Objective 39: Explain why development of self-tolerance is important
Objective 40: Describe cellular and non-cellullar immunity
Objective 41: Summarize developmnet and maturation of B- and T- lymphocytes
Objective 42: Distinguish non-specific, innate, or natural immunity from specific or acquired immunity
I found this MP3 tutor session on our textbooks website under chapter 19. I was trying to figure out a way to just upload the audio version of the tutor session so I didn't have to include the whole passage (since the audio version was about 17 mins by itself), but I've spent the last 45 minutes trying to figure out how to get it on this site and I gave up. When I came across this session, it went over five of our objectives which was very beneficial to me. Listening to the session helped me learn the information because they describe the information accurately, but they also shorten the information into easier language for me to understand. It's hard to grasp the concepts of the different types of immunity, or about the B and T lymphocytes because the book describes them in lengthy detail in scientific words that make it difficult for me to actually know what they are trying to tell me. This passage not only sums up all of these objectives, but it relates the immunities and lymphocytes to real life situations like when they talked about the kid eating someone else's gum or how vaccines help our bodies make antibodies. By this passage giving everyday examples, It helps me relate all these objectives to real life and the information stuck better. This tutor session was more helpful than reading the textbook alone.
Our body is equipped with some of the most amazing defenses we could ask for. Our body is like kind of like a military force, always there to protect us and ward off any dangers that may come our way. Our body is equipped with mechanical barriers ( such as skin) and chemical barriers in charge of destroying those harmful pathogens that come our way. The type of pathogens that our bodies are faced with are bacteria, viruses, fungi and protists. Our skin is a highly effective first line of defense in warding off those pesky pathogens, but when our skin fails to get the job done thats when innate immunity and adaptive immunity come into play. These two immunities, along with cellular and non cellular immunity, work closely together to get rid of the pathogen that threatens to distrupt our bodies normal functioning. With all of this hard work going on, it is very important that our bodies develop a sense of self-tolerance. In other words, it is very important for our body recognize its own antigens and refrain from attacking them. If they do attack them, this is when an auto-immune disease takes place and causes our immune system to attack its own antigens as well as foreign ones. I know how how important self-tolerance is first hand because my mother suffers from a rare auto-immune disease and she struggled for the last few years trying to get help so her body would stop attacking its own antigens, causing her to always be sick from the slightest things. Its an ongoing battle, but thankfully she is winning at this moment in time.
Along with this MP3 tutor session, I came across this slideshow called Defending Against Infection that went along with objective 36 and helped summarize how the body defends itself from these harmful pathogens.
Pearson welcomes you to MP3 Tutor Sessions for Anatomy and Physiology.Differences Between Innate and Adaptive Immunity
Section 1: Tough Topics
HIV, SARS, Ebola virus, STDs. They are all around us. Sometimes it feels like we are losing a war against microbes. But let's take stock for a moment. Little kids play outside all day long. They pick up frogs, eat bugs, and chew someone else's gum and they are almost always fine. In most cases, the worst thing that happens is that they get a runny nose. The fact is that even though you are exposed to millions of different microbes everyday, you seldom get sick. All because of the vigilance of your immune system.
In this tough topics section, we will discuss the two major parts of the immune system: innate immunity and adaptive immunity. Innate immunity is the immunity you are born with, and adaptive immunity, also called specific immunity, is acquired through exposure to pathogens throughout your lifetime. Pathogens can be bacteria, viruses, or parasites. Basically anything that disrupts homeostasis. We will begin by defining immunity, highlighting the key players--the white blood cells. In the next section we will discuss innate immunity. We will finish the discussion with a description of adaptive immunity. Let's get started.
The immune system is composed of millions of molecules and cells working to destroy anything identified as not being part of you. The foot soldiers in this war on microbes are the white blood cells. Let's look at the various types.
White blood cells are large, translucent blood cells with an arsenal of organelles. All white blood cells are leukocytes. Leukocytes form in the bone marrow. After their formation they follow different, preprogrammed destinies to dispose of microbes by engulfing them, lysing them, or synthesizing products to help destroy them.
