VCE Biology Question Thread

[HighTide]

Hey guys,

Can helper t-cells stimulate both b-cells and cytotoxic t-cells at the same time?

thanks,

EDIT: and on that note, how do t-helper cells know which b-cells have the right antibodies on their surface complementary to the antigen and hence stimulate them to proliferate?

From what I've learnt, they can both be stimulated at the same time. The B cell is an antigen-presenting cell (APC). The T-Helper cells will be activated when the B cell presents the antigenic epitope to the T Helper cell. Remember that the antigen is specific to the B cell, and the T Helper cell has a TCR (T-cell receptor) which is also specific. As such, when the antigen is presented via the class II HLA markers, the cell will then secrete the Interleukin II and cause the proliferation of specific cytotoxic T and B cells.
Hope it helps. 

[plants]

From what I've learnt, they can both be stimulated at the same time. The B cell is an antigen-presenting cell (APC). The T-Helper cells will be activated when the B cell presents the antigenic epitope to the T Helper cell. Remember that the antigen is specific to the B cell, and the T Helper cell has a TCR (T-cell receptor) which is also specific. As such, when the antigen is presented via the class II HLA markers, the cell will then secrete the Interleukin II and cause the proliferation of specific cytotoxic T and B cells.
Hope it helps. 

Thanks a bunch!
So in that case, what will happen if the t-helper cell binds to an MHC class II antigen complex on say, a dendritic cell or macrophage? How do the specific b-cells become activated here?
Also, you said the T-helper cell will cause the proliferation of specific cytotoxic t-cells. How does the release of Interleukin II only stimulate the specfic cytotoxic t-cells relevant to the particular MHC-antigen complex?

These are both the same question, really. I think I'm just confused.

  Cheers,

[HighTide]

Thanks a bunch!
So in that case, what will happen if the t-helper cell binds to an MHC class II antigen complex on say, a dendritic cell or macrophage? How do the specific b-cells become activated here?
Also, you said the T-helper cell will cause the proliferation of specific cytotoxic t-cells. How does the release of Interleukin II only stimulate the specfic cytotoxic t-cells relevant to the particular MHC-antigen complex?

These are both the same question, really. I think I'm just confused.

  Cheers,

Just to clear up the confusion, I'll summarize what happens. [Note: This is T dependent antigens only]
When a macrophage detects an antigen it will digest it, cut off the epitopes and present them on MHC Class II markers. To stimulate the the Helper T cells to divide once the specific antigen has been found, the macrophages release a cytokine called Interleukin I. These antigens can be presented to Helper T cells which have the corresponding T-cell receptor to the antigen. When the antigens are presented to the specific Helper T cells, the T cells will become "activated".

Now, if the antigen attaches to an antibody on a corresponding B cell, it will also be digested, and the epitopes presented on MHC Class II markers. These will present the antigens to the corresponding activated Helper T cells. From here, the Helper T cell will secrete Interleukin II, and will cause the activation of B cells.  B cells would proliferate and differentiate into B memory cells and plasma cells.

A similar process occurs for Cytotoxic T cells. They present the epitope. When the right antigen is found, the Helper T cell will secrete interleukins which promote proliferation of that specific cell.

This is called T-cell dependent antigens where you require the T Helper cell to be "activated" in order to form B cells and B memory cells. Remember this is specific immunity. The T cells and B cells interact specifically based on the antigen. So in this case, the Helper T cell, B cell and cytotoxic T cell are all specific to the antigen.

[tiff_tiff]

Heyy

I have a few immunity questions too

1)   What happens after the phagocyte has engulfed the bacteria? How does the body dispose of it? Apoptosis? It just degrades? Recycling of nutrients?

2)   Can phagocytes operate independent of complement proteins? Or do they always need complement proteins because they are unable to recognize bacteria by themselves?

3)   The book says T helper cells are also involved in the cellular immune response (MHC I proteins) but the diagrams drawn always only involve Tc cells? I know that when a infected cell presents an antigen to MHC I, Tc cells recognizes it, proliferates and then kills it, how does Th cells come into play?

