Immuno Week 2 post lect. updates Flashcards
Why is important that MHC proteins are very general in what they bind?
It they were specific then we would have to produce way more MHC proteins to bind all potential antigens, instead we just leave it up to the T cells to figure it out
Which of the MHC molecules is more diverse?
- what is the main contributing factor to this diversity?
MHC class II is more diverse, this can be attributed mainly to the fact that they have BOTH alpha and beta genes that can combine in different ways
What does loss of CLIP/ invariable chain lead to?
Loss of ability to distinguish between intracellular and extracellular pathogens
Why are MHC proteins so important in organ rejection?
Largest degree of polymorphisms in genome means its unlikely to find people whose MHC profiles are identical
What between MHC I and II which is the most likely target for transplant rejection?
MHC I because its located throughout the body
What determines your BO and why are you attracted to people with BO that is different from yours?
MHC haplotype determines BO, and it is evolutionarily advantageous for us to mate with people who have haplotypes that are different than ours.
MHC I proteins exist on all cells but they are more strongly represented on APCs. Why is this so?
APCs must enter secondary tissue for a response to be mounted because the correct T cell is most likely located there.
Also APCs have B7 which is needed to activate niave T cells
What affect does lack of TAP1/2 have on MHC profile of cells?
No TAP1/2, then no proteins are loaded the MHC class I and they will be degraded
What would be bad about upregulating the amount of CTLA-4 on naive T cells?
CTLA-4 would reduce T naive cell activation. This is advantageous for things like cancers
T or F: you need less MHC class II binding to reach the threshold.
True
What is the most important interaction for getting naive cells into 2˚ lymph tissue?
L-selectin to GlyCam-1, this expression is lost on activated T cells which keeps them out of 2˚ lymph
What interaction lets neutrophils out of vascular endothelium into extravascular space?
PECAM-1:PECAM-1 (CD-31:CD-31) interaction
What is IL-8 also known as and what is its function?
AKA CXCL8, it binds neutrophils to slow them down
What will happen to your ability to form germinal centers if you have to B cells?
If you don’t have any B-cell, then you will be unable to form Germinal centers.
T or F: IL-22 and IL-17 are chemotractants secreted by T17 cells
False
IL-17 INDUCES endothelial cells to produce a neutrophil chemotractant
IL-22 INDUCES endothelial cells to produce and antibacterial peptide
Is Treg considered an effector cell?
- why or why not?
NO, it requires B7 co-stimulation
T or F: Tregs are found in the greatest proportions in the blood to prevent cytotoxic cells from reacting to host proteins
False, Treg are found in SECONDARY LYMPH. tissues
- They need to be located here to be in contact with macrophages and prevent proliferation of naive T cells that react to self antigen
T or F: when Treg down regulates, it must be recognizing the same antigen as the cell that it is suppressing
False, there are many antigen types that are presented on a macrophage so it is unlikely they will be bound to the same antigen. BUT if there’s a lot of Treg bound to a macrophage, it has probably ingested host material and most presented antigens will be self-antigens, so any effector cell that binds is probably one the snuck by during negative selection and its proliferation should be limited.
What are the 3 things the NK cells look for when going out to kill cells?
- Amount of MHC class I- if you lack MHC class I, you will be killed
- MIC - presence of MIC indicates stress and NK will kill that cell
- IgG1 and IgG3, NK cells see these and kill any cell with these bound (opsonization aka ADCC)
T or F: NK cells are good at clearing out intracellular bacterial infections
False
What is the link between TH1 responses and activation of NK cells?
TH1 response leads to the formation (via B cell activation) of opsonizing types of antibodies (IgG1 and IgG3), these are detected by NK cells which will then kill them
Even though TH1 is responsive to intracellular pathogens the NK cells really only get fired up during viral infections
What does GM-CSF do?
Simulates bone marrow to make more macrophages and neutrophils
T or F: BOTH IFN-gamma and CD-40 are needed for macrophage activation
True
Besides macrophage activation, what does CD40 act to do?
Both TH1 and TH2 need it to activate B cells
T or F: T cells are needed for granulomas to form
True
Why does CD8+ T cell response to an intracellular infection also trigger a TH1 response?
No matter what there will always be some cross presentation of antigens so some of the MHC class II that is for extracellular antigen will present some intracellular peptides leading to TH1 cells getting upregulated
What is the main function of TH2?
- what does it use to do this?
Drives B cells to make neutralizing antibodies (IgA, IgE, IgG2, and IgG4)
IL-4 stimulates IgE formation via class switching IL-5 stimulates IgA formation via class switching
T or F: IL-2 is required for B cell mediated response (humoral) and for cell mediated response.
True