White blood cells can be divided into different subsets based on the type of immunity that is triggered for defense. Monocytes, which become macrophages, neutrophils and eosinophils, are all considered phagocytes. Phagocytes destroy pathogens by engulfing them in vesicles, internalizing them, breaking them down, and spitting out the remains. Another important subset of white blood cells is the lymphocytes, which include B cells, T cells, and natural killer cells. Lymphocytes are more subtle assassins. They poke holes in cells, injecting enzymes that kill the microbe, or they produce antibodies that smother the intruder, targeting it for destruction.
Phagocytes and natural killer cells are important members of innate immunity, while B cells and T cells are active members of specific immunity. Let's discuss innate immunity and the leukocytes that play an important role in its success at stopping pathogens.
Innate immunity is your first line of defense. This defense begins with your skin and mucous membranes. But what happens if you get a cut that breaches the skin's defenses, and it gets infected? At that point, the internal defenses take over, using immune cells and chemicals to attack invading pathogens. We will discuss the cellular defenses first.
Innate immunity relies on two broad categories of cells for defense: phagocytes and natural killer cells. As we discussed, phagocytes destroy pathogens by engulfing them in vesicles, after which they break them down and spit out the remains.
Natural killer, or NK, cells are derived from lymphocytes. They migrate over all the tissues of the body looking for and destroying abnormal cells like cancer cells and virally-infected cells. The NK cells can recognize these cells as different because they lack the appropriate signals identifying the cell as being "you." This lack of "you" traits is usually in the form of a tag such as a specific cell membrane receptor or the presence of unidentified sugars that belong to the pathogen.
Unlike phagocytes that engulf their prey, NK cells come in direct contact with the target cell, poke holes in the membrane, and inject it with toxic chemicals. This type of attack is very similar to another lymphocyte we will talk about later called the T cell. NK cells also secrete potent chemicals that act like flare guns to augment the inflammatory response. This flare gun signals macrophages, other lymphocytes and some of the chemical defenses to help combat the infection.
Okay, we've discussed the various cellular responses to microbial attacks. Now let's talk about how your immune system wages chemical warfare on invading pathogens. The arsenal of chemical weapons includes the inflammatory response, the secretion of antimicrobial proteins, and fever. The inflammatory response kicks into gear when you suffer from some physical injury, such as getting kicked. It also becomes activated by injury from intense heat, irritating chemicals, or infection from viruses, bacteria, or fungi. Let's look more closely at the inflammatory response.
At some point, you have probably experienced an infected cut. You knew it was inflamed because it was red, swollen, hot, and painful--the four signs of inflammation. Inflammation begins with a warning siren made up of chemicals secreted by the injured tissues. These chemicals act as a homing beacon for macrophages and mast cells to migrate to the injury site. Macrophages start engulfing bacteria and debris while mast cells secrete histamine. Histamine is a very potent inflammatory chemical that causes the symptoms we associate with allergies, like a runny nose, hives, and watery eyes. Histamine causes the surrounding arterioles to dilate. This brings warm blood to the area and increases the local temperature. In addition to this, the histamine increases permeability of the local capillaries to promote exudation, the leaking of capillary fluid into the tissues, carrying antibodies and clotting factors with it. This is what causes the swelling. And the swelling in turn presses on nerves, causing the pain.
If the injury is badly infected, pus can develop. This creamy-yellow substance is a mixture of dead white blood cells, ruined tissue, and living and dead pathogens. If the area is very badly infected, it can be walled off from the rest of the body by scar tissue. The scar tissue is made from collagen fibers and can form an abscess. At this point, the pus and fluid build-up within the abscess will have to be drained before the injured area will heal properly.
Besides the inflammatory response, innate immunity also includes antimicrobial proteins. These antimicrobial proteins include the interferons and complement proteins. Interferons are proteins secreted by infected cells in a last ditch effort to save adjacent uninfected cells from viral attack. Interferons diffuse into adjacent cells and cause the still healthy cell to synthesize proteins that stop viral protein synthesis and degrade the viral RNA.
The complement system, usually just called complement, includes a group of more than twenty plasma proteins that circulate in an inactive state. Their function is to "jack up" the response by the immune system to its highest active status. It does this through chemical mediators that enhance every aspect of immunity—hence the name complement. Complement can be activated either by antibodies or when certain complement factors interact with microbial molecules and target them for destruction.
