Placeholder Image

字幕列表 影片播放

  • >>Dr. Ketchum: So we are going to go ahead and continue our discussion of the immune

  • system, and well be discussing innate immunity. Now before we discuss innate immunity, you

  • need to understand that there’s actually two different types of immunityone of those

  • being innate immunity, which is also called nonspecific immunity, and the other is called

  • acquired or adaptive immunity, which is also known as specific immunity. But just to give

  • you a quick overview of both of these, when you first think about the nonspecific or the

  • innate immunity, it’s a very rapid response. This is your first line of defense. And what

  • this does is it gives your body time for the specific immunity to kick in. So innate immunity

  • is always there. It’s present; it’s going to happen as soon as your body is invaded

  • by a foreign object, and then the specific immunity will take over after that. It’s

  • rapid, and it’s also not selective. So it’s not targeting specific species of invaders,

  • for example. It’s not specific. It just wants to kill foreign invaders, and that’s

  • the end of it. The innate immunity involves physical and chemical barriers, and it also

  • includes cellular defenses. Now once the innate immunity has occurred, then the next type

  • of immunity that will occur or kick in is the acquired immunity. It’s a slow response.

  • And so because it’s a slow response, it’s very selective in what it’s killing. It

  • may kill a specific bacterial cell or a specific virus, and specific immunity includes two

  • different types of responseshumoral responses, which are also called antibody-mediated responses,

  • and cell-mediated responses, which are also called cytotoxic lymphocytes. Here’s our

  • analogy. When you think about an innate response, the castle is the body. And the first thing

  • that this innate response wants to do is it wants to prevent that invader from entering

  • the body. And once that invader invades the body, then the innate response will have some

  • other methods for killing the invaders as well. These things are all taking place as

  • the acquired response is just getting startedbut remember it’s slow, so it takes a while

  • to get the acquired response going.

  • So neutrophils, the eosinophils, basophils and monocytes are all cells that are important

  • in an innate response. The lymphocytes, on the other hand, are the type of white blood

  • cell that are important in the acquired response. You don’t have to memorize the amount of

  • each of these cells in a microliter or their diameters or any of that. You need to understand

  • their anatomical features and their functions. So these are important columns here, but you

  • do also have to know their abundancetheir relative abundance. So again, if you remember

  • Never Let Monkeys Eat Bananas,” that tells you the most abundant leukocyte all

  • the way to the least abundant leukocyte, which are yourbananasor your basophils,

  • so that way you don’t have to memorize the amount per microliter. The reason this is

  • important is because if youre looking at a slidelet’s say you take a blood smear

  • on a microscope slideand, and this is a healthy person, and youre going through

  • and youre identifying all the various white blood cells. Well if youre finding more

  • basophils than you are neutrophils, then youre probably not correctly identifying those cells.

  • Okay, so here’s a flow chart that I put together to help organize the innate versus

  • the adaptive response. So youre definitely going to want to use this as your road map.

  • Were discussing the innate responses in this part, in part two.

  • First let’s start with the physical and the chemical barriers; you think about these

  • as being the wall of the castle. So the first thing I’d like to discuss are the lysozymes.

  • So you have lysozymes that are in your tears and other secretions. These are not lysosomes;

  • lysosomes are different. Lysozymes are antibacterial. So when you cry, it’s actually a good thing

  • because youre killing any kind of bacteria that’s on your skin. You also have the skin,

  • then, and the skin is a physical barrier. The skin also has fatty acids and normal flora

  • as well thatll affect the pH and some foreign invaders cannot survive on the skin just because

  • of the normal flora on our skin. Then you have the mucus and the cilia that line the

  • trachea. The mucus traps any formed particles, and then the cilia works that debris up the

  • respiratory tract and into your mouth so that you can either swallow it or spit it out.

  • If you swallow it, it goes down into your stomach. And remember, the stomach has a pH

  • of two; it’s very acidic. So it’s likely to kill most invaders, but not all. Now taking

  • a closer look at the skin, were not going to spend time on the skin. This isn’t anatomy,

  • but you should realize in this course that you do have two major skin layers: the epidermis

  • and the dermis. So pay attention to those two layers and know where those two layers

  • are locatedwhich one’s on the outermost which ones on the innermost.

  • The dermis, then, the only thing that you need to know about the dermis are the sebaceous

  • glands, and I want you to use your textbook to figure out what’s the function of those

  • sebaceous glands? Why are they important in the immune response? Then we have inflammation.

  • So inflammation is part of the innate immunity as well. When you think about inflammation,

  • it’s your body’s response to tissue damage or microbial invasion. So youve sprained

  • your ankle and your ankle is now inflamed. You stepped on a nail, andso now you have

  • tissue damage and microbial invasion by stepping on a nail. So the goals of inflammation are

  • listed here for you. You want to bring phagocytes to the injured area, because if you can control

  • those invaders at the area that theyve invaded, then they can’t spread throughout

  • the body. You want to stop them there. So if you can bring those phagocytes to the

  • injured area, you can destroy, inactivate invaders, you can remove any kind of cellular

  • debris, and you can start preparing for healing. So let’s take a look at this flow chart.

  • The leukocyte that automatically will start phagocytizing as soon as invaders enter into

  • that wound are your macrophages. So those macrophages are there, and they immediately

  • start attacking foreign invaders that enter the wound. The bacterial invasion itself and

  • the tissue damage as well can cause the mast cells to release histamine. Histamine then,

  • we know, causes vasodialation. So when an arterial vasodialates that means you have

  • less resistance, right, and therefore more blood flow to the injured area. So because

  • there’s more blood flow to the injured areathat’s why it becomes red and that’s why it gets

  • hot. So because there’s more blood there, that means that you have an increase in certain

  • plasma proteins that may be important in the healing process. So these may be clotting

  • factors, for example, that would prevent you from bleeding out.

