A/P Exam 2: Immune System (pmuch done)

What’s Lympth/Lymphatic fluid?

• When does it form?

• What’s another fluid Lymphatic fluid contains?

• What does Lympth fluid house?

• What do Lympth vessels begin as, and what is that composed of?

Lympth = Clear white liquid CT

• Lympth fluid forms when water and dissolved proteins drain from tissues

• Lympth fluid contains chyle fluid from intestines that contains proteins/fats

• Lympth fluid houses lots of WBC’s, esp lymphocytes

• Lympth vessels start as fenestrated capillaries made of 1 layer of endothlium attatched to a basement membrane

What are the walls of Lymph vessels similar to, and what do the vessels do?

Lympth vessels are similar to veins but thinner, and its vessels merge to form lymph trunks

Lympth system: Flow of Lympth

1. How is Lympth transported?

2. What do Larger lympth vessels contain?

3. Where do Right Lympth duct and left Lymph duct drain into? What are their pathways?

4. What is Cisterna Chyli?

1. Lympth transported through progessively bigger vessels —> lymph nodes —> vein

2. Larger lymph vessels contain 1-way valves and smooth muscle

3. R/L LD’s drain into subclavian duct. Right LD brings fluid only from right arm/right side of torso.  Left LD is longer, takes fluid from entire left side of body and all of lower body (like ¾ of the drainage). 

4. Cisterna chyli = well of lymph fluid in center of abd center that leads up and into thoracic duct.

The Right and Left lumbar lymph trunks enter _____, and bring fluid from the ____. Same with the ____ trunk.

R/L Lumbar lymph trunks enter Cisterna Chyli, brings fluid from legs. Same w intestinal trunk

What are Primary Lymphatic organs?

Places where most leukocytes are produced/mature

Redbone marrow

• What is it the starting point for?

• What stem cells does it have and what do they differntiate into?

• What cells mature here? (2)

1. RBM = starting point for all blood cells

2. RBM has hematopoietic stem cells —> either myeloid stem cells or lymphoid

3. Granulocytes + B-lymphocytes mature here

What’s site of Leukopoiesis?

What do some B-cells/T-cells perform, allowing them to not have to be produced via leukopoeiosis?

What can B-cells learn to do in lymph nodes?

1. LP begins in BM

2. Some B/T-cells perform mitosis, so not all lymphocytes produced via LP

3. B-cells can learn what ABD to make in Lymph nodes or other location rather than BM

What are the 2 Primary Lymphatic organs?

1. RBM

2. Thymus

A flat, bi-lobed organ located in superior mediastinum above heart

Thymus

Site of maturation for most T-cells, and enlarges as child, inactive puberty, atrophies in 20’s

Thymus

Lobes connected by areolar CT, and each lobe (right and left) has a medullary and cortical region

Thymus

What type of BV are lymph vessels similar to?

Which Lymph duct sevices most of body?

What are 2 primary lymph organs?

1. Veins

2. Left Lymph duct

3. Thymus + RBM

What’s Lymph nodes considered in terms of primary/secondary

secondary lymph tissue/organ

What are lymph nodes?

(what are they surrounded by)

Structure made of Lymph/non-lymph cells surrounded by lymph capillary network

Lymph nodes are found ____ the body, housing numerous lymphocytes

throughout

What’s function of Lymph node?

What supplies, and drains lymph nodes?

What does the outer cortex, inner cortex, and medulla of the lymph node contain?

Where do B-cells perform mitosis to make more B-cells?

What’s name of space that allows enterance of BV into lymph node or exit via efferent vessels?

lymph nodes filter lymph,

afferent vessels supply lymph node, and efferent vessels drain it.

B + t-cells

B-cells perform mitosis in germinal centers in nodules/follciles in outer cortex of lymph node

Hilum

What’s function of spleen? (4)

1. Filter blood and remove old/defective RBC’s/Platelets

2. Store RBC’s

3. Recycle iron 

Where’s Spleen located?

Next to stomach between 9th/11th rib on left side of body

What’s the function of Red pulp found in the Spleen?

(Red pulp ____ ___ ____, ____, and ___/___ ____.)