The final component of innate immunity is fever. While inflammation is a localized response, fever is a systemic response—that means it affects your whole body. Fever usually occurs if the infection is widespread and internal. Fever is an increase in the body temperature that occurs when your internal thermostat—regulated in your hypothalamus—is reset to a higher point. The reason your thermostat gets reset is because leukocytes and macrophages secrete chemicals called pyrogens. Low and moderate fever is an effective immune response; it speeds up the body's metabolic rate, which in turn accelerates the repair process.
Let's summarize what we have discussed so far. Immunity is your body's defense against pathogens. There are two types of immunity: innate and adaptive. Innate immunity is the immunity you are born with and includes both physical barriers such as the skin and internal defenses. Internal defenses include cellular defenses performed by phagocytes and natural killer cells, as well as inflammation, antimicrobial proteins, and fever.
Now let's talk about adaptive or specific immunity.
Adaptive immunity is the body's specific immunity. Unlike your innate immunity which is nonspecific and attacks anything it recognizes as foreign, damaged or unknown, adaptive immunity is very choosy. Adaptive immunity will only attack specific threats. Adaptive immunity is carried out by two types of lymphocytes, the B cells and the T cells. Like all blood cells, the lymphocytes first develop in the bone marrow. B cells stay and mature there. Immature T cells migrate to the thymus where they mature. These lymphocytes become immunocompetent and have to be self-tolerant. In other words, these cells have to be able to evoke an immune response and make sure that response isn't against your own normal cells.
Adaptive immunity has three underlying traits. First, it is specific. It recognizes and attacks only specific pathogens. Secondly, it is systemic. This is a widespread reaction, not limited to a localized region of the body. Lastly, adaptive immunity has memory. In many cases, once you are exposed to a virus, your body remembers and you become resistant to reinfection.
Adaptive immunity has two components: humoral immunity and cellular or cell-mediated immunity. Humoral immunity produces antibodies. Cell-mediated immunity relies on a particular lymphocyte called a T cell, rather than antibodies, to defend the body. Both of these components work by recognizing antigens. Let's talk about antigen recognition next.
Antigens are cell surface proteins. You, as an individual, have a unique set of self-antigens called your Major Histocompatibility Complex, or MHC. However, when cells are infected by a pathogen or are abnormal, like a cancer cell, non-self antigens are presented. The change can be initiated by the infectious agent or because the cell no longer responds to normal control signals. It is these changed cells that the humoral and cell-mediated immune processes recognize and destroy.
There are two classes of MHC proteins. Class 1 MHC proteins are on all the cells of your body. Class 2 MHC proteins are only found on specific cells of the adaptive immune response. Let's talk in more detail about the humoral and cell-mediated immune responses next.
Humoral immunity works like this. The B cells are formed in the red bone marrow where they mature and become immunocompetent. These are the cells responsible for producing antibodies against foreign antigens. Once a B cell is exposed to a foreign antigen it becomes activated and undergoes cell division. One of the daughter cells becomes a memory cell. That is why you can be resistant to reinfection of say, chicken pox, once you have been exposed. These memory cells may live up to 20 years or longer. The other daughter cell has a different fate. It will continue to divide and produce an army of B cells. Each B cell will go on to produce antibodies that are secreted into general circulation to seek out and destroy the antigen they were exposed to. Antibodies mark the target cells for destruction by causing them to clump together, smothering their surfaces, acting like beacons for complement proteins and phagocytes and causing toxic cell by-products to precipitate out of solution.
But there are limitations to their defenses. B cells can only detect an obvious threat, like bacteria floating around in your blood. They can't detect viruses and bacteria that infiltrate the cells. For this, another defense is mounted by the cell-mediated arm of immunity. Cell-mediated immunity has a more direct approach. Let's look at that next.
T cells are formed in the red bone marrow, and then migrate to the thymus where they become immunocompetent. T cells recognize infected or abnormal cells differently than B cells. They recognize antigens that have been processed into fragments and sent to the cell surface. Once it detects one of these fragments, the T cell binds to it and becomes active. The T cell then divides like the B cell, with one daughter cell becoming a memory T cell and the other the cytotoxic T cell that targets cells with that antigen fragment for destruction "up close and personal." The cytotoxic T cell binds to the foreign cell, pokes holes in it, injects enzymes and toxins into it, and breaks up the cell membrane.
