Biology Unit 3 Questions Megathread

[Kaille]

i know i'm being pendantic. i'm fussing over a MHC question.

so there are tumour cells in tasmanian devils that can be transmitted to other uninfected tasmanian devils and go unoticed as they are accepted as self cells.

Should i say that the protein displayed on the MHC 1 marker is similar, therefore they are not identified as non self cells, or should i say that the MHC 1 marker is similar.

[Russ]

That's not pedantic, that's an important difference. Cells are defined as self if they have the same (or similar enough) MHC marker

[Kaille]

so what if the mhc marker is the same, but display a non self protein? wouldn't this occur in viral cells?

[Russ]

I don't understand your question but I hope this answers it:

T cells are trained by the body to not target "self" MHC - if they did, they'd spontaneously target every cell in your body. If you get a foreign cell transplanted with non-self MHC, you get a response to it (transplant rejection). If it is the same, your body will respond to it as normal - ie only when it has a foreign peptide displayed.

When a cell is infected with a virus, viral components are expressed on MHCI...this obviously leads to recognition and immune response.

[Kaille]

hah. i see, thanks for the help

[TrueLight]

was just looking around and here this might also make things clear what Russ said is correct
 http://chickenoreggblog.wordpress.com/2010/04/13/tasmanian-devil-facial-tumour-disease-too-good-a-match-for-the-immune-system/

"Devil populations in eastern Tasmania have low levels of genetic diversity due to reductions in population size over the last 150 years.  DFTD is so virulent in these populations because the tumours have the same MHC type as healthy devil cells.  Being an infectious cancer, transmission of DFTD between individuals is a bit like a skin graft or organ transplant. If the tissue’s MHC type matches, the transplant is accepted, if not it is rejected.  Because the MHC types of the tumour and the devil match, DFTD cells are not recognised as foreign so no immune response is mounted.  And because of the low genetic diversity, all devils in the population have similar MHC types meaning the disease can easily spread from one individual to another...
Here the story gets a little (more) complicated: Tasmanian devils have multiple MHC genes (up to 7 genes each), which fall into two groups on the basis of their DNA sequence.  The tumour cells have both group 1 and group 2 variants, as do the individuals from the susceptible eastern populations.  However the northwestern populations harbour a greater diversity of MHC types, and many individuals from these populations have MHC types which have only either group 1 or group 2 sequences.  None of these individuals have succumbed to DFTD, suggesting they are resistant to the disease.  Belov’s group proposes that in individuals with only group 1 sequences, the immune system will recognise the group 2 sequences on the tumour as foreign and resist it (and vice versa for individuals with only group 2 sequences).   This has yet to be tested in practice, as it is obviously difficult to get permission to infect an endangered species with a deadly disease.  However, these findings are promising for the continued survival of the species and may have a significant impact on their conservation management."

[Kaille]

thanks truelight, you didn't have to go to so much trouble. yeah it was this question that tripped me up.

[TrueLight]

haha na it was nothing just a google search .... mmm trifle...who watched masterchef lol

[Kaille]

ahaha hells yeyahh. ah i digress.

[Lesliel1]

how do memory B cells work? i know they remember the certain pathogen so that the next time they come, the immune response is quicker but i was wondering how it actually works.. like to they divide or like activate stuff or something? :S LOL

[TrueLight]

yes your right in that memory B cells respond much faster in a secondary immune response but there are some differences...like they are long lived, circulate in the periphery, hardly divide with no antigen stimulation...also
memory b cells have differentiated from b cells that have been primed and activated so they have already gone through the various stages of b cell development. So their antibodies are of much higher affinity. Also memory B cells in a secondary immune response produce large amounts of the effector antibody ie: IgG... not IgM...
they also have larger amount of MHC on their surface and CD80/86 therefore there is less of a requirement for costimulation and you don't need as much antigen to stimulate the memory b cell and therefore the response is quicker.
they also have different molecules (or different levels) on their surface that help memory b cells with adhesion, activation threshold, cell survival etc...
but the way in which of memory b cells are activated is the same as naive b cells in that it recognises antigen, uptake, process, present to Th cells, activate, proliferate, differentiate and go along to do their thing but the response in doing all these is much faster and greater.

[Kaille]

are cysts like spores? can they exist on childrens toys etc?

[Russ]

What context?
A cyst in the body is not a spore, no

[Kaille]

oh hang on, wrote something completely stupid. just ignore.

[WhoTookMyUsername]

After the Calvin Cycle finishes, and PGAL is produced, do 2 molecules combine to form fructose (as NOB says) , and then into glucose, or into glucose directly?

Also, can someone please explain how electrons in chloroplasts absorb energy and transfer this to the water molecule?
cheers

3)

Does  negative feedback work by simply causing a change in the variable being detected, or does it act directly on the gland (i'm sure its the first one but some sources imply otherwise) i.e. when drawing a negative feedback diagram, should i draw the feedback arrow to the stimulus, or the gland producing the hormone?

4) Is a protein glycolipid just a protein + carb attached to an already present lipid in plamsa membrane and
is a glycolipid just a carb molecule attached to an already present phospholipid?

5) Do leukocytes phagocytose eukaroyttc pathogens? Neap says they do but Campbells  says otherwise