What is red pulp made of? (4)

What is white pulp made of? (2)

Red pulp filters out AG’s, microbes, and defective/old RBCs. Made of MP, RBC’s, platelets, granulocytes, etc.

White pulp = lymphocytes + macrocytes.

What are Lymphatic nodules?

(___ of lymphocytes w.o a ___ ____)

Where are they located in general?

(areas with ____ ____ of ____ ____)

Where are the majority found?

1. Lymph nodules = clusters of lymphocytes w.o surrounding capsule

2. Lymph nodules are located in areas with highest risk of pathogen exposure

3. Lyph nodules are mostly found in resp. + digestive tracts.

What are tonsils considered in terms of Lymph?

Lymph nodules

Lymph nodules: Tonsils

1. Where are they found?

2. What are they important in developing immunity to? (___ pathogens)

3. What does swollen tonsils indicate? 

4. What’s the outer layer invaginate to form? What do these contain? What do they encourage?

1. Tonsils are found on inner surface of Pharynx

2. Tonsils are important in developing immunity to oral pathogens

3. Swollen tonsils = active IR to infection

4. Outer layer of tonsil invaginates to form crypts which accumulate debris from eating or breathing, which then encourages pathogens to penetrate into tissues where they can be destroyed by leukocytes. Basically catches pathogens as you eat/breathe to prevent from reaching digestive system.

In terms of Lymph, what is Mucosa-Associated Lymphoid tissue (MALT) considered?

Lymph nodule

Mucosa-associated lymph tissue (MALT)

1. What’s its shape, and where is it generally found? What are 3 examples of locations its found?

2. Where are Peyer’s patches specific to and what do they defend against?

3. What do Peyers patches contain? What do they transport?

1. MALT = dome shaped lymph tissue in mucous membranes like tits, lungs, and eyes

2. Peyer’s patch in SI and protect vs foodborne pathogens

3. Peyers patches have cells called Microfold/M cells, which sample material in intestinal lumen —> transport to follicles/nodules so lymphocytes can see

Peyers patch are considered…

MALT, form of lymph nodule

What form of lymph tissue does appendix fall under?

lymph nodules

What does the Appendix contain?

What is the Appendix a resevoir for?

What’s Appendix relationship with C.dif, for example?

What systems is Appendix active in?

1. Appendix has lymph tissue that holds T-cells + B-cells mediated IR

2. Appendix is resevoir for good bact that outcompete pathogens

3. C.dif common in env but only infects people whose natural gut biome has been killed off by AB’s

4. Appendix active in digestion/immune system

What’s Appendicitis?

What are symptoms? When is it deadly?

What’s treatment for appendicitis, what do astronots have to do before going to space?

1. Overproduction of bact causes IF of appendix and pus due to appendix getting blocked by poop, foreign body, cancer

2. Severe pain in LRQ, deadly in appendix bursts and floods AP cavity with bacteria

3. Appendicitis treated via surgical removal, astronots must have their appendix removed as safety measure.

Where are most Lymph nodules found?

Respiratory and Digestive tracts

Why is the appendix considered lymph tissue?

Contains T/B cells and is a resevoir for good bact.

What’s an Antigen?

What does the Immune system recognize?

What are most AG’s made of? (2 most common)? Can all molecules act as AG’s?

What are common AG’s? (5)

1. AG = anything to trigger an IR

2. Immune system recognizes epitopes, a region on AG that ABD’s or T-cell receptors can attatch to

3. Proteins most potent, and then sugars. All molecules can act as AG but protein/sugars more potent.

4. Common AG’s = bacteria /viral components, pollen, food, drugs, animal dander

What do B-lymphocytes kill?

Where do T-lymphocytes begin development, and finish maturation? What do they kill? What do they release and what does this cause, and what type of feedback loop is this?

How are B and T-cells classified?

Cytotoxic T-cells express ____ on their surface

1. B-cells kill pathogens, develop and mature in BM

2. T-cells kill infected self cells (cancerous, infected via covid etc), begin in BM finish in thymus, release Interleukin-2 (IL2) which causes growth of B/T cells. Form of positive feedback loop for fighting off pathogens and recruiting B/T-cells

3. B and T cells are classed by proteins on surface called Cluster of Differntiation markers (CD markers)

4. Cytotoxic T cells have CD8 on surface.

What is the exception to T-cells killing infected cells? What part of immunity is this?

