Re: how does a suppressor cell stop an immune answer?

The cytotoxic/suppressor component of T cells are characterized by 
the presence of CD8 antigen on their surface. These cells recognize 
antigen presented on the surface as antigenic peptide complexed 
with class I MHC molecules, which are classically known as 
transplantation antigens because genetic differences in these 
molecules induce rapid graft rejection. Class I molecules are found 
on virtually all cells and are specialized to present antigen 
synthesized endogenously, within host cells, such as cell associated 
viral or tumor antigens. In this manner, the cytotoxic (killer) T cells 
bind to cells that express the antigen to which they react (usually virus 
or tumor) and kill those cells through the release of cytokines (also 
called lymphokines)

T suppressor cells act to inhibit T helper cells from function, thereby 
preventing the initiation of the response. They can also act directly on 
B cells or effector T cells to inhibit their activity, but this is probably 
less important than their inhibition of T helper cell activity. Some 
autoimmune diseases (immune responses against one's own 
tissues) are thought result from defects in T suppressor cell function. 

The suppressor situation has become somewhat complicated, since 
some suppression can be explained by the reciprocal inhibition of T 
helper 1 (Th1) and T helper 2 (Th2) cells. For example, addition of 
Th1 cells to a culture in which antibody synthesis was the measure of 
T cell help would look like T suppressor cell activity. Indeed, antibody 
synthesis would be inhibited in a situation where it would be 
expected without the addition of Th1 cells. However, one would also 
see an increase in delayed hypersensitivity if it were also measured 
in the system.

Both T and B memory cells are cells that have undergone 
differentiation and clonal expansion. These cells continue to circulate 
and upon exposure to antigen will undergo rapid clonal expansion to 
provide a secondary immune response. This process ensures that 
the second response is much faster than the primary immune 
response to a foreign antigen.