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Edexcel A2 Biology SNAB 6BI04 ~ 6BIO5 June 2016 Watch

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    (Original post by noctisff)
    Do all retroviruses use reverse transcriptase?
    Yes
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    Anyone else interested in Skype revision? We're in a call now.
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    (Original post by PhysicsIP2016)
    Macrophages are the first cells to act as APCs because they function to activate the correct T helper cell with the complementary receptor upon infection.
    When the B cell acts as an APC the now activated T helper cells stimulate clonal selection which produces the correct antibodies for the pathogen.

    Think of macrophages turning into APCs being mainly present in primary infection. In the case of secondary infection the B memory cells recognise the same antigen so they can differentiate immediately (with the aid of T memory cells) without needing the macrophage to activate them.
    Hi, can you please give the generic marking points that we should use in regards to the non-specific and specific responses when concerning APCs?

    I do not recall coming across clonal selection etc in mark schemes which is why a model answer would be appreciated
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    EDIT - Came back to do this later without realising others had replied, ignore if you understand ;-;

    Susta1nz and ABeingOnEarth


    The pathogen (ANY PATHOGEN, even HIV) has antigens which are recognised as 'non-self' and are engulfed by a phagocyte (e.g. a macrophage) through the process of phagocytosis. The pathogen is now contained within a phagocytic vacuole and is broken down when a lysosome fuses with it, releasing it's hydrolytic enzymes.

    The phagocyte then presents the pathogen's antigen using a major histocompability comlex (MHC) on it's surface. The phagocyte is now an antigen presenting cell (APC). This is a non-specific immune response,

    Humoral response
    This stimulates the activation of T cells. These T cells (using their COMPLEMENTARY RECEPTORS) will bind to the antigens presented by the phagocyte. Remembering, only the SPECIFIC T cell with the COMPLEMENTARY receptor will bind to that SPECIFIC antigen. This causes the T cell to divide and differentiate to produce T-helper cells, T-killer cells (involved in the cell mediated response) and T-memory cells.

    T-helper cells activate B cells. These are another type of white blood cells covered in antibodies (each antibody is the same around one same B cell, but antibodies on different B cells are different to the first one). These antibodies are COMPLEMENTARY to the antigen. When a successful antigen-antibody complex has been formed, the B cell will divide by mitosis (with the help of cytokines produced by T-helper cells) into plasma cells (which produce an armada of these COMPLEMENTARY antibodies) and destroy the pathogen.

    Cell mediated response
    T-killer cells (produced after the activation of a T cell (see above)) attach to body (self) cells infected by the pathogen and destroy them.

    Oh and Susta1nz, the specification requires that you actually know the specific antigen on HIV. It's called GP120 and attaches to CD4 receptors on T-helper cells to infect them

    Hope this helped
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    (Original post by study2016)
    Hi, can you please give the generic marking points that we should use in regards to the non-specific and specific responses when concerning APCs?

    I do not recall coming across clonal selection etc in mark schemes which is why a model answer would be appreciated
    1. macrophages engulf pathogens via endocytosis, and is contained inside the cell within a vacuole called a phagosome
    2. lysosomes fuse with the phagosome to form a phagolysosome. the phagolysosome contains the hydrolytic enzymes which digest the bacteria.
    3. some bacterial antigens remain in the vacuoles, this is known as antigen processing.
    4.a second vacuolecontaining some small fragments of the bacterium buds from the main vacoule and fuses with the cell membrane. the digested contents are released from the cell(due to being toxic).
    5. the antigen combines with the mhc proteins on the cell membrane. the antigen is said to have been presented on the surface of the macrophage.
    6. the macrophage with these antigen/mhc complexes are now known as an antigen presenting cell (apc)
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    (Original post by study2016)
    Hi, can you please give the generic marking points that we should use in regards to the non-specific and specific responses when concerning APCs?