If someone could please clarify it would mean a lot

Thanks in advance

[vox nihili]

Heyy

I have a few immunity questions too

1)   What happens after the phagocyte has engulfed the bacteria? How does the body dispose of it? Apoptosis? It just degrades? Recycling of nutrients?

2)   Can phagocytes operate independent of complement proteins? Or do they always need complement proteins because they are unable to recognize bacteria by themselves?

3)   The book says T helper cells are also involved in the cellular immune response (MHC I proteins) but the diagrams drawn always only involve Tc cells? I know that when a infected cell presents an antigen to MHC I, Tc cells recognizes it, proliferates and then kills it, how does Th cells come into play?

If someone could please clarify it would mean a lot

Thanks in advance

1. The bacterium fuses with lysosomes and they degrade it.

2. Independent. Antibodies can also promote phagocytosis, for instance.

3. By helping the Tc cell to become activated

[kimmytaaa]

hi
Just wondering if I failed 2 sacs in a row, what are my possible outcomes? Will be able to still get a ss of 35? or should I drop biology?

thanks

[biy]

Need some help with these questions:

1). How do cells distinguish between self and non self?

[biy]

Macrophage recognises the MHC markers of a bacterium as no self, and engulfs it.


How can a macrophage recognise the MHC markers of a bacterium? Do the MHC markers of the macrophage actually bind or attempt to bind with the MHC markers of the bacterium?

Also how does a macrophage come into contact with the bacterium in the first place? Do macrophages flow in the blood stream?

Thank you <3

[biy]

Sorry if the inflush of questions

How do B lynphocytes recognise an antigen? Do they specifically bind to the antigen or are they stimulated by other molecules that an antigen is presents

My book says that the antigen binds with a B cell antibody on the cell surface, and as a result the production of antibodies is triggered, is this true ?

[Sine]

How do B lynphocytes recognise an antigen? Do they specifically bind to the antigen or are they stimulated by other molecules that an antigen is presents

My book says that the antigen binds with a B cell antibody on the cell surface, and as a result the production of antibodies is triggered, is this true ?

B lymphocytes recognise free moving antigen they bind to the antigen using their surface Antibodies which are in a fixed position on the cell membrane.

[biy]

B lymphocytes recognise free moving antigen they bind to the antigen using their surface Antibodies which are in a fixed position on the cell membrane.

Thanks Sine

But what happens next?

[biy]

Here comes the in flush of questions again

- How would you define antigen? Is it okay to just say that an antigen is any foreign carbohydrate or protein molecule that stimulates an immune response? I don't feel right saying that it triggers antibody production, because it does more than that, right?

- How do phagocytes recognise and engulf foreign pathogens? Is it when the MHC markers of the pathogen are not recognised by the MHC markers of the phagocyte, hence labelling it as a non-self, and engulfing it?

- Is it right to define antibody as a protein molecule that is produced in response to an antigen?

- When a B lymphocyte forms an antigen-antibody complex with a transmembrane antibody, is it true that Th cells are responsible for the clonal production of the same B cell, into plasma B cells and memory B cells?

- What happens when B memory cells are produced? Do they get stored in lymph nodes? If so, why is it that next time the same antigen is detected, the immune response is much more rapid? Is it because these pre-made memory cells are concentrated in the blood, and when an antigen is detected, an influx of antibodies are produced by these millions of B cells?

- What exactly do antibodies do? I know they bind to the antigens on the pathogens, but what has that got to do with anything?

- What happens after an antibody has done it's job? Is it reused or is it degraded?

- How can you define inflammation? Can you just say that it occurs when tissue fluid is damaged? And the responses of inflammation include the vasodilation of blood vessels, which means more blood is flowing into the infected region, causing a battalion of leucocytes to be present on the site, to fight the pathogen?

- "A doctor takes a blood sample from a patient, who has a microbial infection. What should the doctor expect to see in the blood sample, to prove that there is a bacterium infection?" I said that the doctor would obviously see a lot of leucocytes as they are working to fight the bacteria. This answer is correct, but I also wrote antibodies. Is this true? Can antibodies by detected free-roaming in the blood?