NK-T cells, which can kill pathogens and are part of innate immunity

Majority B/T cells are part of this immunity

Adaptive

Cytotoxic T-cells

1. What cells do they destroy (2)

2. What do they release? (3)

1. CT-T cells kill tumor cells + virus infected cells

2. CT-T cells release enzymes called perforins that poke holes in inf. cell, and then from there can release Granzymes (causes apoptosis) or Granulysin (disrupts ion balance and damages mitochondria)

What’s function of Memory-T cells?

Memorize past AG exposure even after pathogen with that AG has left body

What’s function of Regulatory T-cells? (2)

1. Prevent ____ of T-cells through ____ to ____ _____ attack

2. Stop ____ ____ ____ at end of ____ window.

1. Prevent overactivity of T-cells through repression to prevent autoimmune attack

2. Stop T-cell mediated IR at end of response window.

Lymphocytes: T cells and the T cell receptor

1. Where are T-cell receptors embedded

2. What are T-lymphocytes on the lookout for, and on what cells? (2)

3. What happens if the T-cell finds what its looking for?

4. What does the variable region of the T-cell receptor do?

5. What is each T-cell specific to?

6. What’s the most common T-cell receptor?

7. T-cell receptors have a similar job to _____.

1. T-cell receptors are on T-cell membrane

2. T-cells on lookout for non-self AG’s on infected or cancer cells

3. If AG’s present, receptor matches it and attatches

4. Varible region determines what AG’s T-cell will see as threat/other

5. T-cells are specific in type of AG’s they interact with

6. Alpha-Beta T-cell receptor

7. Antibodies

Memory B cells carry the memory of _____ ______ to an AG.

Memory B cells are made after ______ to AG by _____ ______.

Plasma B cells are ____-____, ____-_____, _____-_____ cells.

Plasma B cells arise after ______ __ Antigen

What do B-cells specifically attack?

Memory B cells carry memory of previous exposure to an AG

Memory B cells are made after exposure to AG by cytokine signaling

Plasma B cells are long-lived, non-proliferating, antibody producing cells

Plasma B-cells arise after exposure to antigen

B-cells attack virus/bact AG’s not normally found in body

What’s another term for a B-cell?

What is the variable region responsible for binding?

What is the constant region respondinble for binding and mediating?

(binds ____ or ______ and mediates _____ ____)

What is the Light chain of the B-cell’s 2 types?

What does the heavy chain of the B-cell tell us?

B- cell = immunoglobin

Variable region is AG binding specific to AG/Disease/Epitope its learned to ID

Constant region binds compliments or proteins and mediates cell response

Light chain = Kappa or lambda, 2 types that differ in size

Heavy chain = Defines isotype of ABD

If the body see’s an AG, it will make an automatic ABD for it right?

In general, how does VDJ recombination work for producing antibodies and receptors?

Where does VDJ recombination occur for T-cells, and B-cells?

Body can’t see an AG and just make a custom ABD or T-cell receptor as its lots of trial and error

VDJ-C, there’s V,D and J cells in genomes

• When making new ABD/T-cell receptor, body takes a part of V (v1, v2, etc) and repeats with D, and J, to make combo of AG receptor protein, and then can further add variability by add/removing final AG receptor protein product. All trial and error, constantly adjusting until something sticks to AG and works. Can take several days, all based on luck of random combos.

T-cells VDJ recombination occurs in the Thymus, and B-cells in BM

Major Histocompatability Complex (MHC)

1. There are ___ classes of MHC proteins and individuals ______ ____ _____ of each MHC _____ from each _____.

2. MHC proteins are ______ to each person and how cells recognize ____ __ _____.

1. 2 classes of MHC proteins and people inherit 1 copy of each MHC gene from each parent

2. MHC proteins unique to each person and how cell recognizes self vs other

Where is MHC1 found? Where is it not found? What does it allow them to do?

What does MHC1 dock with, and on what cells? What does this lead to?

MHC1 are on surface of all cells except RBCs, allows them to be AG presenting cells

MHC1 docks with CD8 protein on surface of Cytotoxic-T cells, and interaction with CD8 causes apoptosis

Where is MHC2 found? (3)

What does it dock with and on what cell? What does its interaction lead to growth of?

