The primary job of the immune system is to defend the body against infectious agents such as viruses, bacteria, fungi, and parasites.
The process is dauntingly complex.
For one thing, the immune system must tell the difference between cells that are normal parts of the body and cells that are invaders, in immunologic jargon, distinguishing between “self” and “non-self.” Somehow, the immune system can remember what every cell in your body looks like, and any cells that lack your distinctive cellular signature (for example, bacteria) are attacked.
Moreover, when your immune system does encounter a novel invader, it can even form an immunologic memory of what the infectious agent looks like, to better prepare for the next invasion, a process that is exploited when you are vaccinated with a mild version of an infectious agent in order to prime your immune system for a real attack.
Such immune defenses are brought about by a complex array of circulating cells called lymphocytes and monocytes (which are collectively known as white blood cells; cyte is a term for cells).
There are two classes of lymphocytes: T cells and B cells. Both originate in the bone marrow, but T cells migrate to mature in the thymus (hence the T), while B cells mature in the bone marrow. B cells principally produce antibodies, but there are several kinds of T cells (T helper and T suppressor cells, cytotoxic killer cells, and so on).
The T and B cells attack infectious agents in very different ways.
T cells bring about cell-mediated immunity. When an infectious agent invades the body, it is recognized by a type of monocyte called a macrophage, which presents the foreign particle to a T helper cell. A metaphorical alarm is now sounded, and T cells begin to proliferate in response to the invasion.
This alarm system ultimately results in the activation and proliferation of cytotoxic killer cells, which, as their name implies, attack and destroy the infectious agent.
It is this, the T-cell component of the immune system, that is knocked out by the AIDS virus. By contrast, B cells cause antibody-mediated immunity.
Once the macrophage–T helper cell collaboration has occurred, the T helper cells then stimulate B-cell proliferation. The main task of the B cells is to differentiate and generate antibodies, large proteins that will recognize and bind to some specific feature of the invading infectious agent (typically, a distinctive surface protein).
This specificity is critical, the antibody formed has a fairly unique shape, which will conform perfectly to the shape of the distinctive feature of the invader, like the fit between a lock and key. In binding to the specific feature, antibodies immobilize the infectious agent and target it for destruction.
There is an additional twist to the immune system.
If different parts of the liver, for example, need to coordinate some activity, they have the advantage of sitting adjacent to each other.
But the immune system is distributed throughout the circulation. In order to sound immune alarms throughout this far-flung system, blood-borne chemical messengers that communicate between different cell types, called cytokines, have evolved.
For example, when macrophages first recognize an infectious agent, they release a messenger called interleukin-1. This triggers the T helper cell to release interleukin-2, which stimulates T-cell growth (to make life complicated, there are at least half a dozen additional interleukins with more specialized roles). On the antibody front, T cells also secrete B-cell growth factor.
Other classes of messengers, such as interferons, activate broad classes of lymphocytes. The process of the immune system sorting self and non-self usually works well (although truly insidious tropical parasites like those that cause schistosomiasis have evolved to evade your immune system by pirating the signature of your own cells).
Your immune system happily spends its time sorting out self from non-self: red blood cells, part of us. Eyebrows, our side. Virus, no good, attack. Muscle cell, good guy…. What if something goes wrong with the immune system’s sorting? One obvious kind of error could be that the immune system misses an infectious invader; clearly, bad news.
Equally bad is the sort of error in which the immune system decides something is a dangerous invader that really isn’t. In one version of this, some perfectly innocuous compound in the world around you triggers an alarm reaction.
Maybe it is something that you normally ingest, like peanuts or shellfish, or something airborne and innocuous, like pollen.
But your immune system has mistakenly decided that this is not only foreign but dangerous, and kicks into gear. And this is an allergy. In the second version of the immune system overreacting, a normal part of your own body is mistaken for an infectious agent and is attacked.
When the immune system erroneously attacks a normal part of the body, a variety of horrendous “autoimmune” diseases may result. In multiple sclerosis, for example, part of your nervous system is attacked; in juvenile diabetes, it’s the cells in the pancreas that normally secrete insulin.
As we’ll see in tomorrow's post, stress has some rather confusing effects on autoimmune diseases. So far in this overview of the immune system, we’ve been concentrating on something called acquired immunity.
Suppose you’re exposed to some novel, dangerous pathogen, pathogen X, for the first time. Acquired immunity has three features.
First, you acquire the ability to target pathogen X specifically, with antibodies and cell-mediated mediated immunity that specifically recognize that pathogen. This really works to your advantage, a bullet with pathogen X’s name written on it.
Second, it takes some time to build up that immunity when you are first exposed to pathogen X, this involves finding which antibody has the best fit and generating a zillion copies of it.
Finally, while you will now be geared up to specifically go after pathogen X for a long time to come once that specific defense is on line, repeated exposure to pathogen X will boost those targeted defenses even more. Such acquired immunity is a pretty fancy invention, and it is found only in vertebrates.
But we also contain a simpler, more ancient branch of the immune system, one shared with species as distant as insects, called innate immunity. In this realm, you don’t bother with acquiring the means to target pathogen X specifically with antibodies that will be different from those that would target, say, pathogen Y.
Instead, the second any sort of pathogen hits your system, this nonspecific immune response swings into action. This generalized immune response tends to occur at the beachhead where a pathogen gets its first foothold, like your skin, or moist mucosal tissue, like in your mouth or nose.
As a first step, your saliva contains a class of antibodies that generically attack any sort of microbe that it encounters, instead of acquiring a means of targeting specific invaders.
These antibodies are secreted and coat your mucosal surfaces like an antiseptic paint. In addition, at the site of infection, capillaries loosen up, allowing cells of the innate immune response to slip out of the circulation to infiltrate the immediate area of infection.
These cells include macrophages, neutrophils, and natural killer cells, which then attack the microbe. The loosening of the capillaries also allows fluid containing proteins that can fight the invasive microbes to flow in from the circulation.
And what happens as a result of that?
The proteins fight the microbe, but the fluid also makes the area swell up, causing edema. This is your innate immune system leaping into action, causing inflammation.
This gives us a broad overview of immune function. Time to see what stress does to immunity. Naturally, as it turns out, a lot more complicated things than used to be suspected.
We will look at this in the next article
This is information was taken from the book why zebras don't get ulcers