- Do MHC markers actually bind with MHC markers of other cells in our bodies? And is it true that when a MHC marker binds to a MHC marker that is not recognised, it initiated an immune response? If so, are the MHC markers that bind with these MHC markers of other cells, including pathogenic cells, considered the MHC Class II?

Any help is greatly appreciated <3   And I apologise about the number of questions, but biology is so intriguing, and my teacher isn't much help at all as he probably hates the subject

[jyodesh.com]

Okay its been a while and im pretty rusty with this stuff so someone correct me if i make a mistake,
anyway to answer all your questions biy, the process of the adaptive immunological response follows:
1) During their development adaptive immune cells (T-cells and B-cells) are randomly generated and any T-cell or B-cell that responds to self molecules are destroyed before they can mature. I don't know the exact mechanism for this though but the result is that you get a random collection of T-cells and B-cells that don't attack self cells. The genes that control the variable region of the T-cell receptor and B-cell receptor (antibody) that allows them to recognise an antigen are generated by recombination and are not inherited.
2) Phagocytes have genes, inherited from your parents, that allow them to recognise non-specific proteins that are common to pathogens e.g. a protein that is found on all bacteria. These phagocytes are found in the blood and lymph as neutrophils and monocytes. They can move into the tissues where monocytes mature into macrophages. Here they can phagocytose pathogens and then they will move into the lymphatic system. This is part of the innate immunological response.
3) The phagocyte breaks down the pathogen using lysosomes resulting in a whole bunch of non-self protein fragments inside the phagocyte. These protein fragments (antigens) are then presented in the groove of a membrane protein called the Major Histocompatibility Complex II (MHC II). So its like putting rotten fruit (antigen) in a basket labelled rotten fruit (MHC II). For this reason cells that have MHC II are called antigen presenting cells (APC)
4)The APC travels to lymph nodes and the spleen where it will find a whole bunch B-cells and T-cells. What happens next is like finding true love. The antigen presenting cell has to find a CD4 helper T-cell with a T-cell receptor that matches the antigen. There are a lot of different T-cells each with different T-cell receptors so its like trying to find your one true love in a sea of ugly people. After a while the APC will find its corresponding CD4 helper T-cell and the T-cell will become activated and will begin to proliferate.
5) Some of the CD4 helper T-cells will differentiate into CD8 cytotoxic T-cells. CD4 helper T-cells will help to activate the corresponding B-cells causing them to differentiate and proliferate.
6)a)CD8 cytotoxic T-cells target cells target virus infected cells. All nucleated cells express MHC I (not II) and present protein fragments in their groove. If they present a viral protein fragment the CD8 cytotoxic T-cell will kill it.
b) B-cells have antibodies/immunoglobulins expressed on their surface. Initially these are IgG (i think). Once activated they unergo isotype switching. This is when the antibody changes into different isotypes i.e. IgG --> IgA or IgM or IgE. The isotype it switches to depends on the purpose of the antibody. Some antibodies exist to neutralise bacterial toxins, some are excreted onto the internal surface of organs e.g. lungs, some are excreted and exist in the blood to bind to their target making a ball of pathogens stuck together which phagocytes can eat up, some remain on the surface of the B-cell.
I hope that answers your questions

[biy]

