VCE Biology Question Thread

[Biology24123]

What did you get in biology, GrannySmith

[cosine]

You need to know what it is and its implications, but not any specifics on how its done (just a general idea i.e. genes are shuffled).
You need both the IgE and mast cell to release the histamine. In this way, the pair act as a unit.

Okay, so histamine will only be released if enough allergens bind so as to form cross linkages. You can think of it as a threshold level - you need a certain number of allergens to bind to the IgE in order to activate the mast cell. Yeah I was inferring cells=mast cells, and that they degranulate=release histamine (this is because histamines are stored in granules within the cell).

Cheers brah. So when mast cells release histamines in response to inflammation, does this mean this is a team effort with the IgE antibodies as well? Cheers.

[Biology24123]

Cheers brah. So when mast cells release histamines in response to inflammation, does this mean this is a team effort with the IgE antibodies as well? Cheers.

No, histamine causes inflammation. When antigens bind to igE on the mast cells, they release histamine

[cosine]

If viruses enter host cells and present their non-self antigens on the MHC I markers of the host cell, does this mean that T cells will specifically bind with the MHC of host cells? Also, if this is the case, then viruses are not engulfed by phagocytes, right?

[Biology24123]

If viruses enter host cells and present their non-self antigens on the MHC I markers of the host cell, does this mean that T cells will specifically bind with the MHC of host cells? Also, if this is the case, then viruses are not engulfed by phagocytes, right?

Viruses are intracellular so they will be in host cells most of the time

[cosine]

Viruses are intracellular so they will be in host cells most of the time

My main question was if viruses enter host cells, they present their nonself antigens on the MHC I molecules, right? When this MHC I molecule displays the nonself antigens, do Tc cells destroy the cells?

Also, can B cells specifically bind with pathogens/antigens, using their transmembrane antibodies?

[cosine]

Can I post my understanding of the immune system, and can anyone, anyone, improve anything or point out any misconceptions, please?

There are three lines of defence against foreign pathogens:
- First line of defence: Non-specific chemical or physical barriers that prevent entry of pathogens into our body
- Second line of defence: Non-specific structural (cells) or processes that occur when the first line of defence has been infiltrated.
- Third line of defence: Specific immune response in which lymphocytes recognise specific antigens and respond to them.

First line of defence:
Physical barriers:
- Intact skin: provides immunity against any pathogens as it prevents entry
- Ciliated membranes: these hair-like projections trap foreign materials in the trachea tract and sweep them up, to either be swallowed or coughed out
- Natural flora: Naturally occurring bacterial cells compete against harmful pathogens

Chemical barriers:
- Mucous: sticky substances that traps foreign pathogens
- Stomach acid: Acidic environment kills many pathogens
- Tears and secretions: Contain enzymes that break down and dehydrate pathogens
- Urine: Urine flow wipes out pathogens

Second line of defence:
When the first line of defence is breached, the second line of defence mechanisms come into play.
- Phagocytes: Certain leucocytes such as dendritic cells, neutrophils and macrophages that engulf foreign materials and are known as phagocytes. Once these pathogens are engulfed, they are contained within vesicles within which lysosomes fuse with to degrade the pathogens.
- APCs: Antigen Presenting Cells engulf pathogens, degrade them and release antigenic fragments onto MHC II markers onto the cell membrane. APCs include B Cells, Dendritic cells and macrophages
- Mast cells: Mast cells have IgE antibodies embedded on their cell membranes. Mast cells release histamines and are granulocytes.
- Inflammation: Inflammation is a process whereby mast cells release histamines to vasodilate blood vessels and increase skin capillary permeability so that an influx of leucocytes are present in the infection site. Certain macrophages at this site release chemicals known as interleukins that stimulate the hypothalamus of the brain to increase the body temperature, known as fever. This increase in temperature will reduce pathogenic metabolism or activity.
- Complement proteins: Complement proteins are secreted by phagocytes and are inactive in the blood plasma until recognition of a pathogen. Once activated, they cause a cascade of events and more complement proteins are activated. They typically respond to bacterial cells. They can either bind to the cell membranes of bacterial cells in massive amounts to attract more phagocytes onto the scene, or they can lyse the membranes of bacterial cells.
- Interferons: Interferons are released by virally infected cells that stimulate nearby cells to produce viral-resistant enzymes to protect themselves.

