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T helper cells, B cells and cytokines

So basically when a B cell engulfs a pathogen, it presents the antigen on its cell surface membrane and becomes and APC. Then the T helper cell would bind to it and release cytokines which stimulates clonal selection; the B cells divide to produce clones of B memory cells and B effector cells.

Now when a macrophage becomes an APC and the T helper cell bind to them, they release cytokines which make the T helper cells themselves divide. Why don't they divide as well when the APC is a B cell and not a macrophage?

Also what is the function of active T helper cells?
I didn't think B cells were phagocytosing cells.
Reply 2
Original post by The Angry Stoic
I didn't think B cells were phagocytosing cells.


I'm quoting the Edexcel A2 book: "The B cell then engulfs the whole pathogen by endocytosis."
Original post by Kurraiyo
I'm quoting the Edexcel A2 book: "The B cell then engulfs the whole pathogen by endocytosis."


They do I've just checked. I'm not sure they do it particularly often compared to the main phagocytosers though.

I really need to go back over B cells...
I've heard that the b cells are stimulated by the macrophages ( when they encounter a pathogen) once stimulated the b cells divide by mitosis to form memory cells( which stay in the blood, and when the.pathogen enters again it divides to produce plasma cells) and plasma cells which secretes antibody in the blood. This all is written in the CIE Biology coursebook. T helper cells, when encounters a pathogen secretes cytokines which stimulates b cells to divide to form appropiate plasma cells.

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(edited 10 years ago)
Reply 5
Original post by Kurraiyo
So basically when a B cell engulfs a pathogen, it presents the antigen on its cell surface membrane and becomes and APC. Then the T helper cell would bind to it and release cytokines which stimulates clonal selection; the B cells divide to produce clones of B memory cells and B effector cells.

Now when a macrophage becomes an APC and the T helper cell bind to them, they release cytokines which make the T helper cells themselves divide. Why don't they divide as well when the APC is a B cell and not a macrophage?

Also what is the function of active T helper cells?




So an active T helper cell releases cytokines which stimulates the division of the B cell into B effector clones and B memory clones. The B effector cells then differentiate into plasma cells which can produce antibodies.

T helper cells are a very vital part of our immune system, without active T helper cells, antibody production is decimated. For example, the effects of HIV

So basically Active T helper cells are involved in the activation of B cells, therefore the production of antibodies and the activation of T killer cells and some other immune cells


Regarding your first question, if you mean why don't the macrophages divide it's because cytokines are complimentary to the cell that releases them, in terms of their cell surface receptors. If you mean why don't the Active T helper cells divide during the activation of B cells, the Active T helper cell is already active. Division has already occured to produce that Active T helper cell, there's kinda no need to as they only need to carry out their activation functions

I hope that helps.
(edited 10 years ago)
There are a couple of reasons for all of this and most of them boil down to the fact that at A level immunology is taught at a very simple level, as it should be, but if you want answers to regurgitate in exams then learn what the textbooks tell you!

There are two big reasons why B cells don't activate T cells when they present antigens. The first (and simplest) is that they don't produce the activating cytokines that macrophages and dendritic cells do when they present antigens. Secondly, think about what you know about B cells. They all have unique receptors for antigen. There are therefore only a few B cells in the body that will recognise any specific pathogen. The chances of one of these finding antigen in a lymph node, engulfing it and then activating a T cell (if it were able to) are small. Meanwhile tons of macrophages and dendritic cells are in the periphery, at the site of infection, omnomnomming all the delicious pathogens and then coming back to the lymph nodes to present antigen to T cells.

Active T helper cells do a lot of things. They produce a lot of different cytokines that do all sorts of things to improve the immune response or tailor it towards a pathogen type. They also help to activate T killer cells and B cells, stimulating them to divide and differentiate into active forms.
Reply 7
Original post by Kurraiyo
So basically when a B cell engulfs a pathogen, it presents the antigen on its cell surface membrane and becomes and APC. Then the T helper cell would bind to it and release cytokines which stimulates clonal selection; the B cells divide to produce clones of B memory cells and B effector cells.


Yes, in essence this is correct. B-cells can be activated in two main ways: by T-cells or T-cell independently. T-cell dependent activation occurs when an APC (can be macrophages, dendritic cells, or B-cells themselves) takes in and processes the antigen and presents it on the surface of the cell, associated with a special membrane protein called HLA. The T-cell receptor of the Helper T-cell then binds to the HLA-antigen complex and the helper T-cell produces various cytokines, which have a wide range of effects. One of the cytokines produced stimulates B-cell differentiation and proliferation.

T-cell independent activation is basically when certain types of antigen bind to the B-cell receptors and trigger activation directly.

Now when a macrophage becomes an APC and the T helper cell bind to them, they release cytokines which make the T helper cells themselves divide. Why don't they divide as well when the APC is a B cell and not a macrophage?


They do, but this is a rare event since B-cells can only process one antigen, whereas macrophages can process many antigens.


Also what is the function of active T helper cells?


Really what we have already described - they release cytokines. Don't really know much about the A-level course but some of these cytokines are:

Colony stimulating factor - stimulates the production of white blood cells
gamma-interferon - activates macrophages
tumour necrosis factor - various effects, inflammatory mediator, kills tumour cells, macrophage activation
Interleukins - lots of types with various effects, IL-1 causes fever, inflammation, T-cell activation. IL-4 is the main one that stimulates B-cell proliferation and differentiation.

That's a summary to give you the general idea. In short, cytokines make other immune system cells work better and cause fever and inflammation.

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