoblast = stem cell for all formed elemetns
fork in the path, myeloid stem cell of lymphoid stem cell

hemocytoblast
=> lymphoid stem cell (stem cell)
=> lymphoblast (committed cell)
=> lymphocyte (product)

hemocytoblast
=> myeloid (stem cell )
=> myeoblast (committed)
=> eosinophils, neutrophils, basophils (possible products)

hemocytoblast
=> myeloid (stem cell )
=> mono blast (committed)
=> monocyte (product)

Question 15

leukocyte disorders

Answer 15

leukemia
infectious mononucleosis
leukopenia

Question 16

leukemia

diff types
will lead to
treatment
death bc

Answer 16

cancer of WBC
usually a single cell remains unspecified and mitotic

acute = derives from a cell early in differentiation pathway

chronic = from a cell at a later stage

bone marrow taken over by cancer cells
= anemia, clotting problem, fever, weight loss, bone pain

WBCs are numerous but non functional
death to internal bleeding or overwhelming infections

treatment = irradiation
anti-leukemics drugs
bone marrow transplant

Question 17

infectious mononucleosis

Answer 17

excessive number of enlarged and abnormal shaped lymphocytes

symptoms = tired, achy, chronic sore throat, fever

Question 18

leukopenia =

Answer 18

abnormally low WBC count
due to drugs or chemotherapy drugs

Question 19

the immune systems, 2 defences

Answer 19

innate, non specific, defenses
there all the time, dealing w something going wrong in the body,
all it knows is something wrong, not what. doesn’t have to specifically identify to attach

adaptive, specific, defences,
subpopulations of lymphocytes recognize specific target
each sub pop recognizes + deals w specific type of micro org.

Question 20

how does innate immune system get informed/activated

Answer 20

triggered by micro orgs entering from outside or by tissue damage w/o external infection

Question 21

PAMPs

Answer 21

pathogen associated with molecular patterns
when molecules are present when not normally should be
recognized by toll-like receptors on surface of phagocytic cells = informs active immune system to carry out a responseD

Question 22

DAMps

Answer 22

molecules in the wrong place in your body
sprain ankle = tissue damage = signal

Question 23

DAMps and PAMPs working together

Answer 23

notify the innate immune system that smth is wrong
don’t need to know what is it

+
together
DAMPS = cut on your finger
PAMPs = open to env to pathogens enter

Question 24

innate defenses

Answer 24

things present all the time in our bodies that help us
effective but can be breached, not fool prood, things can get passed so rest of immune system takes over

Question 25

examples of innate defences

Answer 25

Acid = acidity of skin, vaginal and stomach secretion stop bacteria growth enzymes = saliva, resp mucus and lacrimal fluid have lysozymes enzymes in stomach can digest microrgs. mucin = in digestive and resp pathways, can get to nasal cavity or back of throat but not further, traps micro orgs defensin = anti-microbial peptides secreted by mucus mb of GI and resp system and by skin, other chemicals = some lipids in sebum and dermicidn in sweat that are toxic to bacteria

Question 26

inflamation what, how signs

Answer 26

response to any type of injury cut, sprain, twist, burns occurs as part of innate, can be amplified as adaptive immune response redness, heat, swelling, pain

Question 27

why inflammation

Answer 27

prevents spread of micro orgs to nearby healthy tissues disposes of cell debris and pathogens brings in growth factors for repair process alerts the adaptive immune system

Question 28

inflammatory chemicals

Answer 28

histamine, complement system, kinins, prostaglandins released by injured cells, macrophages and lymphocytes promote arterole dilation, + cap leakiness, + attract other immune cells to come to site of injury/inf

Question 29

what causes pain during inflammation

Answer 29

chemicals released by cell fighting infections + P of the build up fluid coming from circ system (accumulating in tissues)

Question 30

process of infection promoting inc neutrophils at site

Answer 30

neutrophils enter blood from bone marrow caps become more leaky, opens up spaces in bn adj epi cells neutron are singled to slow down, cling to wall, find an opening and squeeze through towards site of infection

Question 31

margination diapedesis chemotaxis

Answer 31

Margination = rolling along insideof tinu blood vessel Dia = squeezing through opeingin into intersitial spaace Chemo = following trail of inc concentration of inflamm cjemicals that are closer to the cell gets to site of injury and site of infection

Question 32

flowchart

Answer 32

tissue injury = release of inflammatory chemicals and chemical mediators 1. vasodilation of arterioles = inc blood flow to area 2. inc permeability of caps = fluid in tissue 3. attract neutrophils and other immune cells *** leukocytes migrate to injured area migration, diapedesis phagocytosis of pathogens and dead tissues healing *** tissue injury also = release of leukocytosis inducing factor = stim leukocytosis = inc number of WBC in blood stream WBC migrate to injured area, pick off over here

