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Human Body > Physiology (Immunology 1) > Flashcards

Physiology (Immunology 1) Flashcards

1
Q

History of Innate Immunity

A

Innate immunity is highly conserved
- Compared to the adaptive which is only in vertabrates
- Drosphilla = have innnate immunity
- Startfish = have macrophages
- Frogs + Zebra fish = models of immune system (have a similar immune system to humans but it is more simple)

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2
Q

Challenge for innate immunity

A

Innate immunity has to recognize many classes of organisms of wide variety that can cause problems
- Recognizes things of varying sizes (Small - Virsus -> Bacteria –> Protoza –> Fungi –> Parisites)
- Have four main chatagories = viruses + bacteria + protozoa + fungi AND each catagory has many different specieis
- All different in shape and size
- Have extracellular and intracelular things + different species have different replcation stradegies + RNA vs. DNA

Example -
Small - Have to recognize viruses that hijak cell machinery
Large - Have to recognize larger exrtacellular bacteria + have to recognize fungi that cause cause tissue daamge

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3
Q

Goal of the innate immune system

A

Overall: To swiftly and effeciently idetfy potential health threats

  1. Slow and halt the invasion of the threat
  2. Alter he adaptive immune system
  3. Minimize damage to the organism (Damage control)
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4
Q

Is the innate immune system effective?

A

RESULT of innate - because the innate immune system is so effective –> the majority of potential threats are no threat at all
- We are exposed to things all of the time but most threats don’t reasult in anything because immune system is good at controling them

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5
Q

Innate Vs. Adaptive immune

A

Innate - INflimation + complement activation + phagocytosis + destruction of the pathogen
- Tyical time after infection to start a response = minautes
- Duration of the response = Says

Adaptive = Specilized actors
- Typical time to initiate = hours - days - weeks

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6
Q

Main Pillars of Innate immunity

A
  1. Avoidance
  2. Resistence
  3. Tolerance
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7
Q

Innate immunity (Avoidence)

A

Avoid things using chemical and physical barriers - avoid the ability of the pathogen to get in and establish infections (prevent infection)

Uses:
1. Epithelial barriers (EX. Skin, intesitines etc.)
2. Mucus (Ex. oral mucosa)
3. Enzymes
4. pH (Ex. change in pH organism can’t handle)
5. Commernsal microflora

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8
Q

Innate immunity (Resistnce)

A

Innate immune tries to resist infection - Profesional profilers

Uses:
1. Humoral components
2. Cellular components

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9
Q

Innate immunity (Tolerance)

A

Prevention of damage (tolerance of the tissue to be damaged to a certain extent and still be able to heal)
- IF you get an infection = you tolerize the area to make sure the area is not too sensitive

Ex. Liver is very tolerant to damage - sees many microoranisms but it can still heal and recover

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10
Q

Cellular components of the adaptive immune system

A
  1. Macrophages
  2. Dendritic cells
  3. Nuetrophils
  4. Eosenophils
  5. Basophils
  6. Mast cells
  7. NK cells
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11
Q

Macrophages

A

Overall: Phagocytosies and activation of bactericidal mechanisms + antigen presentation
- Eating machine (eat everything it comes into contact with that shows signs of being forign)
- Engulf and kill pathogens = first line of defense (primary source of blockade of infection because the are in tissues and most infections occur in tissues)
- Destroy pathogens with oxidative reagents
- Put out chemokines and cytokines to tell other cels = prevents other cells from getting infected AND draws in cells to help
- Once infection happens - they complete tissue repair post infection (Ex. when wound gets red –> heals –> because macorphages healed it) ; can heal well or can cause fibrosis = not healing properyly = get organ dysfunction

Location - resident in most tissues ; found in every tissue in body

Arise during emrogensis + get new ones through monocyte differentiation

Long lived cells (Ex. Microglia)

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12
Q

Monocytes vs. macrophages

A

Monocytes + macrophaes BOTH phagocytose but most infectsion occur in tissues where macrophages already are = macrophages is the #1 phagocytic cell

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13
Q

Dedritic cells

A

Overall - Antigen uptake in peripheral sites + Antigen presentation
- 2nd class of phagocytic cells
- Mostly do mucoperocytosis = drinking around the are a
- Have long dedirtic extenstions
- Complete survelince in tissue (at the first line of defense) - survery for infection –> leave first line of defense and report infection to specilize cells in lymph nodes (leave the tissue after infection)

