So how does a 2nd infection response occur so fast for extracellular bacterium if no memory T-helper cells are produced?
Will we ever have to refer to memory T-helper cells(at all for VCAA) or is it sufficient to state they are "activated" by interleukin-1 produced by dendritic cells and that it activates T-cytotoxic cells to proliferate and differentiate into memory T-cytotoxic cells and active T-cytotoxic cells by secreting interleukin-2?
Why are you neglecting the humoral response in this immune response?
For VCAA, memory T cells are not required but they do certainly exist.
Say the first time a bacteria infects an organism. It will respond by producing memory B cells and plasma B cells. But this can only occur when T-helper cells are activated through APCs (phagocytes). The T-helper cells are not restricted to only B cells, and when they are activated (the t helper cells) they also proliferate into effector (the ones that will be in charge of activating) and the memory T helper cells (stored for later use). The effector T-Helper cells will then activate both B and T-cytotoxic cells to proliferate. Both of these will produce memory and effector (for B cells, it's formally known as plasma) cells. The memory cells are stored in lymph nodes or spleen for second invasion response, and the effector cells act upon the current pathogen.
The chemicals required are not necessary, as Mr. T-Rav has said before, and also the memory T cells are also not required, but they do exist.
I guess in terms of VCE biology, only memory B cells are significant. Let's just assume that naive T-helper cells and naive Cytotoxic T cells must get activated for every pathogenic invasion, and only memory B cells exist. So if a recurrence occurs, and you want the humoral response to rapidly kick in, a T-helper cell would have to encounter an APC, and this is activated. The activated will encounter one of THE MANY MEMORY B CELLS (more chance of finding one than before) which has already also internalised the antigen and presented it onto it's MHC II markers. This complex (TCR-MHC II) will activate the memory B cells to proliferate into MORE MEMORY AND PLASMA B CELLS causing an even more amplified and rapid response for the next response - which is generally why the second/third vaccinations are more effective and sought.
I guess it really depends on the context of the question, but I have never seen a VCE biol question regarding memory T cells, and I had to learn this the hard way to just relay my knowledge of memory cells onto B cells.
How do antibodies actually get to the site of infection if they are produced in the lymph node? Travel in the lymph fluid?
Also, do cytotoxic T cells travel in the lymph fluid to the infected cells?
Yes, antibodies travel in the lymph fluids and as well as the blood plasma.
Yes, cytotoxic T cells are mobile immune cells. Think of it this way, cytotoxic T cells mainly attack and destroy virally infected cells that display non-self antigens on their MHC I markers, then how would the embedded cells travel to the lymph nodes? Right, so the cytotoxic T cells must 'regulate' the body for their target cells - also think of cancerous cells, and transplanted organs, the transplanted cells would not travel to the lymph nodes, they're embedded onto the organ, so cytotoxic T cells would need to locate these themselves.
I think, not too sure though, that only
inactivated B and T cells are found in the lymph nodes. Not too sure about this though, hopefully someone else can confirm it.