Question 33

interferon main pathway

Answer 33

cell 1 is infected by virus. virus enters the cells, duplicates interferon gene is switched on by presence of virus mRNA for interferon is made interferon (the protein) is produced by cell 1and released interferon binds to cell 2 induces synth of protective proteins stimulates cell to turn on gene for antiviral protein s antiviral portion blocks viral production in cell 2 nothing can be done for cell 1, it died

Question 34

interferon other roles

Answer 34

when released in ECF can activate macrophages, and mobilize natural killer cells = anti cancer effects killer cells kills infected cells

Question 35

complement system

Answer 35

group of at least 20 plasma proteins circulating in the blood stream in an inactive state once activated = variety of components amplify inflmaroty proves propagation of activation, one activates 2, 2 activates 3, and so one

Question 36

effects of complement system

Answer 36

main goal = destruction of invading microbes by mb attack complex 1. vasodilate and inc permeability of caps and venules to proteins, so WBC can go to site of inf 2. chemotaxis = following trail of inc concentration of inflamm cjemicals that are closer to the cell gets to site of injury and site of infection 3. enhancement of phagocytosis

Question 37

C3b functions as a opsonin

Answer 37

C3b is a tag on bacteria that help immune cells recognize and destroy threats opsonin = coding on a bacteria to a specific molecule binds to bacteria, makes it easier for phagocytic cells, makes more visible

Question 38

Membrane attack complex = MAC activation

Answer 38

classical pathway = adaptive immune system activated by antibodies coating target cell lectin pathway= lectin binds to specific sugars on micro orgs surface alternative pathway = lack of inhibitors in micro orgs surface = can proceed in killing it

Question 39

MAC step

Answer 39

C3 gets split into C3a and C3b C3a = enhances inflammation (inc histamine, inc vessel permeability, attracts phagocyte) C3b = coats pathogen surfaces, enhance phagocytosis C5b is created = C6-9 proteins join together form MAC MAC is formed insert into target cell mb create pores that lyses target cell, and many almost like a hole punch, takes away ability to regulate internal env

Question 40

fever high is= moderate is =

Answer 40

innate response to systemic infections usually body temp = 37 deg C when leukocytes and macrophages are exposed to bacteria and other foreign substances, they release pyrogens high = dangerous s leads to proteins being denatured = can't fn as normal moderate = helpful = speeds up metabolic rate , helps immune sys fn more rapidly causes liver and spleen to hold on to Fe and Zn, minerals that help bacteria reproduce if not available, dec replication from bacteria

Question 41

natural killer cells

Answer 41

type of lymphocytes not specific to anything no recongition of specific antigen kill anything suspicious

Question 42

process of to kill or not to kill healthy vs infected

Answer 42

there are two triggers, expression fo a stress marker and a lack of protective MHC 1 MHC 1 will bind to killer inh receptor = stop the NK from attacking, saying "im part of the body chill" low stress marker infected, high stress marker = "something is wrong, kill me" no MHC1 to bind with the inh receptor, no inh = will get killed

Question 43

killing method, how?

Answer 43

trigger cells to commit cell suidicde perforin = creates holes in mb of target cell granzymes = enzymes that enter through holes and triggers programmed death

Question 44

adaptive mechanism 3 key players

Answer 44

B lymphocute = humeral immunity = antibodies to fight infections, pathogens in bloodstream (bac, virus) T lymphocyte = cell-mediated immunity = direct attack and killing infected/abnormal cells, inf w virus or cancer cells Macrophages (antigen presenting cells) tell immune system of what they have found

Question 45

lymphocytes self tolerance vs immunocompetence

Answer 45

originate in red bone marrow from hemocytoblasts initially all identical, then becomes either B or T depends on where matured bone marrow or thymus maturing = tested fro s and I s = ability to ignore bodies own cells and not attach them I = recognize and respond to foreign antigens, attack pathogens fail = death

Question 46

antigen

Answer 46

antibody generating substance can have multiple anitgenic determination = can activate diff B cells

Question 47

Major histocompatbiltu complex

Answer 47

grp of cell surface glycoportines that mark the cell as self, "I belong to the body" each one has a groove where a self-antigen or a foreign antigen can be interred self = no kill = im safe foreign = kill me

Question 48

lymphocyte development, maturation and activation

Answer 48

both B and T cells precursors originate in red bone marrkw T cell precursors travel to thymus , B cells stay In bone marrw they develop immunocompetence and self tolerance they leave the thymus and bone marrow patrol secondary lymphatic organs and circulate through blood/lymph when encounter an antigen, they bind to it, become activated they will multiply their numbers, differentiate and carry out response