Okay its been a while and im pretty rusty with this stuff so someone correct me if i make a mistake,
anyway to answer all your questions biy, the process of the adaptive immunological response follows:
1) During their development adaptive immune cells (T-cells and B-cells) are randomly generated and any T-cell or B-cell that responds to self molecules are destroyed before they can mature. I don't know the exact mechanism for this though but the result is that you get a random collection of T-cells and B-cells that don't attack self cells. The genes that control the variable region of the T-cell receptor and B-cell receptor (antibody) that allows them to recognise an antigen are generated by recombination and are not inherited.
2) Phagocytes have genes, inherited from your parents, that allow them to recognise non-specific proteins that are common to pathogens e.g. a protein that is found on all bacteria. These phagocytes are found in the blood and lymph as neutrophils and monocytes. They can move into the tissues where monocytes mature into macrophages. Here they can phagocytose pathogens and then they will move into the lymphatic system. This is part of the innate immunological response.
3) The phagocyte breaks down the pathogen using lysosomes resulting in a whole bunch of non-self protein fragments inside the phagocyte. These protein fragments (antigens) are then presented in the groove of a membrane protein called the Major Histocompatibility Complex II (MHC II). So its like putting rotten fruit (antigen) in a basket labelled rotten fruit (MHC II). For this reason cells that have MHC II are called antigen presenting cells (APC)
4)The APC travels to lymph nodes and the spleen where it will find a whole bunch B-cells and T-cells. What happens next is like finding true love. The antigen presenting cell has to find a CD4 helper T-cell with a T-cell receptor that matches the antigen. There are a lot of different T-cells each with different T-cell receptors so its like trying to find your one true love in a sea of ugly people. After a while the APC will find its corresponding CD4 helper T-cell and the T-cell will become activated and will begin to proliferate.
5) Some of the CD4 helper T-cells will differentiate into CD8 cytotoxic T-cells. CD4 helper T-cells will help to activate the corresponding B-cells causing them to differentiate and proliferate.
6)a)CD8 cytotoxic T-cells target cells target virus infected cells. All nucleated cells express MHC I (not II) and present protein fragments in their groove. If they present a viral protein fragment the CD8 cytotoxic T-cell will kill it.
b) B-cells have antibodies/immunoglobulins expressed on their surface. Initially these are IgG (i think). Once activated they unergo isotype switching. This is when the antibody changes into different isotypes i.e. IgG --> IgA or IgM or IgE. The isotype it switches to depends on the purpose of the antibody. Some antibodies exist to neutralise bacterial toxins, some are excreted onto the internal surface of organs e.g. lungs, some are excreted and exist in the blood to bind to their target making a ball of pathogens stuck together which phagocytes can eat up, some remain on the surface of the B-cell.
I hope that answers your questions

Thank you so much, <3!

Just a small question with the red part on your post. What do you mean by this? Can you answer just these questions for me too?

- Do MHC markers actually bind with MHC markers of other cells in our bodies? And is it true that when a MHC marker binds to a MHC marker that is not recognised, it initiated an immune response? If so, are the MHC markers that bind with these MHC markers of other cells, including pathogenic cells, considered the MHC Class II?

- How would you define antigen? Is it okay to just say that an antigen is any foreign carbohydrate or protein molecule that stimulates an immune response? I don't feel right saying that it triggers antibody production, because it does more than that, right?

Thanks so much jyodesh.com <3!!

[jyodesh.com]

-The innate immunological response is fixed and cannot adapt to the target presented. This is because it is based on inherited traits passed on from parents. In this way they cannot change. (In contrast for adaptive immunity cells they undergo a genetic lottery shuffle thing where they select different combinations of DNA and get rid of the rest. So this means that adaptive immune cells have a different set of DNA from other cells in the body.) There are specific receptors on the surface of phagocytic cells which can recognise pathogen structures. These pathogen structures tend to be repetitive sequences that could be found in viral RNA or DNA or in bacteria specific carbohydrates or pathogen specific wall components.

-Im pretty sure MHC markers don't bind with other MHC markers. MHC markers bind to T-cell receptors. MHC markers are like flag proteins. They say hey I found a pathogen, come look (MHC II), or hey im infected by a virus (MHC I)

- An antigen is any foreign substance that elicits an adaptive immunity response, which could be any foreign substance because the T-cell receptors and B-cell receptors are kinda designed in a way so that there are a lot of different possibilities of what they can end up recognising as an antigen. Along with carbohydrates and proteins, i'm pretty sure even metals can be recognised as antigens. In cases where things go wrong and you produce a B-cell or T-cell that ends up recognising self cells as foreign, you get an autoimmune disease, and the targets would be known as autoantigens. An example of an autoimmune disease is type 1 diabetes where the immune system destroys the beta cells in the islets of of Langerhans resulting in a reduced ability to produce insulin.