What are MHC-2 also called?

MHC-II found on macrophages, B-cells and dendritic cells

• MHC-II dock with CD4 protein on surface of T-helper cells —> Interaction causes clonal growth of T-helper cells. (positive selection)

MHC2 are professional AG presenting cells

Positive and Negative selection of B/T-cells

1. What is Positive selection?

2. What is negative slection?

3. What does CD stand for, and BCR?

What’s purpose of Positive/Negative selection?

Where does it occur for B cells? What about T-cells?

1. Positive selectioon = Making more of B/T-cell that make ABD/T-cell receptor specific to AG of bact

2. Negative selection: Removes cells that attack our own AG’s

3. CD = cluster of differentiation marker, BCR = B-cell receptor

4. Purpose is to keep certain receptors that we need, and get rid of others that take up space

5. Occurs in BM, and Thymus for T-cells

What are the possible outcomes of negative slection of lymphocytes? (4) (RAAI)

1. Receptor editing: Change lymhpcyte receptor so it can’t recgonize self AG’s

2. Anergy: inactivate lyphocyte so it can’t make IR

3. Apoprotis: Programmed cell death

4. Ignorance = Immune system doesn’t deactivate and cells continue to mature and make more of cells that attack self cells causing autoimmune disease

What do B-cells attack?

What do T-cells attack?

What is VDJ recombination?

• Pathogens

• Inf. self cells

• VDJ recombination - how body makes different combos of genes for aBD to attack initial exposure to pathogen

Physical barriers are part of ____ immunity

innate

What’s the feature of Epithilial tissues as a physical barrier?

tightly packed cells prevent pathogens getting in

What’s the purpose of Physical Barrier, Mucous membarane

• What’s it composed of?

• What does it create, and what does it serve as?

• What do mucous membranes contain?

• Mucous membrane part of innate immunity physical barriers is epithilial tissue

• Creates mucus as barrier to pathogens

• Mucous membranes have lyozymes, anti-pathogenic substances.

What’s the first line of defense against foreign threats?

skin

Physical barriers: The skin

• What is the waterproof portion, and what is resistant to?

• What’s function of its glands? (2)

• Skin has epithelial  epidermis thats waterproof and chem resistant to bact enzymes

• Skin has glands that block microogranism growth and mantain pH of 3-5

What’s innate immunity?

Features of immune system we’re all born with that are largely the same for most people

Fever, Inflammation, and physical barriers like stomach acid, sebum, and saliva are parts of what immunity?

Innate immunity

Cytokines affect both the ____ and _____ immune system

Innate and adaptive for cytokines

Cytokines

• What are they? What cells specifically secrete them mostly? (2)

• What do they act as? (3)

• What is there effect based on?

• What does overproduction of cytokines lead to?

• T-cells destroy our own cells, why is this important to remmeber?

• What’s an example of a cytokine being released?

• What were majority of deaths in covid due to?

1. Cytokines = proteins secreted by immune cells for communication (mostly T-helper cells and macrophages)

2. Act autocrine (same cell) paracrine (local) and endocrine (distant) manner

3. Effect of cytokine is based on type of cytokine releaesd

4. Overproduction cytokines = cytokine storm, leads to sick/death

5. T-cells destroy our own cells, so we don’t want overstim’d cytokines

6. T-H cell sees pathogen, releases cytokine messenger to direct other cells to do things

7. majority of deaths in covid due to cytokine storm killing lungs during covid

What’s the most abundant leukeocyte?

What is the first responder to infection?

What does this cell release? (2)

1. Neutrophils

2. Neutrophils first to respond to infection and most abundant

3. Neutrophils release anti-microbial enzymes and NETS (neutrophil exterior traps)

Where are mast cells found?

What do they regulate? (2)

What symptoms are they responsible for?

1. Mast cells found in CT, not in blood.

2. Mast cells regulate VD + angiogenesis

3. Mast cells responsible for allergy symptoms

Basophils comprise ___% of leukeocytes

Basophils release histamine, what do these do?

Basophils = 1% leukeocytes

Basophils release histamine that cause allergic reaction and which removes allergens from site of infection

Eosinophils are ___% of leukeocytes

Eosinophils also release _____

Eosinophils are effective against….