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14
Q

Dendrites vs. Macrophage

A

Macrophages = take things up to kill them

Dendirtic = take up things to tell suroundings to help + to present things to the lymphoid organs

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15
Q

Granulocytes

A

Nuertophils (majority) + Eossenphis + Basophiles

Work horses of immunity

In H and E stain = have very big granuales

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16
Q

Nuertophils

A

Overall - Phagocytosis (destroy pathogen) and activation of bactericidal mechanisms
- Important in initial response
- Catches pathogens around them and destorys them
- Produce cytokines and kemokines to pull in more cells
- Not present in tissue prior to infection (makes them different from macrophages)
- Kill selves — spill out insides – surrounds area = kills everything around it
- 24 hour life cycle - Leave bone marrow at night –> die at the end of the day

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17
Q

Eosenophils

A

Overall - Killing of antibody coated parisites
- Also affects allergy repsonse

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18
Q

Basophils

A

Overall - Promotion of allergic repsonses and augmentaion of anti-parasiic immunity

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19
Q

Mast cells

A

Overall - Release of granials contaiing histamine and active agents
- Affects allergies
- Engaged with IgE –> in response release histamine

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20
Q

NK cells (natural killer cell)

A

Overall - Release of lytic granuals that kill some virus infected cells
- Bridge between the innate and adaptive immune system
- Has more specificity than other innate cells but not as much specificty as adapative cells (looks like adaptive cell but functions like innate cell because has broad affects)
- Looks for cells that are not showing self (no MHC I prsenting healthy peptide) = kills them
- Released granzymeB to kill pathogens
- Kill tumor cells

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21
Q

Circulating innate immunity

A
  1. Nuertrophis
  2. Basophils
  3. Eosenphils
  4. Mast Cells
  5. Monocytes (because become macorphages)
  6. NK cells
  7. Platlets - express receptors on surface + bind AB + bind to monocytes and facilitate monocyte entry to the brain
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22
Q

Tissue/Cavity innate immunity

A
  1. Macrophages
  2. Dendritice cells (found in lymphid tissue + in gut)
  3. Innate-like lymphocytes - cells that look like lymphocytes (adaptive) but have innate function becayse they are not very specific
    Includes:
    • ILCs (in gut)
    • NK T Cells - Mix of NK cell and T cell (have TCR but not variant + kill like NK cells)
      -Gamma delta T cells (skin defense) - very invarinat responses = only respond certain way = innate like
    • B-1 B Cells (mouth + cavity Defense/tooth decay)
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23
Q

Antigen presenting cell

A

Macrophages + Dendrtites - both antigen presenting cells
- Link adaptive and innate immune systems (transition from innate to adaptive response)
- Present antigens to B and T cells t get adaotive response –> B cells will induces AB and T cells will have specific responses

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24
Q

How does the immune system identify potential threats?

A

The immune system recognizes many things through Patterns Recognition Receptors (PRRs)

25
Q

Partern Recognition Receotors

A

Overall - allow the innate system to repsond within hours

  1. Optimize speed and efficiencey
    • invarint in the genome = don’t need recombination to be made/functional = can be made faster
    • consituntly expressed (always expressed in most immune cells - don’t need activation signal)
    • Inherited through passage of gene
    • Trigger imediatley to responses when see repsonse 9might ned mutiple reposne becaue dont want innate triggering to everything
  2. Accutley idetofy threates
    • Recognize sturctural patterns common/conserved on pathogens = recognize PAMPs (pathigen associated molecular patterns)
26
Q

Pathigen Assocated Molecular patterns (PAMPs)

A

Bacteria - Lipteichoic acid (LTA) + Peptodoglycan (PGN) + Lipoporteins + DNA + Flagellin + Lipopolysaccridies (LPS)
- Tend to be bacteria cell walls (Ex. LSP)

Virus - Coat protein or nucelic acid that is expressed in virus

Parasite - GPI anchor

Yeast - Zymosan (beta-glucan) –> cell wall of yeast

ALL building blocks of pathigens that can’t go away (invariant they can’t change) = innate immune system co-evoloved to recignize them
- very senstive - small amount of PAMPs causes cell to react