Let's summarize the difference in your humoral and cell-mediated immune responses. The B cells are responsible for the humoral response. This response involves identification of foreign antigens. This activates the B cells to produce antibodies specific for the targeted antigen. They attack and destroy these antigens or antigen-producing cells by clumping, lysing, and precipitating them out of the blood. So humoral immunity can be considered an indirect attack on pathogens by the B cells. In contrast, the T cells initiate a specific immunity response in which the T cell is presented with antigen fragments that cause the T cell to become immunocompetent. Once this occurs, the T cells destroy the unwanted cell by poking holes in the membrane and injecting enzymes to break the targeted cell into pieces.
With adaptive immunity, the first time the B and T cells are exposed to a new antigen, the response is slow. So you get really sick. This is called the primary response. The second time you are exposed, the B and T memory cells have a record of this antigen or antigens like it. So they can respond and divide really quickly, acting like a first strike against the developing infection. That is why you don't get sick when exposed at a later time. This is called the secondary response. So, when you are exposed to chicken pox the first time, you get an intense illness. But you don't get it a second time because your B and T cells can very quickly replicate and destroy the pathogen. That is how vaccines work. A vaccine initiates a primary response at low levels, deliberately introducing the B cells to the antigens. The B cells produce antibodies against the antigens and form a memory of these antigens. Then the next time you get infected, the B cells can respond quickly because they already know to attack the pathogen.
Let's summarize adaptive immunity. It is specific and self-tolerant. B and T cells are the major players. Upon exposure to an unknown antigen, they produce memory cells. B cells produce antibodies, which mount an indirect attack on the infected cells and noncellular pathogens. T cells attack directly to kill the cells by poking holes into them and injecting cytotoxic compounds.
That's the end of this section.
In this tough topics section, we will discuss the two major parts of the immune system: innate immunity and adaptive immunity. Innate immunity is the immunity you are born with, and adaptive immunity, also called specific immunity, is acquired through exposure to pathogens throughout your lifetime. Pathogens can be bacteria, viruses, or parasites. Basically anything that disrupts homeostasis. We will begin by defining immunity, highlighting the key players--the white blood cells. In the next section we will discuss innate immunity. We will finish the discussion with a description of adaptive immunity. Let's get started.
The immune system is composed of millions of molecules and cells working to destroy anything identified as not being part of you. The foot soldiers in this war on microbes are the white blood cells. Let's look at the various types.
White blood cells are large, translucent blood cells with an arsenal of organelles. All white blood cells are leukocytes. Leukocytes form in the bone marrow. After their formation they follow different, preprogrammed destinies to dispose of microbes by engulfing them, lysing them, or synthesizing products to help destroy them.
White blood cells can be divided into different subsets based on the type of immunity that is triggered for defense. Monocytes, which become macrophages, neutrophils and eosinophils, are all considered phagocytes. Phagocytes destroy pathogens by engulfing them in vesicles, internalizing them, breaking them down, and spitting out the remains. Another important subset of white blood cells is the lymphocytes, which include B cells, T cells, and natural killer cells. Lymphocytes are more subtle assassins. They poke holes in cells, injecting enzymes that kill the microbe, or they produce antibodies that smother the intruder, targeting it for destruction.
Phagocytes and natural killer cells are important members of innate immunity, while B cells and T cells are active members of specific immunity. Let's discuss innate immunity and the leukocytes that play an important role in its success at stopping pathogens.
Innate immunity is your first line of defense. This defense begins with your skin and mucous membranes. But what happens if you get a cut that breaches the skin's defenses, and it gets infected? At that point, the internal defenses take over, using immune cells and chemicals to attack invading pathogens. We will discuss the cellular defenses first.
Innate immunity relies on two broad categories of cells for defense: phagocytes and natural killer cells. As we discussed, phagocytes destroy pathogens by engulfing them in vesicles, after which they break them down and spit out the remains.
Natural killer, or NK, cells are derived from lymphocytes. They migrate over all the tissues of the body looking for and destroying abnormal cells like cancer cells and virally-infected cells. The NK cells can recognize these cells as different because they lack the appropriate signals identifying the cell as being "you." This lack of "you" traits is usually in the form of a tag such as a specific cell membrane receptor or the presence of unidentified sugars that belong to the pathogen.
Unlike phagocytes that engulf their prey, NK cells come in direct contact with the target cell, poke holes in the membrane, and inject it with toxic chemicals. This type of attack is very similar to another lymphocyte we will talk about later called the T cell. NK cells also secrete potent chemicals that act like flare guns to augment the inflammatory response. This flare gun signals macrophages, other lymphocytes and some of the chemical defenses to help combat the infection.
