The humoral immune response B-cells (so-called because they mature in the bone marrow) are white blood cells that work chiefly by producing soluble substances known as antibodies. Each B cell is programmed to make one specific antibody. When a B cell encounters its specific or eliciting antigen (along with various accessory cells), it differentiates into a plasma cell. The latter is essentially a factory for producing that one specific antibody. Antibodies play a crucial role in a cascade of events called the humoral immune response that ultimately leads to the destruction of some of the invading bacteria. Like all immune responses, the humoral immune response can be subdivided into activation and effector phases. The activation phase begins when invading bacteria are phagocitized by an antigen-presenting cell (APC), such as a dendritic cell or macrophage. The bacterium is digested and its antigens processed and presented in combination with the MHC Class II complex on the surface of the APC. The antigen-MHC complex is recognized by a type of immune cell called a CD4+ or helper T cell (Th). The helper T cell begins the attack by docking its antigen receptor to the displayed antigen. The docking process requires the presence of co-stimulatory molecules like B7 and CD28. After successful docking, the helper T cell releases a class of chemical messenger called cytokines. This achieves the following: it causes the helper T cells to multiply, and stimulates both the APC and the helper T cell to exchange chemical messages between themselves and with other cells of the immune system. The helper T cell also releases a cytokine called interleukin-2 (IL-2): this cytokine has a panoply of immune functions, one of which is the proliferation of lymphocytes following activation by a specific antigen. The APC releases cytokines called interleukin-1 (IL-1) and tumor necrosis factor (TNF). The latter steps up the production of IL-1 and performs many of the same functions as IL-1, including the induction of fever in Brian so that his body can assist in fighting off the bacterial infection more effectively. The proliferating helper T cells release substances that signal another type of lymphocyte, the B cell (that also specifically recognizes the antigen), to begin multiplying and differentiating into antibody-producing cells. This initiates the effector phase of the humoral immune response. The antibodies released by the B cells bind in a lock-and-key fashion to antigens on the surfaces of bacterial invaders that survived the initial attack by macrophages and bacterial products. The binding of the antibody to the bacterial antigens achieves two things: first, it makes it easier for â€œkillerâ€ cells to attack and destroy the invading bacteria by both phagocytosis and the release of other factors that can directly lyse the bacteria. Second, it activates another immune military unit called complementâ€”a group of proteins that act like the special forces of the immune defense system because their duty is to begin the lethal process of punching holes in the cell walls of the residual invading bacterial army.