27
Q

Pathogens avoiding Innate system

A

Some pathogens can get around innate system’s ability to recognize PAMPs

Example - viruses have envelope or bacteria hide in cell
- Example - Salmonella hides inside vacuale inside macrophages and then leaks out of the cell

28
Q

Types of PRRs

A
  1. Humoral
  2. Ceullular
29
Q

Humoral PRRs

A

Includes:
1. Ciruclating (in blood) - causes a bacteria = bacteria die bevause they losse the Na+ gradient
- Includes - C1 complex of compliments (main circulating) + Monnose Binding lectin (MBL) + C reactive protein
2. Surfactant proteins A and D (in lung) - causes a pore in envelope = bacteria die bevause can’t replicate
- Degrade bacetria that it comes into contact with
- Like enzymes in the lungs

Made in the liver

30
Q

C1 complex

A

First compoenent of compliment- binds to AB that are biund to a bacteria/virus –> triggers pathway of complememt

End of pathway - cause pores in cell wall of bacteria or infected cell = causes cell death

MBL = also intiates complement but it doesn’t bind to AB - binds to mannose on bacteria cell wall =intiates compliment

C reactive = signal that there is something going - also binds to bacteria and intitaes compliemnt cascade)

31
Q

Ceullular PRRs

A

Includes:
1. Extraceullar memebrane bound - found on cell surface -> primari;y respond to bacteria and parisites because outside the cell
- Have phagocytic receotors (Macrophage mannose receptor + Scavanger receperts) - invraints receotors that binds to parts f bacteria/viruses –> pulls Pathogen in to be phagocytosed
- Have signaling receptors (Toll like Receptors (TLR) 1, 2, 4, 5, 6) - found on DCs + NK cells + Macrophages - reacts to

  1. Intracellular
    • Have membrane bound (TLRs 3, 7, 8, 9) - found on endosomal vesicles + mostly resond to virsues
    • Have cytosolic (NOD1/2 and Inflamasomes) - NODA1/2 recgnize RNA and DNA inflamasomes react to viruses or general negative climate/off balance of homeostasis
32
Q

Scavenger receptors

A

Recognize MCL or C reactive pritein or C1 complex of compliments bound to cells

33
Q

TLRs

A

TLRs = react to specific PAMPs
- Bind to many ligands BUT the ones listed are primary ligands

TLRs = extra or intracellular in endocytes vesicles or in cytolsol –> virsues get into cytosol or has envelope –> TLR recognizes RNA/DNA
- Intraceullar = recgonise virsues –> viruses is negative
- TLRs recignize years + bacteria + fungu + virsues
best known TLRs:
1 and 2 form heterodimer - on surface - bind to proteins found on yeast + bacteria

2 and 6 form heterodimer on surface - bind to proteins found on yeast + bacteria

4 + CD14 + MD2 = recongnizes LPS (gram neg) or lipotratic acid (gram pos)

5 = Recognize flagelin

3 = recognize dsDNA

7 = recognize ssRNA

8 = recginizes G-Rich oligionucleotides

9 = Unmethylated DNA

Look a red boxes in picture

34
Q

Downstream of TLRs

A

Multiple pathways depedning on whcih TLR is signal = get multiple responses depending on TLR signals

Have TLR 4 –> LPS binds –> Get MYD88 cascade –> Get NF kapp B Dimers –> make pro-inflmatory cytokines

OR

Have TLR 4 –> LPS binds –> get TRIF cascade –> Get interferon production

OR

TLR 7 –> reacts to vriuses –> different STAT pathway –> Get NF Kappa B –> get cytokines

When TLR is engaged it turns on transcription to get cytokines (Ex. inteferons or NF Kappa B)
- Downstream response of inflimation - always result in pro-inflamatory cytokines

35
Q

What happens when a PAMP binds to a PRR

A
  1. Destruction of PAMP’s source (destroy invading pathogen)
  2. Recruitment of other cells
  3. Priming of PRR bearing cell

ALL occuring simultanously

36
Q

Destruction of PAMP’s source

A

Occurs through:
1. Phagocytosis
2. Cytotoxin Killing
3. Secreation Tyoe I IFNs: IFN alpaha + IF beta
4. Inducing “climate change”

37
Q

Destruction of PAMP’s source (Phagocytosis)

A

Opsonization vs. Direct cell-cell
- Opsonization - bind bacteria with AB –> macrophages phagocytose
- Direct cell-cell – macrophages to bacteria –> phagocytose bacteria –> destory with enzymes in lysosome (destroy in phagolysasome)