Okay, we've discussed the various cellular responses to microbial attacks. Now let's talk about how your immune system wages chemical warfare on invading pathogens. The arsenal of chemical weapons includes the inflammatory response, the secretion of antimicrobial proteins, and fever. The inflammatory response kicks into gear when you suffer from some physical injury, such as getting kicked. It also becomes activated by injury from intense heat, irritating chemicals, or infection from viruses, bacteria, or fungi. Let's look more closely at the inflammatory response.
At some point, you have probably experienced an infected cut. You knew it was inflamed because it was red, swollen, hot, and painful--the four signs of inflammation. Inflammation begins with a warning siren made up of chemicals secreted by the injured tissues. These chemicals act as a homing beacon for macrophages and mast cells to migrate to the injury site. Macrophages start engulfing bacteria and debris while mast cells secrete histamine. Histamine is a very potent inflammatory chemical that causes the symptoms we associate with allergies, like a runny nose, hives, and watery eyes. Histamine causes the surrounding arterioles to dilate. This brings warm blood to the area and increases the local temperature. In addition to this, the histamine increases permeability of the local capillaries to promote exudation, the leaking of capillary fluid into the tissues, carrying antibodies and clotting factors with it. This is what causes the swelling. And the swelling in turn presses on nerves, causing the pain.
If the injury is badly infected, pus can develop. This creamy-yellow substance is a mixture of dead white blood cells, ruined tissue, and living and dead pathogens. If the area is very badly infected, it can be walled off from the rest of the body by scar tissue. The scar tissue is made from collagen fibers and can form an abscess. At this point, the pus and fluid build-up within the abscess will have to be drained before the injured area will heal properly.
Besides the inflammatory response, innate immunity also includes antimicrobial proteins. These antimicrobial proteins include the interferons and complement proteins. Interferons are proteins secreted by infected cells in a last ditch effort to save adjacent uninfected cells from viral attack. Interferons diffuse into adjacent cells and cause the still healthy cell to synthesize proteins that stop viral protein synthesis and degrade the viral RNA.
The complement system, usually just called complement, includes a group of more than twenty plasma proteins that circulate in an inactive state. Their function is to "jack up" the response by the immune system to its highest active status. It does this through chemical mediators that enhance every aspect of immunity—hence the name complement. Complement can be activated either by antibodies or when certain complement factors interact with microbial molecules and target them for destruction.
The final component of innate immunity is fever. While inflammation is a localized response, fever is a systemic response—that means it affects your whole body. Fever usually occurs if the infection is widespread and internal. Fever is an increase in the body temperature that occurs when your internal thermostat—regulated in your hypothalamus—is reset to a higher point. The reason your thermostat gets reset is because leukocytes and macrophages secrete chemicals called pyrogens. Low and moderate fever is an effective immune response; it speeds up the body's metabolic rate, which in turn accelerates the repair process.
Let's summarize what we have discussed so far. Immunity is your body's defense against pathogens. There are two types of immunity: innate and adaptive. Innate immunity is the immunity you are born with and includes both physical barriers such as the skin and internal defenses. Internal defenses include cellular defenses performed by phagocytes and natural killer cells, as well as inflammation, antimicrobial proteins, and fever.
Now let's talk about adaptive or specific immunity.
Adaptive immunity is the body's specific immunity. Unlike your innate immunity which is nonspecific and attacks anything it recognizes as foreign, damaged or unknown, adaptive immunity is very choosy. Adaptive immunity will only attack specific threats. Adaptive immunity is carried out by two types of lymphocytes, the B cells and the T cells. Like all blood cells, the lymphocytes first develop in the bone marrow. B cells stay and mature there. Immature T cells migrate to the thymus where they mature. These lymphocytes become immunocompetent and have to be self-tolerant. In other words, these cells have to be able to evoke an immune response and make sure that response isn't against your own normal cells.
Adaptive immunity has three underlying traits. First, it is specific. It recognizes and attacks only specific pathogens. Secondly, it is systemic. This is a widespread reaction, not limited to a localized region of the body. Lastly, adaptive immunity has memory. In many cases, once you are exposed to a virus, your body remembers and you become resistant to reinfection.
