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Illustration shows the steps involved in one method of activating a humoral or cell-mediated immune response. The first step shows a bacterium being engulfed by a macrophage. Lysosomes fuse with the vacuole containing the bacteria. The bacterium is digested. Antigens from the bacterium are attached to a MHC II molecule and presented on the cell surface. The next step shows the activation of a helper T cell. A T cell receptor on the surface of the T cell binds the MHC II-antigen complex presented by the macrophage (also called an antigen-presenting cell). As a result, the helper T cell becomes activated and both the helper T cell and macrophage cell release cytokines. The cytokines induce the helper T cell to clone itself. The cloned helper T cells release different cytokines that activate B cells, causing them to clone and begin the humoral immune response; and other T cells, turning them into cytotoxic T cells and beginning the cell-mediated immune response.
A helper T cell becomes activated by binding to an antigen presented by an APC via the MHCII receptor, causing it to release cytokines. Depending on the cytokines released, this activates either the humoral or the cell-mediated immune response.

Immunological memory

The adaptive immune system has a memory component that allows for a rapid and large response upon reinvasion of the same pathogen. During the adaptive immune response to a pathogen that has not been encountered before, known as the primary immune response    , plasma cells secreting antibodies and differentiated T cells increase, then plateau over time. As B and T cells mature into effector cells, a subset of the naïve populations differentiates into B and T memory cells with the same antigen specificities ( [link] ). A memory cell    is an antigen-specific B or T lymphocyte that does not differentiate into an effector cell during the primary immune response, but that can immediately become an effector cell on reexposure to the same pathogen. As the infection is cleared and pathogenic stimuli subside, the effectors are no longer needed and they undergo apoptosis. In contrast, the memory cells persist in the circulation.

Art connection

Illustration shows activation of a B cell. An antigen on the surface of a bacterium binds the B cell receptor. The B cell engulfs the antigen, and presents the antigen on its surface in conjunction with a MHC II receptor. A T cell receptor and CD4 molecule on the surface of a helper T cell recognize the antigen–MHC II complex and activate the B cell. The B cell divides and turns into memory B cells and plasma cells. Memory B cells present antigen-specific antibody on their surface. Plasma B cells excrete antibodies.
After initially binding an antigen to the B cell receptor, a B cell internalizes the antigen and presents it on MHC class II. A helper T cell recognizes the MHC class II- antigen complex and activates the B cell. As a result, memory B cells and plasma cells are made.

The Rh antigen is found on Rh-positive red blood cells. An Rh-negative female can usually carry an Rh-positive fetus to term without difficulty. However, if she has a second Rh-positive fetus, her body may launch an immune attack that causes hemolytic disease of the newborn. Why do you think hemolytic disease is only a problem during the second or subsequent pregnancies?

If the pathogen is never encountered again during the individual’s lifetime, B and T memory cells will circulate for a few years or even several decades and will gradually die off, having never functioned as effector cells. However, if the host is re-exposed to the same pathogen type, circulating memory cells will immediately differentiate into plasma cells and T C cells without input from APCs or T H cells. This is known as the secondary immune response    . One reason why the adaptive immune response is delayed is because it takes time for naïve B and T cells with the appropriate antigen specificities to be identified, activated, and proliferate. On reinfection, this step is skipped, and the result is a more rapid production of immune defenses. Memory B cells that differentiate into plasma cells output tens to hundreds-fold greater antibody amounts than were secreted during the primary response ( [link] ). This rapid and dramatic antibody response may stop the infection before it can even become established, and the individual may not realize they had been exposed.

Bar graph plots antibody concentration versus primary and secondary immune response. During the primary immune response, a low concentration of antibody is produced. During the secondary immune response, about three times as much antibody is produced.
In the primary response to infection, antibodies are secreted first from plasma cells. Upon re-exposure to the same pathogen, memory cells differentiate into antibody-secreting plasma cells that output a greater amount of antibody for a longer period of time.

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Source:  OpenStax, Concepts of biology. OpenStax CNX. Feb 29, 2016 Download for free at http://cnx.org/content/col11487/1.9
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