When someone is sick with an infection they often experience swelling of their lymph nodes, or lymphadenopathy. This is colloquially referred to as having "swollen glands" and is usually apparent in the neck region. What is going on when this phenomenon occurs is that immune cells are basically congregating in the lymph nodes and undergoing something akin to a pep rally before they face the invader. These conglomerations occur at sites known as follicles in which germinal centers are formed. The result of this process is an army of elite soldiers armed to the teeth with antibodies exquisitely targeted to the microbe that set off the immune system alarms. When your "glands" feel sore it's basically because the equivalent of troop mobilization is occurring. This massive oversimplification is the standard text book version of the events.
I recently listened to a fascinating lecture by Pitt's immunology chairman, Dr. Mark Shlomchik on this topic -- specifically when it doesn't occur quite as is written in the textbook. The infection that his research group has described an alternate pathway of immune response for is Salmonella. Salmonella is a major infectious disease threat that is responsible for thousands of cases of foodborne illness yearly. One of the intriguing facets of Salmonella is that it can, in certain contexts, turn humans into carriers who chronically shed the bacteria (this is well known with the typhoid species of Salmonella but can occur with the gastroenteritis causing members of the group as well).
It had been known that Salmonella infections produce what is known as an extrafollicular immune response with germinal center formation delayed by one month. This response produces antibodies that are directed against Salmonella. These antibodies are specific to Salmonella but are not the sharpest tools and have a lower affinity than a full-fledged graduate of the germinal center.
Another interesting event that occurs is the germinal centers form only when the bacterial load falls through progression of the infection or via antibiotic therapy.
What could be the purpose of this alternative pathway? What is the evolutionary driver here?
A couple of hypotheses: if Salmonella "wants" to have us as its carriers it has to do two things: 1) not kill us and 2) not be killed by us. Could the suppression of germinal centers -- keeping the immune system's schools closed -- be a way to accomplish that by prompting a less elite team of the immune system to respond? This 2nd string team could keep the bacteria out of the bloodstream and somewhat in check (but not completely).