Adaptive immunity has two components: humoral immunity and cellular or cell-mediated immunity. Humoral immunity produces antibodies. Cell-mediated immunity relies on a particular lymphocyte called a T cell, rather than antibodies, to defend the body. Both of these components work by recognizing antigens. Let's talk about antigen recognition next.
Antigens are cell surface proteins. You, as an individual, have a unique set of self-antigens called your Major Histocompatibility Complex, or MHC. However, when cells are infected by a pathogen or are abnormal, like a cancer cell, non-self antigens are presented. The change can be initiated by the infectious agent or because the cell no longer responds to normal control signals. It is these changed cells that the humoral and cell-mediated immune processes recognize and destroy.
There are two classes of MHC proteins. Class 1 MHC proteins are on all the cells of your body. Class 2 MHC proteins are only found on specific cells of the adaptive immune response. Let's talk in more detail about the humoral and cell-mediated immune responses next.
Humoral immunity works like this. The B cells are formed in the red bone marrow where they mature and become immunocompetent. These are the cells responsible for producing antibodies against foreign antigens. Once a B cell is exposed to a foreign antigen it becomes activated and undergoes cell division. One of the daughter cells becomes a memory cell. That is why you can be resistant to reinfection of say, chicken pox, once you have been exposed. These memory cells may live up to 20 years or longer. The other daughter cell has a different fate. It will continue to divide and produce an army of B cells. Each B cell will go on to produce antibodies that are secreted into general circulation to seek out and destroy the antigen they were exposed to. Antibodies mark the target cells for destruction by causing them to clump together, smothering their surfaces, acting like beacons for complement proteins and phagocytes and causing toxic cell by-products to precipitate out of solution.
But there are limitations to their defenses. B cells can only detect an obvious threat, like bacteria floating around in your blood. They can't detect viruses and bacteria that infiltrate the cells. For this, another defense is mounted by the cell-mediated arm of immunity. Cell-mediated immunity has a more direct approach. Let's look at that next.
T cells are formed in the red bone marrow, and then migrate to the thymus where they become immunocompetent. T cells recognize infected or abnormal cells differently than B cells. They recognize antigens that have been processed into fragments and sent to the cell surface. Once it detects one of these fragments, the T cell binds to it and becomes active. The T cell then divides like the B cell, with one daughter cell becoming a memory T cell and the other the cytotoxic T cell that targets cells with that antigen fragment for destruction "up close and personal." The cytotoxic T cell binds to the foreign cell, pokes holes in it, injects enzymes and toxins into it, and breaks up the cell membrane.
Let's summarize the difference in your humoral and cell-mediated immune responses. The B cells are responsible for the humoral response. This response involves identification of foreign antigens. This activates the B cells to produce antibodies specific for the targeted antigen. They attack and destroy these antigens or antigen-producing cells by clumping, lysing, and precipitating them out of the blood. So humoral immunity can be considered an indirect attack on pathogens by the B cells. In contrast, the T cells initiate a specific immunity response in which the T cell is presented with antigen fragments that cause the T cell to become immunocompetent. Once this occurs, the T cells destroy the unwanted cell by poking holes in the membrane and injecting enzymes to break the targeted cell into pieces.
With adaptive immunity, the first time the B and T cells are exposed to a new antigen, the response is slow. So you get really sick. This is called the primary response. The second time you are exposed, the B and T memory cells have a record of this antigen or antigens like it. So they can respond and divide really quickly, acting like a first strike against the developing infection. That is why you don't get sick when exposed at a later time. This is called the secondary response. So, when you are exposed to chicken pox the first time, you get an intense illness. But you don't get it a second time because your B and T cells can very quickly replicate and destroy the pathogen. That is how vaccines work. A vaccine initiates a primary response at low levels, deliberately introducing the B cells to the antigens. The B cells produce antibodies against the antigens and form a memory of these antigens. Then the next time you get infected, the B cells can respond quickly because they already know to attack the pathogen.
Let's summarize adaptive immunity. It is specific and self-tolerant. B and T cells are the major players. Upon exposure to an unknown antigen, they produce memory cells. B cells produce antibodies, which mount an indirect attack on the infected cells and noncellular pathogens. T cells attack directly to kill the cells by poking holes into them and injecting cytotoxic compounds.
That's the end of this section.
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