system, and we’ll be discussing innate immunity. Now before we discuss innate immunity, you

need to understand that there’s actually two different types of immunity—one 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 responses—humoral 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 started—but 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 abundance—their 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 your “bananas” or your basophils,

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

important is because if you’re looking at a slide—let’s say you take a blood smear

on a microscope slide—and, and this is a healthy person, and you’re going through

and you’re identifying all the various white blood cells. Well if you’re finding more

basophils than you are neutrophils, then you’re 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 you’re definitely going to want to use this as your road map.

We’re 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 you’re 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 that’ll 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, we’re 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 located—which 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 you’ve sprained

your ankle and your ankle is now inflamed. You stepped on a nail, and—so 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 they’ve 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 area—that’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 you’re going

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

Remember that we’ve 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 much—that 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 here—these are all cardinal signs

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

changes in blood vessel function—the blood vessel vasodialated.

When we talk about phagocytosis—this 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

more—any 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.

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

does— once the cell is invaded by the virus—the

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 they’ll inhibit protein synthesis. Now

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

We’re 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. They’re important in the innate response,

and they’re going to release some chemicals called perforins that we’ll discuss here

in a second. They’re going to target cancer cells and they target virally infected cells,

and they’re 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 we’ll 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 they’re located; they’re 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. They’re quick, but they have their limitations. They’re

not specific; they’re not going to kill specific bacterial species, for example. And

they’re also short-term—they don’t last very long. So the problem with it is that

because they’re short term and they’re not specific, then you have to have a smart

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

going to start discussing adaptive immunity, and specifically, we’re going to look at

characteristics of your B and your T cells.