Complexity_ A Guided Tour - Melanie Mitchell [81]
The main problem facing the immune system is that it doesn’t know ahead of time what pathogens will invade the body, so it can’t “predesign” a set of lymphocytes with receptors that will bind strongly to just the right shapes. What’s more, there are an astronomical number of possible pathogens, so the immune system will never be able to generate enough lymphocytes at any one time to take care of every eventuality. Even with all the many millions of different lymphocytes the body generates per day, the world of pathogens that the system will be likely to encounter is much bigger.
Here’s how the immune system solves this problem. In order to “cover” the huge space of possible pathogen shapes in a reasonable way, the population of lymphocytes in the body at any given time is enormously diverse. The immune system employs randomness to allow each individual lymphocyte to recognize a range of shapes that differs from the range recognized by other lymphocytes in the population.
In particular, when a lymphocyte is born, a novel set of identical receptors is created via a complicated random shuffling process in the lymphocyte’s DNA. Because of continual turnover of the lymphocyte population (about ten million new lymphocytes are born each day), the body is continually introducing lymphocytes with novel receptor shapes. For any pathogen that enters the body, it will just be a short time before the body produces a lymphocyte that binds to that pathogen’s particular marker molecules (i.e., antigens), though the binding might be fairly weak.
Once such a binding event takes place, the immune system has to figure out whether it is indicative of a real threat or is just a nonthreatening situation that can be ignored. Pathogens are harmful, of course, because once they enter the body they start to make copies of themselves in large numbers. However, launching an immune system attack can cause inflammation and other harm to the body, and too strong an attack can be lethal. The immune system as a whole has to determine whether the threat is real and severe enough to warrant the risk of an immune response harming the body. The immune system will go into high-gear attack mode only if it starts picking up a lot of sufficiently strong binding events.
The two types of lymphocytes, B and T cells, work together to determine whether an attack is warranted. If the number of strongly bound receptors on a B cell exceeds some threshold, and in the same time frame the B cell gets “go-ahead” signals from T cells with similarly bound receptors, the B cell is activated, meaning that it now perceives a threat to the body (figure 12.3). Once activated, the B cell releases antibody molecules into the bloodstream. These antibodies bind to antigens, neutralize them, and mark them for destruction by other immune system cells.
The activated B cell then migrates to a lymph node, where it divides rapidly, producing large numbers of daughter cells, many with mutations that alter the copies’ receptor shapes. These copies are then tested on antigens that are captured in the lymph node. The cells that do not bind die after a short time.
FIGURE 12.3. Illustration of activation of a B cell via binding and “go-ahead” signal from a T cell. This signal prompts the B cell to produce and release antibodies (y-shaped molecules).
The surviving copies are unleashed into the bloodstream, where some of them encounter and bind to antigens, in some cases more strongly than did their mother B cell. These activated daughter B cells