Complexity_ A Guided Tour - Melanie Mitchell [82]
This cycle continues, with the new B cells that best match antigens themselves producing the most daughter cells. In short, this is a process of natural selection, in which collections of B cells evolve to have receptor shapes that will bind strongly to a target antigen. This results in a growing arsenal of antibodies that have been “designed” via selection to attack this specific antigen. This process of detection and destruction typically takes from a few days to weeks to eradicate the corresponding pathogen from the body.
There are at least two potential problems with this strategy. First, how does the immune system prevent lymphocytes from mistakenly attacking the body’s own molecules? Second, how does the immune system stop or tone down its attack if the body is being harmed too much as a result?
Immunologists don’t yet have complete answers to these questions, and each is currently an area of active research. It is thought that one major mechanism for avoiding attacking one’s own body is a process called negative selection. When lymphocytes are born they are not immediately released into the bloodstream. Instead they are tested in the bone marrow and thymus by being exposed to molecules of one’s own body. Lymphocytes that bind strongly to “self” molecules tend to be killed off or undergo “editing” in the genes that give rise to receptors. The idea is that the immune system should only use lymphocytes that will not attack the body. This mechanism often fails, sometimes producing autoimmune disorders such as diabetes or rheumatoid arthritis.
A second major mechanism for avoiding autoimmune attacks seems to be the actions of a special subpopulation of T cells called regulatory T cells. It’s not yet known exactly how these regulatory T cells work, but they do secrete chemicals that suppress the actions of other T cells. A third mechanism has been hypothesized to be the competition among B cells for a limited resource—a particular chemical named BAFF needed for B cells to survive. B cells that slip through the negative selection process and still bind strongly to self-molecules find themselves, due to their continual binding to self-molecules, in need of higher amounts of BAFF than non-self-binding B cells. Competition for this limited resource leads to the increased probability of death for self-binding B cells.
Even if the immune system is attacking foreign pathogens, it needs to balance the virulence of its attack with the obligation to prevent harm to the body as much as possible. The immune system employs a number of (mostly little understood) mechanisms for achieving this balance. Many of these mechanisms rely on a set of signaling molecules called cytokines. Harm to the body can result in the secretion of cytokines, which suppress active lymphocytes. Presumably the more harm being done, the higher the concentration of suppression cytokines, which makes it more likely that active cells will encounter them and turn off, thus regulating the immune system without suppressing it altogether.
Ant Colonies
As I described in chapter 1, analogies often have been made between ant colonies and the brain. Both can be thought of as networks of relatively simple elements (neurons, ants) from which emerge larger-scale information-processing behaviors. Two examples of such behavior in ant colonies are the ability to optimally and adaptively forage for food, and the ability to adaptively allocate ants to different tasks as needed by the colony. Both types of behavior are accomplished with no central control, via mechanisms that are surprisingly similar to those described above for the immune system.
In many ant species, foraging for food works roughly as follows. Foraging ants in a colony set out moving randomly in different directions. When an ant encounters a food source, it returns to the nest, leaving a trail made up of a type of signaling