How Our Innate and Adaptive Defenses Protect Us
Innate, or non-specific, defenses are the tools our bodies use to attack foreign invaders regardless of their ilk. Adaptive, or specific, defense is part of the lymphatic system that protects our bodies from foreign invaders.
How our innate defenses protect us
Germs can be bacteria, viruses, fungi, or other microorganisms, and other foreign particles (pollen, toxins) can be problematic. Our innate defenses target all of these.
First and foremost is our skin—the body’s largest organ and our first line of defense. Along with our other mechanical barriers, such as mucus and tears, most of the potential invaders are never even allowed entry. Should one make it into the body we have other innate strategies for our second line of defense:
- Chemical barriers
- Enzymes (in saliva, gastric juice) break down cell walls.
- Interferons block replication (especially of virus and tumor cells).
- Defensins poke large holes in cell membranes.
- Collectins group together pathogens for easier phagocytosis.
- Inflammation: Dilates blood vessels, sending more resources to the area where the pathogen was identified
- Fever: Weakens microorganisms and stimulates phagocytosis
- Natural killer cells (NKs): Secrete perforins to poke tiny holes in, or perforate, cell membranes
- Phagocytosis: Consumption of foreign invaders by specialized white blood cells
Unfortunately, the occasional pathogen makes it past these defenses so our bodies mount a targeted attack. Furthermore, if we relied solely on our innate defenses, there would be massive amounts of collateral damage to our own cells (which is responsible for many of our symptoms of illness in the first place).
How our adaptive defenses protect us
The lymphatic system mounts a two-tiered attack—cell-mediated and humoral—that targets specific pathogens.
An adaptive system minimizes collateral damage but takes time to get started. This process is dependent on molecules that stick off the surface of cells called antigens. All cells have them, unique to their variety, and that’s how our immune cells distinguish self versus non-self. A type of white blood cell called a macrophage destroys a pathogen by phagocytosis; however, it leaves the antigens intact and displays them on itself. This way, it’s one of our own cells that looks foreign searching for the matching lymphocytes to initiate our adaptive response.
There are two varieties of lymphocyte that carry out this response: T cells which mature in the thymus and B cells which mature in the bone marrow (see the connection?). The action of T cells is called cell-mediated immunity and of B cells it is called humoral immunity.
Once a macrophage finds a T cell with receptors that match its displayed antigens, they bind together. The lymphocyte, called a helper T cell, releases a chemical called interleukin-2, which activates another matching T cell. This stimulates the now cytotoxic T cell to begin proliferating (making copies of itself). These cytotoxic Ts (sometimes called killer Ts) will bind with antigens on the invader and release perforins, killing the pathogen. So only cells with this particular antigen will be targeted.
When the battle has waned, suppressor T cells signal the adaptive immune process to stop. Some T cells will remain as memory T cells once the pathogen has been defeated. This way, if it invades again, it won’t take long for the macrophage to find a match and the pathogen will be destroyed before you even show any symptoms—thus providing you immunity.
B cells, with matching receptors, will bind to the pathogen or the antigen-presenting macrophage. When the helper T cell is activated it also releases cytokines which, in turn, activate the B cell. It begins to proliferate into plasma B cells and memory B cells. The memory Bs hang around with the memory T cells in the lymph nodes for protection later. The plasma Bs begin manufacturing antibodies, which are proteins that will bind to the antigens on the pathogens. When bound with antibodies, the pathogen is now neutralized.
Since they have two binding sites, antibodies can also cause agglutination, clumping together the invaders for more efficient phagocytosis. They also can activate the complement cascade, a series of chemical reactions that can directly destroy the pathogen.
The faster we can locate the matching B and T cells, the less damage the pathogen can cause. Lymphocytes are generated with random receptor shapes and researchers argue that we all have one cell in us somewhere to match any pathogen we could possibly encounter—the issue is, can we find it before the pathogen does irreversible damage.