Biology Unit 3 Questions Megathread

[HERculina]

Thanks Russ.

2 more questions

1) why do injected antibodies not trigger the immune response as they are foreign particles?
Is it because the body would then attack all antibodies?

Douchy said lone antigens can trigger t helper cells, is that wrong?

antibodies are more like 'self' i guess. If anitbodies were treated like antigens, then there would be nothing to kill the free antigens!
O, and antibodies aren't cells, so i guess they wouln't need the MHC markers? not sure :|

yea i dont think lone antigens can trigger helper T cells cause helper T cells can only bind to an antigen presented by a macrophage.

Oxygen isnt actually used in krebs cycle but its presence is required for the krebs cycle to occur!

yep, its needed for the oxidation of pyruvate to acetyl CoA that enters the cycle.

i thought it was solely needed for the ETC, to form water?
my teacher said that cytochrome = always the last electron acceptor in the ETC and then the rest in the ETC were different proteins. can anyone else confirm this?

And helper T cells, do they activate cytotoxic T cells, other helper T cells and B cells? When they activate cytotoxic T cells does it mean cytotoxic T cells start undergoign clonal expansion or does this only happen to Helper T cells. Or are they just activated to move to lymph nodes and meet with the infect cell and kill it.
also, are all T cells that come from the thymus gland, helper T cells?
Thanks

EDIT: are dendritic cells part of 2nd line of defence and are lymphokines a type of cytokine

[lexitu]

Oxygen isnt actually used in krebs cycle but its presence is required for the krebs cycle to occur!

yep, its needed for the oxidation of pyruvate to acetyl CoA that enters the cycle.

i thought it was solely needed for the ETC, to form water?
my teacher said that cytochrome = always the last electron acceptor in the ETC and then the rest in the ETC were different proteins. can anyone else confirm this?

And helper T cells, do they activate cytotoxic T cells, other helper T cells and B cells? When they activate cytotoxic T cells does it mean cytotoxic T cells start undergoign clonal expansion or does this only happen to Helper T cells. Or are they just activated to move to lymph nodes and meet with the infect cell and kill it.
also, are all T cells that come from the thymus gland, helper T cells?
Thanks

EDIT: are dendritic cells part of 2nd line of defence and are lymphokines a type of cytokine

The oxygen in the krebs cycle doesn't necessarily come from atmospheric oxygen, it comes from lysis of water molecules but that's way too, complicated you don't need to know that. Oxygen is ONLY an input in electron transport. The last electron acceptor is oxygen as far as I know... You don't need to know anything about the cytochrome complex other than that is a group of proteins that transfer H+ ions and electrons (and that you need to know this is unlikely)

Helper T cells activate everything, generally. The other cells need co-stimulation before they can proliferate. A VN pro can expand on this

Dendritic cells are definitely 2nd line. Lymphokines are cytokines but slow down there's NO WAY you need to know that!

[Russ]

RE: helper cells, they don't activate other helper cells, they lack MHCII. thymus produces several types of T cell, the only ones you need to know are CD4 and CD8 though

1) why do injected antibodies not trigger the immune response as they are foreign particles?

They're self molecules. Every Ab has two regions, the Fab for antigen binding and the Fc for host recognition. All human Ab have the same Fc regions, so you can transfer them. Mouse Ab are different, you'll eventually get an immune response if you try it.

2) do ige antibodies bind to allergens before or after binding to mast cells?

Potentially both, but predominantly after. The concentration of serum IgE is something like 10 million times less than IgG.

Edit: are single celled Protista engulfed by phagocytes?

Doubt it, they're pretty big, but i suppose degranulation could chip away at them.

Douchy said lone antigens can trigger t helper cells, is that wrong?

Why would it be wrong? Anything presented on MHCII will trigger a Th response, regardless of where it came from

What does Pr stand for ? (as in something red light, Pr and Pfr)(can someone explain the shade avoidance response?)

Polyrefringence at a guess?

[HERculina]

RE: helper cells, they don't activate other helper cells, they lack MHCII. thymus produces several types of T cell, the only ones you need to know are CD4 and CD8 though

Oh thanks lexitu and russ
ok, but i read  that the interleukin-2 released by Helper T cells activate other Helper T cells (tsfx bklets). what do they mean by this

[Russ]

Oh, my bad, I thought you meant by direct TCR/MHCII binding. Yeah they secrete all sorts of cytokines that are responsible for causing other Th cells to differentiate etc.