Question 49

T cell maturation more detail

Answer 49

testing if they can see MHC? hopefully yes and if activated by self antigens (hopefully no, if yes = autoimmune disease)Ç positive selection = must recognize self MHC be able to bind to MHC if can't recognize = death by cell suicide can = MHC restrictions = survivors can now only recognize antigens that are placed on self MHC go to negative selection Negative selection = must not recognize self antigens make sure don't bind and attack bodies own cell bind too strongly/recognized = eliminated failure to recognize = survive

Question 50

B cells

Answer 50

immature lymphocutes undergo maturation in bone marrow self reactive weeded out when immunocompetent = display unique receptor on cell surface, makes them Abe to react to one nad only on foreign antigen

Question 51

B cells and humeral immune response

Answer 51

Primary response: usually in spleen or lymph nodes there is an antigen there are 3 diff B cells, each w diff receptor only second gets activated, only one that can hepl so only one being cloned (inc in #) form plasma cells = secrete antibody molecules to the specific antigen antibodies circulate and bind to antigen = marks for destruction also some clone cells, don't become plasma = stay as memory cells, can be called on years later for another response = immunological memory same challenge but faster response

Question 52

Immunoglobin classes

Answer 52

IgM = antibody = first one secreted by plasma cells during primary response IgA = dimer = found in body secretions, salvia, sweat, intestinal juice, milk stops pathogens from attaching to epi cell surfaces IgD = acts as receptor on surface of B cells IgG = mist abundant antibody in plasma protect against toxins, bac, and viruses circulating IgE = ALLERIC RESPONSES,

Question 53

comparing concentration of antibodies vs time days after exposure to antibodies

Answer 53

day 0 = exposed to antigen A day 4-5 = drastic inc in conc of antibody to A conc decreases gradually till day 28 practically 0 day 28 = 2nd exposure to A, 1st exposure to B = instance jump of antibody to A concentration. response is faster and larger day 32 = slight jump in conc of antibodies to B.

Question 54

how do vaccines factor in

Answer 54

memory cells are most important = carry the info of the antigen if 2nd appearance can boost repsonse in size and time. antibodies disappear after some time, vaccines trigger you to make more memory cells, keep the response quick and efficient.

Question 55

humeral immunity types and subtypes

Answer 55

humoral = involved antibodies fighting against pathogens active = only one able to establish immunological memory naturally acquired = infection = contact w pathogen artificially acquired = vaccine = dead/weakened pathogens passive naturally acquired = from mother to fetus via placenta or to child through milk artificially acquired injection of exogenous antibodies

Question 56

cell mediated immune response (T cells)

Answer 56

activated T cells kill body cells that are infected/abnormal or cancerous or foreign various types of T cells CD8 = cytotoxic T cells = killer T cells = attack and kill using perforin = CD4 - helper T cells = stimulate proliferation and activity of other lymphocyte sub populations (including plasma cells) regulatory T cells = stop immune response, small subset of CD4

Question 57

difference in binding requirement bn diff types of T cells and how they go about forming a response

Answer 57

CD8 cell link w MHC I molecules, found on all cells recognize antigens presented her CD8 binds to a region of the MHC I, so T cell receipt recognizes the presented antigen, if activated, will kill the cell itself CD4 have to link with MHC II molecules found on antigen presenting cells (APCs) like dendritic cells, macrophages etc. CD4 binds to a region of the MHC II so T cell receptor can recognize the presented antigen once activated, they activate B cells, CD8 T cells to enhance immune defense class II MHC = I am not infected, only showing what I found"

Question 58

macrophages

Answer 58

formed from monocytes in bone marrow 1. engulf foreign substances, present fragments of antigen on their own surface so can be recognized by T cells (antigen presenters) 2. secrete soluble proteins that activate T cells = secrete factors that activate macrophages

Question 59

effectiveness of immune system to fight disease depends on

Answer 59

ability to recognize foreign antigens by binding to them ability to communicate with one another so whole organism continues a specific immune response to antigens

Question 60

clone formation / clonal selection of T cells

Answer 60

dendritic cell engulfs pathogen, displays its fragment on class II MHC proteins CD4 T cells recognize antigen-MHC complex T cell receptor and CD4 bind to the complex 2nd signal from the antigen presenting cell is needed = co-stimulatory molecule binds to receptor w both signals = T cell is active cloning formation /proliferation differentiate into memory cells and effector cells

Question 61

helper T cells mobilizing both humeral and cellular immunity

Answer 61

humeral immunity = helps activate B cells B cells encounter antigen, displays is on surface helper T cells bind w antigen containing MHC II w antigen helper T cells release co stimulatory signals ot complete B cell activation cellular immunity = help activate CD8 cells helper t cells binds dendritic cell helper T cells stimulate cell to express co- stimulatory molecules dendritic cells now activate CD8 cells w help of the thing secreted by helper T cells