The cytokines send a message to cells, like the white blood cells called polys (polymorphonuclear leukocytes, or PMNLs), to come to help get rid of the invader. There is a crossover here with the adaptive immune system (see Section 7.2) because some of the cytokines will call for help from lymphocytes and others involve even more complex combinations of cells.

The chemokines cause a vast array of chemical responses, from something as simple as releasing histamine to the complex chemical cascade that causes clotting.

As a well-coordinated system, evolved over millions of years, the innate immune system does its best to identify, isolate, neutralize, and eliminate the foreign material. If the body needs more weapons than are available to the innate system alone, it has the capacity to call for further help: the body has evolved the additional ability to adapt itself to any new threat, threats for which the innate system has not evolved an instant response. This second level of defense is the adaptive immune response.

7.2 Adaptive (acquired) immunity

The second kind of immunity is called adaptive because it needs to learn to adapt. Acquired immunity is an older term, but the meaning is the same. The newly learned immune response is acquired by adapting to the new situation. It has to learn how to fight the invader. Adaptive immunity has to take a look at the new invader, and the mechanisms involved actually take tiny bits of it to a local lymph node. Lymph nodes are those glands that become inflamed and swollen, like those under your jaw and in your neck when you have a sore throat. Your body has lots of them scattered about, sitting quietly waiting for the adaptive immune system to bring them evidence of trouble.

Each lymph node has two possible ways of responding to these microscopic and molecular-sized pieces of foreign matter, called antigens. It can develop an antibody (a kind of custom-made protein that circulates in the blood to find, match up with, and neutralize invaders like viruses) or it can train certain types of specialized white blood cells called lymphocytes to recognize, kill, or immobilize the invader. That takes time, sometimes just a few days but often a week or more if the immune system has never “seen” this invader before. The adaptive immune system is always slower to get going than the innate system when something new shows up. Even when it has already learned (from prior exposure) what the invader is, it may take a day or two to get up to speed, but some responses are almost instant. Think about peanut or penicillin allergy, which can onset in minutes with devastating effects. A longer delay is to be expected for some invaders if the original exposure was a long time ago. The innate system is faster because it doesn’t need to process the invading materials again to figure out what the material or foreign invader is. The innate immune system already knows how to react.

Whatever the response of the immune systems, the results are always after the fact in acne. There has to be a trigger. A small population of an organism like P. acnes or Malassezia sitting quietly down in the follicular duct, out of reach of the innate and adaptive immune systems, is not by itself enough to cause acne. If it were, we would all have acne, all the time. The same is true of other things found naturally in the follicular units of the folliculopilosebaceous units (FPSUs). Malassezia live on all of us, as do P. acnes and Demodex and many hundreds (no exaggeration!) of other kinds of organisms. If the “acne bacillus” (P. acnes) were the real primary cause of acne vulgaris, all we would need to do is eliminate P. acnes. It has taken over 60 years to realize that killing P. acnes is not enough to clear this disease. We are just now learning that our attempts may have done more harm than good [3, 4].

7.3 Inflammation as the primary acnegen

A tremendous amount of work has been done looking at the cause of inflammation in the acnes and the mechanisms by which inflammation is produced [5]. This has led to the identification of a large number of inflammatory mediators (messengers) present in various stages and forms of the disease. These are triggered by the cytokines, the group of chemicals produced by the inflammatory cells of both immune systems. Some of these molecules are cytokines all by themselves; others trigger additional cytokine and chemokine activity. Cytokines are basically messengers, rather as hormones are messengers. Chemokines are specialized cytokines that tell specific cells, usually lymphocytes, what to do and where to go. Usually the message is that the cell is needed elsewhere to do battle, and to come quickly. But nature likes a balance, so there are other chemokines and cytokines that are inhibitory.

Related posts:

The handouts Exogenous acnegens and acneform eruptions Appendices The acne hormones Management The three acnes and their impact

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