Third line of defence:
- Humoral: The humoral immunity involves B cells - Plasma B cells or Memory B cells
- Cell-mediated: The cell-mediated immunity involves T cells - Cytotoxic T cells and T helper cells

Humoral:
B cells possess specific antibodies on their cell membrane that will recognise and bind with specific antigens only. Once this antigen-antibody complex is formed, the whole complex, including the pathogen, is engulfed. Once engulfed, antigenic fragments are released onto MHC II markers on the cell surface of the B cell. An activated T helper cell will recognise this MHC II marker and release chemicals to force the B cell to proliferate into: B memory cells and plasma B cells. The memory B cells will be stored in the lymph nodes and spleen for the second infection, to provide long term immunity against the specific antigen. The plasma B cells will produce and secrete the specific antibodies that will go off and bind to the antigens onto the surface of pathogens.

Cell-mediated:
When phagocytes engulf foreign pathogens, they degrade them and release antigenic fragments within the MHC II markers that will display/present them on their cell surface. Once on the cell membrane, these MHC II markers will interact with TCRs of T cells to activate them, and once activated, the T cell will proliferate into Tc and Th cells. The Th cells, as aforementioned, will activate B cells that present the antigens on MHC II markers to proliferate, when the TCR-MHCII complex is formed. Now all of our body cells possess MHC I markers with self-antigens presented on them. These Tc cells will go around and their TCRs will bind with MHC markers and ensure they're self antigens presented on them. If the case of tumour cells or virally infected cells, the virus will present nonself antigens on the host cell and the Tc cells recognise this, and destroy the cells.

If there is any missing information, or any misleading information, please ask away and let me know. This was one topic I really struggled with and I hope I have overcome this, that's why I want anyone to help out and point out any errors. 99.95.

[cosine]

Is there a specific reason as to why organ transplants can be rejected? Is it because the MHC I markers on these cells of the donor have different antigens as compared to our self antigens, and so cytotoxic T cells will recognise this as foreign and destroy them?

[Biology24123]

Can I post my understanding of the immune system, and can anyone, anyone, improve anything or point out any misconceptions, please?

There are three lines of defence against foreign pathogens:
- First line of defence: Non-specific chemical or physical barriers that prevent entry of pathogens into our body
- Second line of defence: Non-specific structural (cells) or processes that occur when the first line of defence has been infiltrated.
- Third line of defence: Specific immune response in which lymphocytes recognise specific antigens and respond to them.

First line of defence:
Physical barriers:
- Intact skin: provides immunity against any pathogens as it prevents entry
- Ciliated membranes: these hair-like projections trap foreign materials in the trachea tract and sweep them up, to either be swallowed or coughed out
- Natural flora: Naturally occurring bacterial cells compete against harmful pathogens

Chemical barriers:
- Mucous: sticky substances that traps foreign pathogens
- Stomach acid: Acidic environment kills many pathogens
- Tears and secretions: Contain enzymes that break down and dehydrate pathogens
- Urine: Urine flow wipes out pathogens

Second line of defence:
When the first line of defence is breached, the second line of defence mechanisms come into play.
- Phagocytes: Certain leucocytes such as dendritic cells, neutrophils and macrophages that engulf foreign materials and are known as phagocytes. Once these pathogens are engulfed, they are contained within vesicles within which lysosomes fuse with to degrade the pathogens.
- APCs: Antigen Presenting Cells engulf pathogens, degrade them and release antigenic fragments onto MHC II markers onto the cell membrane. APCs include B Cells, Dendritic cells and macrophages
- Mast cells: Mast cells have IgE antibodies embedded on their cell membranes. Mast cells release histamines and are granulocytes.
- Inflammation: Inflammation is a process whereby mast cells release histamines to vasodilate blood vessels and increase skin capillary permeability so that an influx of leucocytes are present in the infection site. Certain macrophages at this site release chemicals known as interleukins that stimulate the hypothalamus of the brain to increase the body temperature, known as fever. This increase in temperature will reduce pathogenic metabolism or activity.
- Complement proteins: Complement proteins are secreted by phagocytes and are inactive in the blood plasma until recognition of a pathogen. Once activated, they cause a cascade of events and more complement proteins are activated. They typically respond to bacterial cells. They can either bind to the cell membranes of bacterial cells in massive amounts to attract more phagocytes onto the scene, or they can lyse the membranes of bacterial cells.
- Interferons: Interferons are released by virally infected cells that stimulate nearby cells to produce viral-resistant enzymes to protect themselves.