Done by Nuertrophils and macrophages
- Macrophage have phagocutic receptors that bind microbes (mannose receptor + complement receteptor + lipid receptor + Dectin 1 + Scavanger receptor)
- Nuertophils –> phagoctose bacetria into phagosome –> instead of using lysosome it will make hagosome intercat with granuales that it uses to kill extracellular bacteria

Uses Irreversible oxidative destuction
- Example - Bacteria binds to compleent receptor –> Phagoytose –> merge phagosome will lysosome –> forms phagolysosome –> low pH –> have oxidation destructive pathway = destroy pathogen

38
Q

Destruction of PAMP’s source (cytotoxic killing)

A

Cytotoxix killig = direct killing of infected cells or bacteria

Done through complement membrane attack complex - series of C proetins that go down a chain of domains –> go down activate copplement cascade –> get formation of a pore = pathogen dies because all of the Na leaves the pathogen + all pressure is lost + things spill out of cell (cell can do apoptosis or necrosis)

NK cells can do this - recognize when cell is not presenting self –> kills cells by releasing perforin and granzyme –> kills cell
- Perforin acts on target cell membrane
- Granzyme and granyulin –> leads to apoptosis
- Not 100% specific = can harm bystanding cells it is next to

39
Q

Receptors on NK cells

A

NK cells have positive and negative receptors –> if have many positive receptors to kill then NK cell in engage –> Kill pathigen
- If positive receotors engage more than negative = get hole in memebrane –> pathogen dies because loses Na gradient

40
Q

Destruction of PAMP’s source (Secretion of Type 1 IFNs)

A

Infected cells sees virus in cell –> signals IFN beta —> INF beta signals to surrounding cells –> Bind IFN receptor to surrounding cells –> tells cells to turn on PKR Kinase + Mx + restiction factor + IFN beta/IGN alpha –> continues cascade down = increase host defense
- Inhibits viral replication + silos replication (IF viruses can’t get into cells to replicate = virus dies)
- IFN goal = prevent further viral replication + protect surrounding cells
- bystander cells become resistnt to viral infection because upregulate kinases + Mx genes + rescitictiono factors = will traget viruses when enter cells = inhibits furtehr viral replication in bystander cells

IFN alpha + INF Beta = potent cytokines

41
Q

Destruction of PAMP’s source (Inducing Climate change)

A

Induce fever –> get global climate change to prevent further infection

Macorpages (induce fever) –> IL1beta, IL6, TNFalpahe –> Liver makes acute phase protein synthesis when mannose binds to complement + hypothalumus increases temperture + fat and mulscile cells enter catabolic state

42
Q

IL1beta, + IL6 + TNFalpaha

A

Act on Liver - Make actute phase protens (R-recative proteins, MBL) –> get activatation of complement opsonization

Act on bone marrow –> Get Nuetrophil mobilization (get immeidate release of nuertophils) –> Nuertophils phagocytose pathogen

Act on hypothalumus –> increases body tempertature
- Prevents replication of bacteria/virus (don’t replicate well at high body temps)
- Increases antigen process
- Increases specific immune repsonse

Acts on Fat/muscles - Break down fast/muscle for protein and anergy (allow increased body temp)

Acts on Dedritic cells – TNF alpha stimulates DCs ro leave infection and migrate to lymoh nodes and maturation –> get adpative immune repsonse

43
Q

Recruitment of other cells when PAMPs bind to PRR

A
  1. Vasoactive peptides and cytokines
  2. Activating cytokines and kemokines
  3. End result: Rolling and Diapedesis
44
Q

Recruitment of other cells when PAMPs bind to PRR (Vasoactive peptides and cytokines)

A

Mast cells + monocytes + platlets
- When increase Vasoactive peptides and cytokines = Mast cels + monocytes + platelets respond to histmanine and sertaonoins and cytokine s= leave blood and go to area where infection occurs

Vasodilation - Histaine and seratonin
- Monocytes in the endothelium bind to seratonin and integrin = roll off (immune cells recognize cytokines and kemokienes and go out of blood)

TNF-Alpha –> Increase selectins and integrins (markers on vasculature or cells - increase expression alows cells to stick to vasuclature and leave the blood)

TNF-Alpha –> Increase vascular permability (makes tight juctions wider)