1. Eosinophils = 6%

2. Eosinophils release histaine

3. Eosinophils effective against parasites

Innate Immunity: NK-T cells

• Most T-cells are involved in ____ immunity, NK-T cells take part in ____ immune responses

• NK-T cells can induce _____ in ____-____ cells and ____ cells.

• What do NK-T cells release, and what do they contain?

• What peptides can NK-T cells secrete?

• What do people with an impairment in NK cell development have a higher risk of developing?

• What can NK-T cells attack directly?

1. Most T-cells = adaptive immunity, NK-T are innate immunity

2. NK-T cells can induce apoptosis in pathogen-inf cells + cancer cells

3. NK-T cells release granules containing powerful proteases and perforin

4. NK-T cells can secrete a-defensins (antimicrobial peptide)

5. People with impairment in NK-T cell development = higher risk of blood cancer

6. NK-T cells attack pathogens directly, but usually its B-cells

Innate Immune Cell: Macrophages

• Describe the process of Macrophage phagocytosis (4)(also how does MP drawn to the. AG)

1. Macrophages drawn to area by chemotaxis —> Physical interaction between MP + threat and produce psuedopodia around it —> Psuedopodia fuse threat within vesicle to form phagosome —> phagosome is interalized and fuses with lysosome —> proteases and toxic chems in lysosome kill threat —> parts of threat are exposed on cell surface as AG presentation.

MP drawn by chemotaxis —> MP psuedopodia bind foriegn threat and form vesicle around it called phagosome —> MP eats phagosome which then fuses with lysosome containing protease and toxic chems —> threat broken down and remaining parts exposed on MP surface for AG presentation.

Proteins involved in INNATE IMMUNITY: The compliment system and activation of MAC

• Compliment = A family of over ____ proteiins

• Where are they produced and then released into? 

• What are portions of compliment system part of?

• What are most components of compliment system produced in?

• What are the 3 pathways, there cooresponding immune system, what they’re specific to, and where do they merge to produce what? What does this then lead to and activate?

(Describe classical pathway, lectin pathway, alternative pathway, where the pathways merge to activate)

1. Compliment system = family of over 30 proteins

2. Proteins ar eproduced in liver and released in blood

3. Portions of compliment system are in adaptive immunity

4. Most components of Compliment system are produced in inactive form

5. Classical pathway is in adaptive immunity and is triggered by adaptive cells identifies foreign antigens and is specific. Lectin pathway is in innate immunity and responds to mannose sugar on pathogens surface, its not specific. Alternative pathway is in innate pathway, and isn’t specific and C3 is randomly activated due to instability. All 3 seperate pathways merge to produce C3 Covertase —> leads to activating C5 Convertase —> then to MAC (Membrane Attack Complex)

Classical pathway (specific, adaptive immunity, triggered when A.I cells ID foreign AG)

Lectin Pathway (not specific, innate immunity, triggered when I.I cells ID mannose sugar on pathogen surface)

Alternative pathway (not specific, innate immunity, causes C3 to randomly activate due to instability)

CLA —> merge to activate C3 Covertase —> C5 convertase —> MAC

(Classical, Lectin, Alternative)

What does the MAC open on target cells?

• What does MAC primarily act on and why?

• What does MAC do once its embedded?

• What can other compliment proteins do to help?

MAC mostly targets microbes because MAC works best on non-nucleated cells without defense.

MAC when embedded causes cell to leak/destroy

Compliment proteins C3B + C4B precursors to MAC attack bacteria, attract MP, and trigger phagocytosis.

IF is a _____ _____ IR

IF is a stereotypic innate IR

What’s the primary role of Histamine release during IF?

What’s primary role of Prostaglandins during IF?

What’s primary role of Leukocytosis factors?

What’s primary role of compliment activators? (2)

Increase edema (swelling) and cause increased blood flow + VD for cleanup and repair of damaged area

Prostaglandins = pain signaling

Leukocytosis factors = + WBC production

Compliment activators = trigger compliment system and activate MAC

For inflammation, which factors/activators are considered antimicrobial factors?

1. Leukocytosis factors

2. Compliment activators

Fever is a common part of ____ IR

• How does higher temp in the body affect virus/bact?

