Once a T cell recognizes its specific peptide antigen presented on a dendritic cell or B cell, the T cell becomes activated so that it now goes on to promote an aspect of an immune response. These activated T cells are called helper T cells, although this term does not accurately describe all of their functions.

Helper T cells develop in one of two directions, depending on the cytokine environment in which they are activated. These two types are called TH1 and TH2 cells.

The TH1 cells tend to form when there is lots of strong stimulation by the phagocytized antigen and lots of activation of the innate immune system. The TH2, by contrast, tend to form with weaker, more prolonged stimulation with less activation of innate mechanisms.

We have already discussed one important role that TH1 cells perform. This is to travel around the body to macrophages that have phagocytized the antigen. The TH1 cells bind to these cells and release IFN-gamma (interferon-gamma). In the macrophage, this cytokine increases the fusion of lysosomes with phagosomes, it especially cranks up mechanisms used to kill phagocytized microbes, and it attracts macrophages.

This activation of macrophages by IFN-gamma is important for dealing with sophisticated pathogens such as those that cause tuberculosis or leprosy. These pathogens can remain alive in macrophages after phagocytosis, and indeed, they really are intracellular parasites. They can live and reproduce inside unactivated macrophages for long periods.

Why aren't macrophages always "activated"? This probably is because the killing mechanisms of macrophages and neutrophils can damage the body as well as microbes. If activation of macrophages did not require a specific immune response, they might cause far more unnecessary damage to the body than they do. Consider that in tuberculosis the damage to the body is caused by macrophages fighting the bacteria rather than by anything the bacteria release.

A second role of helper T cells is to "help" B cells respond to antigens. Many antigens cannot by themselves cause a specific B cell to divide into a clone of antibody secreting plasma cells. In addition to binding the antigen, the B also phagocytizes some of the antigen and displays peptides on MHC II molecules. An activated helper T must bind to the cell and also release appropriate cytokines. Only when this happens, can the B cell divide into a clone.

The cytokines secreted are different for different types of helper T cells, which can be either TH1 or TH2. In the case of TH1, cells in the ensuing clone tend to undergo heavy chain switching so that they produce IgG, which is a good opsonin.