Have Nuetrophils and monocytes in the blood (Stay there unless have issue) – have vasoactive peptides and cytokines –> dilated the blood vessle = blood essel becomes leaky = the cell can leave the blood vessel near infection

45
Q

Recruitment of other cells when PAMPs bind to PRR (Activating Cytokines and Chemokines)

A

Cytokines and chemkins pulls specifc cells out of blood

Chemokines:
- Monocytes + macrophages + DCs –> CCL2 –> pull Monocytes to site of infection –> monocytes become macrophages
- Macorphages and endothelal cells –> XKCL8 (IL8) : pull nuertophils and T cells to site of infection
- Cells being pulled out of blood –> see increase recetport –> go in direction of cytokines = pulls cell to site of inflimation

Cytokins:
- Platlets –> RANTES –> Pulls Monocytes
- Macrophages –> produce IL-12 –> Pull NK cells
- Macrophages –> produce IL1B and IL6 –> Pulls lymphocytes
- RANTES + IL12 + IL1Beta and IL6 = drive respective cells to inflamation (drive cells down pathway that is needed)

46
Q

Intercellular vs. extra ceullarly chemokines

A

A and B = intercellular
C = extracellilar –> cytikines pull specilized cells to the site of infection

Epxression of cytokines determine if needs to be anti or pro ifnmatory response - based on how far down line inefction is going
- Lots of iFN gamma = infection is ongoing = signal T cells to respond ; More IL4 or Il5 = signals ingfection so it quiets infection

47
Q

Use of chemokines and cytokines

A

Need chemokines and cytokines to get the cells you want at site of infection

48
Q

Recruitment of other cells when PAMPs bind to PRR (End result)

A

End result of Vasoactive peptides and cytokines + Chemokines = to get cells to enter site of infection (Called “Rolling and Diapedesis”)

Overall: Get cells to slow down in blood vessle and follow cytokines to site of infcetion

Selectins - When have increase in selectins –> nuertophils see inrease –> slows down –> recignizes cytokine –> goes out of Blood vessel

Integrins

Diapedesis - cell binds and starts to move through the endothelium

Migration to site of infection

49
Q

Binding if damps to PRR - Prmining of PRR bearing cell

A

Overall - Cell with PRR needs to be primed - focus on presenting cells

  1. Upregukation of MHC II or MHC I
    2, Induction of Co-stimulatory molecules
  2. Migration to Lymph node
50
Q

Prmining of PRR bearing cell (Upresgulation of MHC II and I)

A

Priming increases MHC II or I - upregulation allows T cells when enter site of infection to know if cell is infected or not

MHC II - On APC –> macrophages and DCs
-MHC II - T cell recognizes and generates a receptor + helps B cells geneerate AB
- Present CD4 T cells what help is needed

MHC I - All cells except RBCs and nuerons
MHC I - T cells kills infected cell

MHCs = present peptides to adaptive immune = adaptive can specifically target infection

51
Q

Presentation of peptides to T cells

A

Phgocytic cells take pathigen –> show T cell the protein

Present the peptide o T cell in complex (T cells can’t kill every time it sees a papetide because there would be too much autoimmunity)
- MHC II/I AND inrtdouction of costimulatory molcules = activates T cell (can’t activate T cell with only 1 you need at least two but usually 3 signalls)
- Occurs in lymph nodes
- DCs go to the closest lymoh nodes

52
Q

Prmining of PRR bearing cell (Induction of Ci-stimulatory molecules)

A

CD80 and CD86 –> Get Signal 2

T cel comes to APC with MHCII but no co stim = T cell won’t do anything

Induction of Co-stimulatory = shows T cell it needs to respond

53
Q

T cells and DCs in lymph nodes

A

In lymphnodes there are T cells curculating –> DCs are preseting as mich as they can (lots of MHCII) –> naive T cell will pump into DC and recognize it –> T cell stops moving – T cell binds to antigen –> T cell differentiates

54
Q

Prmining of PRR bearing cell (Migration to Lumph nodes)

A

DCs otravel through afferent lymoh vessles to get to lymph node –> go to T cell zone (paracortex) and encounter naive T cell –> Activate naive T cell

Have increase in T cells after inflamatory resonse = response can happen faster

55
Q

Overarching goal of innate system

A

Hold infection at bay until the cells can get help

56
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Human Body (31 decks)

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