AS & A Level Biology 9700: Primary vs Secondary Immune Response

A person is infected for the first time with a bacterium that is able to survive and multiply inside body cells. Doctors monitor the concentration of antibodies against this bacterium in the person's blood plasma. Several weeks after recovering, the same person is accidentally exposed to the same bacterium a second time, and their antibody concentration is monitored again.

(a) Describe how the pattern of antibody concentration in the blood plasma after the second exposure would differ from the pattern after the first exposure, and explain these differences in terms of B-lymphocytes. [4]

(b) Name the type of cell that B-lymphocytes differentiate into once activated, and state what this cell type produces. [2]

(c) T-lymphocytes are also essential in defending the body against this bacterium. Describe the different roles of T-helper cells and T-killer (cytotoxic T) cells in this response. [4]

Part (a): Comparing the primary and secondary responses

After the first exposure, the body has no B-lymphocytes already committed to this particular antigen, so there is a lag period of several days while a suitable B-lymphocyte is found, activated and allowed to divide (clonal selection and expansion). Antibody concentration then rises slowly, reaching a fairly low peak, before gradually falling again once the infection is cleared. This is the primary immune response.

During this first response, some of the activated B-lymphocytes differentiate not into plasma cells but into long-lived memory cells, which remain in the body long after the infection has gone.

On the second exposure, these memory B-lymphocytes are already present and already specific to the bacterium’s antigens. They recognise the antigen immediately and divide rapidly, producing large numbers of plasma cells much sooner. As a result, the secondary immune response has a much shorter lag period, a faster rise in antibody concentration, and reaches a much higher peak, which is also maintained for longer, compared with the primary response. This is usually fast and large enough to destroy the bacterium before the person shows any symptoms of disease.

Part (b): What activated B-lymphocytes become

Once activated, B-lymphocytes divide and differentiate into plasma cells. Plasma cells are the cells that actually produce and secrete large quantities of antibodies specific to the antigen that triggered the response.

Part (c): Roles of T-helper cells and T-killer cells

T-helper cells do not destroy the bacterium directly. Instead, once activated (by recognising the antigen, often displayed on a phagocyte’s surface), they release chemical signals (cytokines) that:

stimulate specific B-lymphocytes to divide and differentiate into plasma cells and memory cells, and
stimulate phagocytes, increasing the rate at which they carry out phagocytosis.

T-killer (cytotoxic T) cells have a different job. Because this bacterium survives and multiplies inside body cells, some of the person’s own cells become infected. T-killer cells recognise these infected body cells (via antigens displayed on their surface) and bind to and destroy them, for example by causing the infected cell’s membrane to be broken down. This prevents the bacterium hiding and multiplying further inside the body’s own cells.

Final answers

(a) The secondary response has a shorter lag, a faster rise and a much higher peak antibody concentration than the primary response, because memory B-lymphocytes (formed during the primary response) recognise the antigen immediately and rapidly produce large numbers of plasma cells.
(b) B-lymphocytes differentiate into plasma cells, which produce antibodies.
(c) T-helper cells activate B-lymphocytes (to become plasma/memory cells) and stimulate phagocytes; T-killer cells destroy the body’s own cells once they have become infected by the bacterium.