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Sam's Immunology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Give an example of an incomplete antigen and how it works

A

Poison ivy

It binds with skin —>becomes IA —> produces rash

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2
Q

Explain the general inflammatory response (up until WBCs release ILs)

A

Bacteria damages cell —> mast cells migrate there —> toxin binds mast cell —> mast cell releases H,L,Ps (Arachadonic acid from cell damage lead to L & P release? Maybe they are metabolites of AA) —> bradykinins also in the general area —> bradykinins, H, L, & P cause P selectins* to be expressed on endosurface —> cells contract causing leaky channels —> edema
*P-selectins —> catch WBCs & monocytes as they roll along endothelium —> go through PCAMs —> triggers H,L,P to act like chemokines and attract WBC to infection —> release IL1 & TNFa & IL8

*B,H,L & Ps also act on SMC to vasodilate (increase blood flow, causing redness heat etc)

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3
Q

How does inflammation cause pain?

A

Swelling & bradykinins cause pain via nocioceptors

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4
Q

What do IL1 & TNFa trigger in the brain as a result of acute inflammation?

A

Migrate to brain —> act on hypothalamus—> produce PGE2 —> speeds up metabolism —> causes fever and hostile environment rawr

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5
Q

What do IL1 & TNFa trigger in the liver as a result of acute inflammation?

A

Triggers liver to produce acute phase reactant proteins (ex: CRP)

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6
Q

What do IL1 & TNFa trigger in the bone marrow as a result of acute inflammation?

Bonus: what other IL’s are needed for this?

A

Migrate to BM and with help of IL3 & IL5 they upregulate leukocytosis —> increase production of neutrophils etc

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7
Q

What are the 2 main cell types involved in the cellular inflammation response?

A

Macrophages & neutrophils

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8
Q

Describe how macrophages and neutrophils (in cellular inflammation response) create antigens from bacteria

A

Macrophages phagocytose bacteria —> microbe goes into phagosome —> combines with lysosome —> here they hydrolyze the microbe cell wall/structures —> only antigens remain

**later antigens exocytosed and used by APCs

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9
Q

What is the oxidative burst that neutrophils can do?

A

Neutrophils can create free radicals to destroy tough microbes & sacrifice them selves
(Kamikazes!!)

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10
Q

What are APCs?

A

Antigen Presenting Cells
-only cells w/ MHC2 in somatic circulation

APCs = macrophages!!

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11
Q

How do macrophages become APCs?

A

Gene on Chromosome 6 that can be recombined to make MHC2

Then Ag is presented on the MHC2

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12
Q

What genes are important for MHC2?

A

DP, DQ & DR genes

Hint for remembering MHC2 has 2 letter genes, MHC1 has 1 letter genes

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13
Q

What genes are important for MHC1?

A

A, B, & C genes

Hint for remembering MHC2 has 2 letter genes, MHC1 has 1 letter genes

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14
Q

What MHC is expressed on every cell in the body and what does it present?

A

MHC1! And presents self antigen

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15
Q

Draw a picture of the full inflammation pathway

A

Look at the picture we drew while I was quizzing you as reference

I’m typing these on my phone which means I can’t add pictures right now

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16
Q

What are the 3 parts of the classical pathway of complement inflammation?

A
  1. MAC
  2. Opsonization
  3. C3a & C5a signals
17
Q

What is opsonization?

A

The enhancement of phagocytosis

18
Q

Where is complement produced and how does it get to the site of inflammation?

A

Made in the liver

Get to inflammation site by same process as leukocytes

19
Q

Alrighty, let’s try to explain the classical complement pathway

A

Memory AB (IgG, IgM) attach to recognized Ag’s —> complement attaches to AB in a chain:

C1-c4-c2-c3 —> c3 convertase** splits C3 into c3a & c3b
—C3a breaks off & goes away with C5a to increase inflammatory response (via chemotaxis to attract WBCs)
—C3b allows C5b-C6-c7-c8-c9 to attach—> c5b thru c9 can become MAC —> inserts on the microbe membrane —> lyses microbe

**mast cells release proteases that cleave c3 & c5 into a&b parts. C3 convertase is one of these proteases

20
Q

What happens after complement (MAC) has lysed a microbe?

