Inflammation Flashcards
(39 cards)
Give an example of an incomplete antigen and how it works
Poison ivy
It binds with skin —>becomes IA —> produces rash
Explain the general inflammatory response (up until WBCs release ILs)
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)
How does inflammation cause pain?
Swelling & bradykinins cause pain via nocioceptors
What do IL1 & TNFa trigger in the brain as a result of acute inflammation?
Migrate to brain —> act on hypothalamus—> produce PGE2 —> speeds up metabolism —> causes fever and hostile environment rawr
What do IL1 & TNFa trigger in the liver as a result of acute inflammation?
Triggers liver to produce acute phase reactant proteins (ex: CRP)
What do IL1 & TNFa trigger in the bone marrow as a result of acute inflammation?
Bonus: what other IL’s are needed for this?
Migrate to BM and with help of IL3 & IL5 they upregulate leukocytosis —> increase production of neutrophils etc
What are the 2 main cell types involved in the cellular inflammation response?
Macrophages & neutrophils
Describe how macrophages and neutrophils (in cellular inflammation response) create antigens from bacteria
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
What is the oxidative burst that neutrophils can do?
Neutrophils can create free radicals to destroy tough microbes & sacrifice them selves
(Kamikazes!!)
What are APCs?
Antigen Presenting Cells
-only cells w/ MHC2 in somatic circulation
APCs = macrophages!!
How do macrophages become APCs?
Gene on Chromosome 6 that can be recombined to make MHC2
Then Ag is presented on the MHC2
What genes are important for MHC2?
DP, DQ & DR genes
Hint for remembering MHC2 has 2 letter genes, MHC1 has 1 letter genes
What genes are important for MHC1?
A, B, & C genes
Hint for remembering MHC2 has 2 letter genes, MHC1 has 1 letter genes
What MHC is expressed on every cell in the body and what does it present?
MHC1! And presents self antigen
Draw a picture of the full inflammation pathway
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
What are the 3 parts of the classical pathway of complement inflammation?
- MAC
- Opsonization
- C3a & C5a signals
What is opsonization?
The enhancement of phagocytosis
Where is complement produced and how does it get to the site of inflammation?
Made in the liver
Get to inflammation site by same process as leukocytes
Alrighty, let’s try to explain the classical complement pathway
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
What happens after complement (MAC) has lysed a microbe?
MAC breaks off —> C3b exposed again* = huge signal to macrophages and neutrophils
- basically c3b being exposed again is an opsonin (signal to increase opsonization)
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?
C3b receptor
What is the alternate pathway of complement?
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
Describe the lectin pathway of innate immunity
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
Virus has infected a body cell, how do we kill it using IFNs & TLRs?
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