    I do not recall coming across clonal selection etc in mark schemes which is why a model answer would be appreciated

    Non-Specific Response:
    (I figured that when you said when concerning APCs you only wanted phagocytosis)

    - Not antigen specific
    - Histamine released causing inflammation at the site of infection
    - Which causes more fluid to leak out of capillaries and oedema as a result of increased blood flow.
    - Macrophages and Neutrophils in the fluidflow to the site of infection.
    - Phagocytosis - WBCs engulf and digest bacteria by packaging them into vesicles. (Perhaps mention endocytosis too)
    - Lysosome containing digestive enzymes such as proteases fuse with the vesicle
    - Bacteria digested.
    - Macrophage displays bacterial antigens on its surface

    (Obviously there are lots of other barriers that can be discussed with the non-specific response - they seem to really love asking about lysozyme to break down bacterial cell walls and in the case of viruses it's interferon released from the host cell to inhibit viral protein synthesis.)

    Specific Response:

    - Antigen specific
    -In the primary response Phagocytosis causes the Macrophage to become an Antigen Presenting Cell
    (- You might want to mention the Major Histocompatibility Complex here which is recognised as foreign)
    - T-Helper cell with a complementary CD4 receptor binds to the APC
    - T-Helper cell is activated and divides to form T-Memory cells and clones of T-Helper cells
    - B lymphocyte with a complementary receptor binds to the antigen on a bacterium
    - B Cell becomes an APC
    - T Helper cell binds to APC
    - T Helper cell releases cytokines
    - This stimulates the differentiation of B cells into B effector cells and B memory cells (I honestly think that they would accept clonal selection as I have seen it before, but differentiation or division also works)
    - B effector cells differentiate into plasma cells
    - Plasma cells secrete antibodies which bind to the specific antigens on the bacteria.

    [If the question then asks about the secondary response this only involves memory cells and occurs a lot quicker than primary infection - B memory cells recognise the antigen and differentiate immediately into plasma cells to secrete the antibodies]
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    (Original post by PhysicsIP2016)
    Macrophages are the first cells to act as APCs because they function to activate the correct T helper cell with the complementary receptor upon infection.
    When the B cell acts as an APC the now activated T helper cells stimulate clonal selection which produces the correct antibodies for the pathogen.

    Think of macrophages turning into APCs being mainly present in primary infection. In the case of secondary infection the B memory cells recognise the same antigen so they can differentiate immediately (with the aid of T memory cells) without needing the macrophage to activate them.
    So first there is phagocytosis by a macrophage. T helper cell binds to antigen on macrophage on the MHC. This then releases cytokines which activate B cells and T killer and memory cells.

    THEN the B cells are activated, bind to the antigen and then act as an APC to self and then differentiate in to plasma cells and memory cells and plasma cells produce the anti bodies?
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    (Original post by Susta1nz)
    So first there is phagocytosis by a macrophage. T helper cell binds to antigen on macrophage on the MHC. This then releases cytokines which activate B cells and T killer and memory cells.

    THEN the B cells are activated, bind to the antigen and then act as an APC to self and then differentiate in to plasma cells and memory cells and plasma cells produce the anti bodies?
    Essentially, yes, however once the B cell becomes an APC the complementary T helper cell needs to bind to it and release cytokines before the B cell differentiates
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    (Original post by Romanoff)
    EDIT - Came back to do this later without realising others had replied, ignore if you understand ;-;

    Susta1nz and ABeingOnEarth


    The pathogen (ANY PATHOGEN, even HIV) has antigens which are recognised as 'non-self' and are engulfed by a phagocyte (e.g. a macrophage) through the process of phagocytosis. The pathogen is now contained within a phagocytic vacuole and is broken down when a lysosome fuses with it, releasing it's hydrolytic enzymes.

    The phagocyte then presents the pathogen's antigen using a major histocompability comlex (MHC) on it's surface. The phagocyte is now an antigen presenting cell (APC). This is a non-specific immune response,

    Humoral response
    This stimulates the activation of T cells. These T cells (using their COMPLEMENTARY RECEPTORS) will bind to the antigens presented by the phagocyte. Remembering, only the SPECIFIC T cell with the COMPLEMENTARY receptor will bind to that SPECIFIC antigen. This causes the T cell to divide and differentiate to produce T-helper cells, T-killer cells (involved in the cell mediated response) and T-memory cells.