A

MAC breaks off —> C3b exposed again* = huge signal to macrophages and neutrophils

  • basically c3b being exposed again is an opsonin (signal to increase opsonization)
21
Q

Random fact that idk how else to ask or if it’s right given the shrugging stick man you drew by it:

What receptor do WBC use in the complement pathway?

A

C3b receptor

22
Q

What is the alternate pathway of complement?

A

C3b can attach to Ag directly —> c5b thru c9 can attach and form MAC again —> lyse microbe —> then once C3b free again signals opsonization like normal in classical pathway

23
Q

Describe the lectin pathway of innate immunity

A

Mannose binding lectin protein bINDS mannose Ag —> MBL is ID’d by C4 —> forms a chain with c4-c2-c3b-c5b thru c9 —> c5b thru c9 breaks off as MAC again
C3a & c5a released to increase inflammation response again
C3b is still an opsonin when not attached to other things

*so starts with MBL and binds c4, then otherwise the same as classical pathway

24
Q

Virus has infected a body cell, how do we kill it using IFNs & TLRs?

A

Viral DNA damages cell DNA —> body cell releases IRF —> IRF activates IFN alpha beta & gamma
IFNa & b secreted on nearby cells —> activates protein kinase R production —> PKR destroys incoming virus

25
Q

Virus has infected a macrophage, how do we kill it using IFNs & TLRs? How is this different than in just a somatic cell?

A

Macrophage releases IRF —> IRF triggers production of IFN alpha beta & gamma —> alerts nearby cells —> activates protein kinase R production —> PKR destroys incoming virus (ALL THIS IS SAME AS BODY CELL PROCESS)

Difference is IFNg signals nearby macrophages to proliferate & upregulate MHC1 & 2

IFN a & b also activate NK cells

26
Q

How can interferons be used to target certain diseases as treatment/control?

A

It can be used in drugs to specifically target herpes, hpv, MS

27
Q

What TLRs interact with each other (dimerize) instead of dimerizing with self?

A

TLRs 1, 2 & 6 can interact

28
Q

What do TLR 1 & 2 (together) respond to/recognize?

A

GPI anchoring proteins of parasites
And
Lipoproteins

Remember our hint that if TLR 2 is involved, that diner will always be able to respond/recognize 2 things

Rhyme: TLR 1 & 2, take a fat poo (with parasites in it)
———- fat = lipoproteins, poop is where u usually have parasites

29
Q

What do TLR 2 & 6 (together) respond to/recognize?

A

Zymosin (fungi)
And
Gram positive bacteria

Remember our hint that if TLR 2 is involved, that diner will always be able to respond/recognize 2 things

Hint??: Two 6 year olds go on a play date, they are really fun guys but then both tested positive for strep later that week (2 & 6, fungi, G + bacteria)

30
Q

Which TLRs dimerize with self?

A

3, 4, 5, 7, 8, 9 & 11

Wtf happened to 10? Nobody knows and we just don’t care 😂

31
Q

Which TLR identifies/responds to gram negative bacteria

A

TLR 4

32
Q

What does TLR 5 recognize/respond to?

A

Flagellin protein (usually on E. coli)

Hint/reminder: Fffffive and ffffflagellin and 5 letters in E. coli

33
Q

Which TLR responds/recognizes urogenital bacteria?

A

11!!

Remember 11 looks like your ureters/urinary system

34
Q

Which TLRs respond/act in the macrophage phagosome?

A

3, 7, 8 & 9

35
Q

What does TLR 3 respond to/recognize

A

DsRNA

In phagosome of Mac

36
Q

What TLR responds to/recognizes DNA in the phagosome (instead of RNA like all the rest)?

What type of DNA does it specifically respond to?

A

TLR 9!!

Specifically CPG DNA

Hint: TLR + CPG + DNA = 9 letters? Terrible I know

37
Q

What TLR responds to ssRNA?

A

TLR 7!

Hint: Ssssseven & ssssingle ssstranded rna

38
Q

Which 2 TLRs respond to dsRNA?

A

3 & 8

Hint: the numbers nearly look the same? Just missing some left sides of 3s loops

39
Q

What is the purpose of TLRs or what do they cause after recognizing their specific antigens/invaders?

A

They all cascade to activate genes that code for protein signaling, IFNg, TNF IL1b & IL18. (The last 3 things are all connected or in combination with each other?)

All these things increase inflammatory response

Sam's Immunology (5 decks)

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