• How does brain tolerate high temps, and what can it lead to?

Fever is a common part of Innate IR

• Higher temp in body speeds up healing and and cell factors that fight off pathogens + most bact/viruses evolved for normal body temp, not hot body temp

• Brain low tolerance to high temps, so can result it neurological damage.

Comparison of Innate and Adaptive immunity

• What are non-specific defenses?

• What are specific defense?

1. Non-specific defenses mean cell responds to many different foreign molecules like AG, protein, allergens. Innate immunity is non- specific.

2. Specific defences mean cell responds to specific AG’s, adaptive immunity is specific.

Adaptive Immunity: Active vs PAssive

1. Adaptive immunity is constantly _____.

2. Adaptive immunity involves multiple types of ___ cells and ____ cella, and interactions between ___ and _____.

3. What’s Active adaptive immunity?

4. What’s Passive adaptive immunity?

5. What’s natural adaptive immunity?

6. What’s artificial adaptive immunity?

What is examples of

Active natural 

Passive natural

Active artificial

Passive artificial

1. Adaptive immunity is constantly updating

2. Adaptive immunity involves multiple types of B cells, T cells and interactions between cells and proteins

3. Active adaptive immunity - Adaptive immune system is fully activated and there’s memory of the exposure

4. Passive adaptive immunity - Person gets cells developed in different person after that persons active response (there will be no memory of exposure)

5. Natural - non deliberate exposure, i.e get Antibodies from breast milk or pathogens from a cut

6. Artificial - deliberate exposure, i.e injections and med treatments

Adaptive immunity combos

• Active natural - i.e infection

• Passive natural - i.e antibodies in breast milk

• Active artificial - i.e vaccine

• Passive artificial - i.e antibody injections.

What does Antibody interaction with antigens trigger? (5)

(Functions of antibodies in adaptive immunity)

1. AG Neutralization - ABD interacts with AG to block binding site on AG, so the pathogen can’t bind to body cells

2. AG Agglutination - Clumping/sticking AG’s together so they can be easily recognized and eaten by macrophages

3. AG precipitation - AG’s fall out of bloodstream/ISF making them more easily recognized by Macrophages

4. Compliment activation - Through Fc region; leads to cell lysis and attraction of WBC’s

5. Lyphocyte recruitment and activation: B/T cells are alrted to presence of aninvader.

What’s the most common ABD and where is it found?

What does it protect against?

This immunoglobin can take time form post ____/____.

What is a ability unique to this Ig?

1. IgG, blood/body fluids

2. IgG protects against bact/viral infect. 

3. IgG takes time to form post infect/immunization

4. IgG can cross placental barrier

IgA

• Also a very _____ Ig

• Where is it found lining? (2) What fluids is it found in? (3)

• What does it protect and from what? (3)

1. IgA = common Ig

2. IgA found lining digestive/resp tracts, and in saliva, tears, titty milk (passed on to infant)

3. Protects gastrointestinal, resp, and genitourinary tracts from microorganisms

IgM

• Where is it found? (2)

• When fighting new infection, what’s unique about this Ig?

• Where is it displayed and why’s this unique?

1. Found in blood/lymph 

2. IgM = first Ig to be made when fighting new infect.

3. IgM displayed on surface of B-cells, other Ig get released into blood or are picked up by other WBC’s

IgE

1. Normally found in _____ _____ in blood

2. When can there be higher amounts of IgE in the blood?

3. What do IgE induce?

1. IgE normally in small amounts in blood

2. IgE can be in higher amounts if body overreacts to allergens or if fighting parasite infection

3. IgE causes mast cells to release histamine.

IgD

1. How well is it understood, and how much found in blood?

2. What does igD enhance? (2)

3. What is igD reactive against?

1. Least understood ABD w. small amounts in blood

2. igD enhances mucosal homeostasis and immune surveillance by arming granulocytes, basophils, and mast cells

3. igD is reactive against mucosal AG’s

IgD is least understood ABD w small #’s in blood, and is responsible for enhancing mucosal homeostasis and immune surveillance with granulocytes, basophils, and mast cells. IgD reacts to mucosal AG’s

How are AG’s presented on APC’s? (3)

Infected body cell, is infected by either a virus or bacteria → once protein is in cell, it gets picked up by MHC1 → MHC1 will put intself into a vesicle and move to the cellsurface and get embedded in the membrane to be displayed.