Third line of defence:
- Humoral: The humoral immunity involves B cells - Plasma B cells or Memory B cells
- Cell-mediated: The cell-mediated immunity involves T cells - Cytotoxic T cells and T helper cells

Humoral:
B cells possess specific antibodies on their cell membrane that will recognise and bind with specific antigens only. Once this antigen-antibody complex is formed, the whole complex, including the pathogen, is engulfed. Once engulfed, antigenic fragments are released onto MHC II markers on the cell surface of the B cell. An activated T helper cell will recognise this MHC II marker and release chemicals to force the B cell to proliferate into: B memory cells and plasma B cells. The memory B cells will be stored in the lymph nodes and spleen for the second infection, to provide long term immunity against the specific antigen. The plasma B cells will produce and secrete the specific antibodies that will go off and bind to the antigens onto the surface of pathogens.

Cell-mediated:
When phagocytes engulf foreign pathogens, they degrade them and release antigenic fragments within the MHC II markers that will display/present them on their cell surface. Once on the cell membrane, these MHC II markers will interact with TCRs of T cells to activate them, and once activated, the T cell will proliferate into Tc and Th cells. The Th cells, as aforementioned, will activate B cells that present the antigens on MHC II markers to proliferate, when the TCR-MHCII complex is formed. Now all of our body cells possess MHC I markers with self-antigens presented on them. These Tc cells will go around and their TCRs will bind with MHC markers and ensure they're self antigens presented on them. If the case of tumour cells or virally infected cells, the virus will present nonself antigens on the host cell and the Tc cells recognise this, and destroy the cells.

If there is any missing information, or any misleading information, please ask away and let me know. This was one topic I really struggled with and I hope I have overcome this, that's why I want anyone to help out and point out any errors. 99.95.

Your description of the humoral response isn't wrong. B cells can act as APC's but they usually don't.
Humoral
A macrophage will engulf the pathogen (macrophage is non specific to the antigen). The macrophage displays an antigen on the MHC II on the membrane.  Specific T helper cells recognise the antigen and become active, the T helper cell will activate B cells to proliferate (the B cell must have recognised a free antigen for the pathogen). The B cell proliferates into memory cells and plasma cells. The plasma cells produce large amounts of antibodies

Cell mediated

After the antigen is on the MHC II on the membrane, a T helper cell then recognises the antigen and becomes activated. The specific T helper cells then activate specific cytotoxic T cells (they are originally inactive). The cytotoxic T cells proliferate into active cytotoxic T cells and memory cells.

The MHC I part is right.

Thanks for the summary

[Biology24123]

Is there a specific reason as to why organ transplants can be rejected? Is it because the MHC I markers on these cells of the donor have different antigens as compared to our self antigens, and so cytotoxic T cells will recognise this as foreign and destroy them?

Correct

[StupidProdigy]

What's the difference between Natural killer cells, killer t cells and cytotoxic t cells. Are the latter two the same thing just different names? Thanks

[Biology24123]

What's the difference between Natural killer cells, killer t cells and cytotoxic t cells. Are the latter two the same thing just different names? Thanks

Killer T and cytotoxic T are the same. They are specific to an antigen. Natural killer cells will destroy any cell that has foreign antigens on it's MHC I.

[StupidProdigy]

So nk cells are part of the second line of defence yeah? Thanks mate

[Biology24123]

So nk cells are part of the second line of defence yeah? Thanks mate

2nd line

[Sine]

Killer T and cytotoxic T are the same. They are specific to an antigen. Natural killer cells will destroy any cell that has foreign antigens on it's MHC I.

Natural Killer Cells actual destroy the cells that don't have MHC I markers on them (cancerous/virally infected cells).

EDIT:6000th Reply