[WhoTookMyUsername]

RE: helper cells, they don't activate other helper cells, they lack MHCII. thymus produces several types of T cell, the only ones you need to know are CD4 and CD8 though

1) why do injected antibodies not trigger the immune response as they are foreign particles?

They're self molecules. Every Ab has two regions, the Fab for antigen binding and the Fc for host recognition. All human Ab have the same Fc regions, so you can transfer them. Mouse Ab are different, you'll eventually get an immune response if you try it.

2) do ige antibodies bind to allergens before or after binding to mast cells?

Potentially both, but predominantly after. The concentration of serum IgE is something like 10 million times less than IgG.

Edit: are single celled Protista engulfed by phagocytes?

Doubt it, they're pretty big, but i suppose degranulation could chip away at them.

Douchy said lone antigens can trigger t helper cells, is that wrong?

Why would it be wrong? Anything presented on MHCII will trigger a Th response, regardless of where it came from

What does Pr stand for ? (as in something red light, Pr and Pfr)(can someone explain the shade avoidance response?)

Polyrefringence at a guess?

Thanks russ, i thought i read somewhere that T  helper cells could only read antigens off macrophages?

Do horse antibodies (for snakevenom) trigger the immune response?

[lexitu]

Thanks russ, i thought i read somewhere that T  helper cells could only read antigens off macrophages?

No way, any antigen presenting cell can be read by a T cell, the importance of macrophages is often overstated.

[WhoTookMyUsername]

*eep edit sorry :S

1) i meant can T helper cells only read antigens of APCs :O  

Campbell's bio says - while B cell receptors recognize intact antigens, receptors on T cells recognize small fragments of antigens bound to normal cell - surface proteins called MHC molecues

(i think i meant off cells such as macrophages)


2)
Do horse antibodies (for snakevenom) trigger the immune response?


3) STAV '08 says
(in resposne to a question about growth by plants under shade)

"Chlorophyll absorbs red light for photosynthesis but not far red. the shaded plant will therefore be exposed to  more far red light than red light. this will have the effect of the active P_fr
being converted to the inactive P_r.
The result will be stem elongation as P_fr prevents stem elongation"

can someone please explain this and what the P means (sorry i didn't make it clear before Russ)

[lexitu]

Ah, okay, in that case, as I understand it, the antigen fragments must be displayed on the MHC II proteins of antigen-presenting cells which is what Russ said, I think.

[Russ]

1. Yes, the vast majority of antigens must be presented on MHCII in order to stimulate Th activation and production. Those that don't are irrelevant to VCE.

2. Yes, but it requires several exposures until the response is significant. The Ab Fc region is the immunogenic bit, but it's not particularly so.

3. lolplants

[Kaille]

what is a calcium influx in relation to synaptic transmission?

[HERculina]

influx of calcium ions causes the synaptic vesicles to migrate to the pre synaptic membrane and secrete neurotransmitter molecules into synaptic cleft.

i still dont fully get cell mediated immunity. is it:
APC releases a cytokine which attracts the helper T cell. Helper T cell then nids to the antigen fragment presented by the APC'S MHC 2 marker.
helper T cell is stimulated to release another cytokine which in turn activates B cells and also helper T cells to differentiate into clones including: cytotoxic T cells, more helper T cells, suppressor T cells, and memory T cells?
cytotoxic T cells kill infected cells. After they kill, what happens to Tc cells?
and is there anything else im missing

[WhoTookMyUsername]

Thanks russ




you understand it quite well it appears.
the cytotoxic T cells will naturally degrade and die just as other WBCs do.
cytotoxic T memory cells will remian though




STAV '08 says
(in resposne to a question about growth by plants under shade)

"Chlorophyll absorbs red light for photosynthesis but not far red. the shaded plant will therefore be exposed to  more far red light than red light. this will have the effect of the active Pfr
being converted to the inactive Pr.
The result will be stem elongation as Pfr prevents stem elongation"

can someone please explain this and what the P means (sorry i didn't make it clear before Russ)

[HERculina]

P=phytochrome
its a type of phytoprotein that acts as a receptor to light (red or far red light) for plants

[WhoTookMyUsername]

why will the phytocrome change?

STAV '08 says
(in resposne to a question about growth by plants under shade)

"Chlorophyll absorbs red light for photosynthesis but not far red. the shaded plant will therefore be exposed to  more far red light than red light. this will have the effect of the active Pfr
being converted to the inactive Pr.
The result will be stem elongation as Pfr prevents stem elongation"

can someone please explain this and what the P means (sorry i didn't make it clear before Russ)