Virus/Bact inject protein to infect a cell —> protein picked up by MHC1 —> MHC1 fuses with vesicle and moves to membrane surface to display it —> infected cell is now an APC.

All cells can act as APC except

RBC’s

What are the steps of humoral(antibody)-mediated immunity and antibody production? (3)

1. APC (usually inactive  B-cell) finds invader, gets activated brings AG to a T helper celland if T-cell recognizes it uses cytokines to trigger ABD and memory B cell production to make ABD’s.

Primary vs Secondary ABD responses

1. What’s primary response, and secondary response?

2. What Ig does primary phase start with, and what Ig does secondary phase start with? What’s difference in ABD’s produced from 1st exposure vs 2nd?

3. What’s the big difference in the ABD response to the same antigen when memory cells are present? (aka, second time you’ve been exposed to the same AG)

1. Primary response: 1st time exposed to infection. Secondary response; 2nd time exposed to same infection.

2. Primary phase starts with IgM production to deal with infection (not alot), and secondary phase starts with IgG (lots)

3. Secondary phase has rapid ABD due to memory B-cells, no need for time for VDJ recombination.

Cell mediated immunity: activation of CT-T cells

Describe it

1. Inactive CT-T cell finds infected T-cell, activates and does cell division to create more active CT-T cells, and forms memory T-cells (inactive)

2. CT-T cells destroy the infected cell

• Know the outcome, activation of CT-T cells, inject the APC with foreign AG  will toxins killing cell that was an APC,a nd tells other immune cells to destroy that same AG (executing soldier with message, then telling other soldiers to kill what message said)

APC with MHC-I is seen by CT-T cell, injects the APC w.toxins to kill it, and tells other immune cells to destroy cells with that AG

Cell mediated immunity: activation of T-helper cells

• How does this occur?

(What cells are made through cell division, mitosis to create what, and recruitment of what 3 cells)

APC has MHC-II with AG, binds to a inactive helper T-cell on T-cell receptor to cause activation and cell division to create Active T-Helper cells, mitosis to create memory T-helper cells, and recruitment of NK-T cells, macrophages, and B-cells to sight of infection.

What enables a person’s immune system to launch a stronger attack against a pathogen it has already seen before?

Adaptive immune memory cells create a secondary response.

Organ transplant

• What’s Allograft?

• What’s Xenograft?

• Isograft?

• Autograft?

• What’s rejection? What occurs if there isn’t a 100% match and why? What type of drugs will patient need to take?

• What’s a Graft-Versus-Host disease?

1. Allograft = organ transplant between 2 nonrelated people

2. Xenograft - between 2 different species, i.e pig heart

3. Isograft = between ID twins

4. Autograft - From within same body (skin from tits onto ass)

5. Rejection - host body attacks new donated tissue or vice versa. Cells recognize ‘self’ cells based on MHC I and MHC II complexes on cell surface, if not 100% match, host immune system recognizes new organ as pathogen. Person will have to take immunosuppressive drugs for life to avoid rejection. 

6. Graft versus host disease - Donating blood or marrow results in attacking of host tissues as pathogen causing cytokine storm.

Resistance = Host attacks graft (donor) tissue

GVHD = Graft attacks host (person recieving) tissue

Hypersensitivities

• What are allergies? (what it is and 4 effects) (X interacts with X to cause X release)

• What is Anaphylaxis? (5 effects)

• What is food intolerance?

• What is asthma?

1. Allergies = Foreign AG’s interact with IgE causing excess histamine release —> redness, itching, sore, hives.

2. Anaphylaxis = Heightened allergic reaction with hypotension, throat/tongue swelling, rash, SOB, possible death.

3. Food intolerance = can’t digest certain foods, but no IR

4. Asthma = allergic reaction to env factors like cold, exercise, or air chems

Autoimmune diseases

1. Is the general cause known? What are some beliefs? (3)

2. What are treatments for Autoimmune diseases? (3)

3. For diabetes, what is the target tissue, reaction to, and symptoms? (2)

4. Put Celiac disease/IBS here!

1. General cause of Autoimmune diseases uknown, can be molecular mimicry, IR that bypasses T-helper cells, or T-regulatory cell deficency

2. Immunosuppressants, thymus removal, plasmapheresis

3. All over, reaction to pancreas, polyuria and insulin deficency

4. Celiac disease: Target tissue is SI, reaction to gluten, diahhrea, cramping, loss of appetite, failure to grow properly

The method of attack and severity of effects depends on the type of ____.