    T-helper cells activate B cells. These are another type of white blood cells covered in antibodies (each antibody is the same around one same B cell, but antibodies on different B cells are different to the first one). These antibodies are COMPLEMENTARY to the antigen. When a successful antigen-antibody complex has been formed, the B cell will divide by mitosis (with the help of cytokines produced by T-helper cells) into plasma cells (which produce an armada of these COMPLEMENTARY antibodies) and destroy the pathogen.

    Cell mediated response
    T-killer cells (produced after the activation of a T cell (see above)) attach to body (self) cells infected by the pathogen and destroy them.

    Oh and Susta1nz, the specification requires that you actually know the specific antigen on HIV. It's called GP120 and attaches to CD4 receptors on T-helper cells to infect them

    Hope this helped
    Oh wow haha thanks that was also an amazing answer! Really useful

    (Original post by PhysicsIP2016)
    Essentially, yes, however once the B cell becomes an APC the complementary T helper cell needs to bind to it and release cytokines before the B cell differentiates
    Oooh, I usually just say the T helper cell binds to the antigens on the APC and release cytokines which activate B cells etc.. Thanks so much for the help!
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    (Original post by ABeingOnEarth)
    There is no exam paper for Jan 2016 that isn't IAL. Normal A Level exams no longer take place in Jan, just June.
    Oh! Thanks for the info!
    It's surprising, because for the IAL's, they actually added a new session (November),AS only, staring this year!
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    (Original post by PhysicsIP2016)
    Susta1nz ABeingOnEarth
    B cells have antibodies on their surface and when they bind to the complementary antigen they become APCs. The T helper cell with the complementary receptor then binds to this APC which releases cytokines to trigger clonal selection of the specific B cells into memory cells and plasma cells.

    With viruses, they invade the host cell and do present foreign antigens on the membrane, however in the case of HIV as there is a high rate of mutation within the gene that codes for the antigen the immune response isn't as effective as lots of T Helper cells are being digested by phagocytes and T killer cells and eventually HIV could go undetected.
    I think you may be getting confused with TB, as this evades the immune system by preventing antigen presentation inside the phagocytes. That's why it can lie dormant.
    dont phagocytes form apc


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    (Original post by PhysicsIP2016)
    Yes
    Where do retroviruses come in unit 4?
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    Is it ATPase or ATPsynthase in thylakoid membrane, I've seen mark schemes interchange with this one and I don't which one I should use.
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    Anybody got a list of definitions? for unit 4
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    (Original post by Cakey_101)
    Where do retroviruses come in unit 4?
    HIV is a retrovirus that can be treated with antiretroviral drugs but that's all you need to know.
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    (Original post by Oshoko)
    Is it ATPase or ATPsynthase in thylakoid membrane, I've seen mark schemes interchange with this one and I don't which one I should use.
    It's ATP synthase.

    ATPase breaks down ATP into ADP + Pi

    ATP synthase SYNTHESISES ATP from ADP + Pi
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    (Original post by ranz)
    dont phagocytes form apc


    Posted from TSR Mobile
    Yes but only macrophages. The original posters were asking about B cells
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    (Original post by Romanoff)
    It's ATP synthase.

    ATPase breaks down ATP into ADP + Pi

    ATP synthase SYNTHESISES ATP from ADP + Pi
    👍good I thought so
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    (Original post by PhysicsIP2016)
    When Carbon Dioxide and RuBP combine. Technically GP is reduced to GALP using NADPH and phosphorylated using ATP so there is no transfer of carbon.
    Thank you!
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    I was doing a past paper (June 2014) and did question 4(a) and the answer referred to a phagosome and phagocytic vesicle. In previous papers, it said to only accept phagocytic vacuole.

    Does anyone know if there's a difference between a phagosome, phagocytic vesicle and phagocytic vacuole?

    The markscheme for 2014 is here:
    http://qualifications.pearson.com/co...-June-2014.pdf

    and the answer is on page 26.
 
 
 
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