Immune SystemPosted 4 years ago under Uncategorized
Every moment of every day your immune system remains on high alert, fighting off foreign invaders and protecting the homeland, your body. This highly complex system includes many parts of the bodytissues, organs, cellsand it not only fights the good fight, it retains a memory of each major battle and the foe it defeated so the next attack is more easily won.
The immune system is designed to battle four types of pathogens: bacteria, viruses, fungi, and parasites while it continues its vigilant search for dead and mutated cells and rids the body of them.
Barriers to Invaders
Our first line of defense begins with the skin, mucous membranes, ear wax, stomach acid, and friendly bacteria.
In most places, our skin is dry and slightly acidic. This is not a friendly environment for pathogens. Those that do try to take up residence on our skin have to battle friendly bacteria that will fight off a pathogen to maintain their claim. That works well if we aren’t foolish enough to use anti-bacterial soap that kills off the friendly bacteria. And this is the reason you will find you have less body odor if you stop using antibacterial soaps and switch to organic soaps. Your friendly bacteria will thank you and they will go back to fighting off their smelly cousins.
The hairs in our nose, ear wax, and vaginal secretions are all defenses the body uses to protect and defend against invaders. Mucous membranes are covered with a film of mucous that is either coughed up, sneezed out, or swallowed. Coughing and sneezing rids the body of many trapped pathogens (though it spreads them to other people) and swallowing destroys many more due to stomach acid. All of these barriers make up the first line of defense. The innate immune system with its non-specific response, holds the second line.
Non-specific Response–The Innate Immune System
We are born with an innate immune system. This second line of defense is called into play when a pathogen breaches one of the body’s barriers. For example, if we step on something sharp, bacteria enter the body through the cut and rapidly multiply, using whatever food and resources the body provides. Every twenty minutes, these bacteria double in number until they reach a certain point when the changes they are causing around them begin to damage the body. This signals the immune system to respond, and the first responders, the phagocytes, wage war.
The first phagocytes on the scene are the huge macrophanges. Their claim to fame is that each macrophange is able to swallow and destroy up to 100 or more bacteria. Most of the time this response is all that is needed–the macrophanges save the day single handedly. But if their efforts were not enough to clean up all of the invaders, the macrophanges call for a second phagocyte, nutrophiles, to join the battle as they order the blood vessels to release fluid into the area. The fluid causes inflammation, which is helpful to the immune response, though it is sometimes painful.
Nutrophiles erect barriers to trap and kill bacteria, and they are great killers. Unfortunately nutrophiles are indiscriminate killers. When they go on the rampage, they kill healthy human cells along with invading bacteria. They can be so damaging to the body, they automatically self destruct within five days.
If the invasion has not been stopped, a third phagocyte, the dentritic cell, comes into play. The dentritic cell rips a bacterium to pieces and places these pieces of the enemy along its outer layer (these pieces are called antigens) and it determines whether the invader is a bacteria or a virus. If the pathogen is a virus, the dentritic cell releases interferon that attaches to neighboring healthy cells and aids them in fending off attack. The dentritic cell then goes searching for reinforcements, calling the lymphocytes into play.
Specific Response–Adaptive Immunity
Our bodies produce billions of different kinds of T-cells. The dentritic cell searches for the one T-cell out of the billion whose structure matches the antigens displayed on its surface–those pieces of the ripped apart bacterium. Each T-cell is has one single antigen. When the dentritic cell finds the specific T-cell whose receptors match the displayed antigen, the antigen and receptor fit together like a lock and a key or two puzzle pieces. Then the magic begins. The T-cell quickly clones itself, creating an army to fight the pathogen. Some of these T-cells become memory cells. They stay behind, remembering the specific pathogen to be ready for a faster response if there is a future invasion. A group of the new T-cells travel to the lymph nodes to activate the B-cells, while another group goes directly to the main battlefield.
The immune system may release hormones that trigger a fever and a reduction of iron in the blood. The increased warmth and decreased iron slow the reproduction rate of many bacteria while increasing the activity of the phagocytes. Fever also increases interferon production if the body is fighting a virus.
When the T-cells find the B-cells that match up (once again the puzzle pieces must fit!), the B-cells start rapidly multiplying. B-cells produce B memory cells and plasma cells that produce antibodies. Millions of antibodies saturate the body through the bloodstream. Antibodies are protein structures that bind to the surface of the invading pathogen. They immediate kill and disable bacteria as they provide a structure to aid other killer cells attempting to attach to the pathogen. Once again, macrophages eat up the pathogens.
This is a very simplified overview of how the immune system attacks invading pathogens. In actuality, there are many more types of cells that make up the immune system. So much of the body works together: the circulatory system, the lymphatic system, our bone marrow, our skin, mucous, stomach acid, etc. Everything from the brain to helpful bacteria fight the good fight. And though it makes mistakes and doesn’t always work properly, without an immune system, we would quickly die.
How Your Immune System Works. Harvard Health Publications (c) 2010