  • The release of histamine by the mast cells also increases the capillary permeability.

  • So what I want you to do is think about a capillary here, and I’m just going to draw

  • three endothelial cells that are forming the walls of this capillary. And when you have

  • histamine release, the pore size has increased significantly. So if you increase the pore

  • size, that means more fluid can flow through those pores. So that means youre going

  • to get a local accumulation of fluid, some of that fluid being in the interstitial fluid.

  • Remember that weve talked about swelling or what we call edema, an excess of interstitial

  • fluid. It can also cause pain, because you have excess fluid in an area and the skin

  • can only stretch so muchthat causes pain. Pain is a good thing, because pain actually

  • forces you to rest whatever part of your body is injured, and that way it can repair itself

  • if it’s resting. Because you have this increased capillary permeability, then that’s going

  • to increase the number of phagocytes that can make it to the tissue, like your macrophages.

  • If you have more phagocytes, that’s going to increase their secretions. And their secretions

  • can cause systematic responses like fever, for example. All in all, then, this is an

  • inflammatory response and all of the information in red herethese are all cardinal signs

  • of inflammation. And all of these cardinal signs of inflammation are because you had

  • changes in blood vessel functionthe blood vessel vasodialated.

  • When we talk about phagocytosisthis is a form of endocytosis, but specifically, how

  • is it achieved? So it’s going to be your job to fill in the steps. Don’t go into

  • moreany more detail than what these four steps are asking for here. Opsonins, I do

  • want you to look at opsonins and, and, why do we need opsonins? Why are opsonins important

  • in phagocytosis? Then we have interferon. This is another type of innate immunity, and

  • the goal of interferon is to interfere with viral replication. Now many of you have had

  • Intro Zoology and so you know that when a virus gets inside of a cell, the virus takes

  • over the machinery of that cell. And so it starts producing it’s own viral RNA and

  • it’s own proteins. So there are some other functions of interferon that are listed here,

  • and go ahead and read them and at this point realize that there are other functions for

  • interferon besides interfering with viral replication. So let’s take a look at how

  • this will work.

  • Were going to take a cell, and it’s been invaded by a virus. So what the cell

  • doesonce the cell is invaded by the virusthe

  • cell is going to be releasing interferon. So the interferon is going to enter the extracellular

  • fluid, and it’s going to travel to healthy cells, cells that have not been invaded by

  • the virus. And when it binds to these receptors on an un-invaded cell, this un-invaded cell

  • now will produce inactive enzymes. So basically this cell is just waiting, it’s waiting

  • to be invaded by a virus. Because what these enzymes will do once they become activated

  • is they will break down viral messenger RNA and theyll inhibit protein synthesis. Now

  • here comes our virus; it invades this cell. So those inactive enzymes are now active enzymes.

  • Were going to stop protein synthesis of the virus. So if a virus cannot multiply inside

  • of a cell, the virus is dead. Viruses rely on cells in order to make their own proteins,

  • and they, again, take over the machinery of the cell. So if they can’t do that they

  • have nothing to survive on. This is why we call it interferon. Interferon is interfering

  • with a virus; it’s interfering with its replication. So next we have the natural killer

  • cells.

  • Natural killer cells are kind of like lymphocytes. Theyre important in the innate response,

  • and theyre going to release some chemicals called perforins that well discuss here

  • in a second. Theyre going to target cancer cells and they target virally infected cells,

  • and theyre going to lyse the membranes of those cells. So let’s look at how natural

  • killer cells work. This killer cell here is a natural; so it binds to the target cell.

  • Once they come into contact, the natural killer cell releases perforins. What perforins do

  • is they create a pore in the membrane of the invader. So if we do that then water and ions

  • can rush in. We increase the permeability. So if you increase the permeability for water

  • and ions into the cell, the cell will swell and burst. It’s going to lyse. Then we have

  • the compliment system. The compliment system is activated by two different means. The only

  • one well discuss here is listed here at number one. We will discuss number two here

  • later, but first, let’s focus on number one when we activate a compliment system.

  • So here you have a bacterial cell, and on the surface of it is some carbohydrate. That

  • carbohydrate is recognized by a compliment protein. So these compliment proteins are

  • floating around in your plasma. That’s where theyre located; theyre in the plasma

  • cruising around. And when the compliment protein recognizes this carbohydrate chain, the compliment

  • protein will bind to the plasma membrane of this bacterial cell. And once it binds to

  • the plasma membrane that creates a whole cascade of events that end up developing what’s

  • called a membrane attack complex, a MAC. So this membrane attack complex is essentially

  • a pore. So once you develop the pore, fluid can rush into the cell, and then the cell

  • will burst and it will lyse. So that kills that target cell as well. So compliments really

  • good in killing bacterial invaders.

  • So innate responses are really good. Theyre quick, but they have their limitations. Theyre

  • not specific; theyre not going to kill specific bacterial species, for example. And

  • theyre also short-termthey don’t last very long. So the problem with it is that

  • because theyre short term and theyre not specific, then you have to have a smart

  • system, and that’s what adaptive immunity is all about. So in the next part were

  • going to start discussing adaptive immunity, and specifically, were going to look at

  • characteristics of your B and your T cells.

>>Dr. Ketchum: So we are going to go ahead and continue our discussion of the immune

字幕與單字

影片操作 你可以在這邊進行「影片」的調整,以及「字幕」的顯示

B2 中高級

人體生理學 - 先天免疫系統 (Human Physiology - Innate Immune System)

  • 1418 46
    SylviaQQ 發佈於 2021 年 01 月 14 日
影片單字