Bacteria

Intracellular bacteria go into ____ ____ and ____ within the ____ (may or may not kill the ___)

IC bact go into host cell and reproduce, may or may not kill host cell

Bacteria

Extracellular bacteria ____ ____ by attacking from ____. They can ___ ____ or ___ ____ in membrane.

EC bact kill host cell from outside. Can inject toxins or poke holes in membrane.

Some bact can kill cells by releasing ____ into blood.

toxins

Viruses

• Can they reproduce on their own?

• What genetic info do viruses have?

• What enzyme do viruses have and what does it trigger?

• What does virus borrow from the host cell and what does it make?

• What can some viruses do to the host cell?

• What do symptoms depend on?

• Viruses can’t reproduce on own need host cell.

• Viruses have DNA or DNA.

• Viruses like RNA polymerase-like enzyme to trigger transcription.

• Virus borrows nucleotides + ribosomes from host to make genetic material and proteins.

• Some viruses explode out of host cell to kill it, rather than performing exocytosis.

• Symptoms depend on type of body cell infected.

Retroviruses and AIDS (aquire immune deficency)

• Are Immunodeficency and Autoimmune disease the same?

• What can Retroviruses cause? (2)

• What’s a prominent cause of immune deficency? What’s main disease it causes, the type of virus it is, and what does it destroy?

• No. I.def is when immune system is underactive.

• Retroviruses can cause cancer or viral infection.

• HIV. causes AIDS, form of retrovirus that destroys T-helper cells/CD4 cells.

Retroviruses

• What is their genome like?

• What enzyme do Retroviruses have allowing them to make DNA?

• What enzyme allows Retroviruses to insert their DNA into host cell genome?

1. Retrovirus have single strand RNA genome

2. Retroviruses have reverse transcriptase to make DNA from RNA template

3. Retroviruses have integrase that inserts viral dna into host cell genome.

Fungi

• Fungi are _____ that enter body via breaks in. _____ or inhaled ____.

• Fungi can resist immune defenses by forming _____ (to help ____ from ___ ____) or altering their cell _____.

• Fungi can infect cells directly by ____ ____ or induced ______, which uses cells for _____.

• Fungi can cause damage by releasing _____ that damages ____ and weakens ____.

1. Fungi = eukaryotes entering body via skin breaks or inhaled spores

2. Fungi resist immune defenses by making biofilms (hides from immune system) or altering cell wall

3. Fungi can infect cells directly by forced entry or induced endocytosis, which uses cells for nutrients

4. Fungi can cause damage by releasing toxins that damages tissues and weakens IR.

Parasites

• mostly ____ organisms too ____ to enter cells, but some like prootoza and ameoba are _____.

• Parasites consume ___ ____ and ____ for nutrients

• Some parasites can ____ the hosts ____ ____ to avoid ____.

• Parasites can destroy cells, tissues and organs, cause _____, and rob body of essential _____.

1. Parasites = mostly MC organisms too large to enter cell, but some like protozoa and ameoba are unicell.

2. Parasites consume host cells and tissues for nutrients.

3. Some parasites can quiet host IR to avoid detection

4. Parasites can destroy cells, tissues, and organs, cause IF, and rob body of essential nutrients.

Med that inhibits growth of or destroys microorganisms and only works on bacteria

AB’s

Inhibits growth of and destroys microorganisms and is safe for external use on tissues like skin

Anti-septics

Inhibits growth or destroys microorganisms but isn’t safe for use on living tissues

Disinfectants

The ability of bacteria to survive treatment with antibiotics

AB-resistance

T or F, all AB’s AS and DI’s are 100% effective at killing bact.

F, 99.99% effective, if 1m bact, 99.99% killed, leaves 10k resistant bact.