>>Dr. Ketchum: This is part four of six for the immune system. This—this part is going
to focus specifically on humoral immunity. So before we begin, let’s take a look back
at our outline here. And so once again, here we’ll focus on humoral immunity. And specifically,
when you think about humoral immunity, what I want you to think about again are B lymphocytes.
So when we go through humoral immunity, the big picture here is that we’re going to
be able to take B lymphocytes and we’re going to be able to produce plasma cells,
and those plasma cells are going to be able to produce antibodies. And then we’ll be
able to discuss what those antibodies are going to do. So you may want to add to your
flow chart here the function for those antibodies, and there are several things that the antibodies
can do.
Now B lymphocytes can also get converted over to memory cells. Memory cells, then, when
they get exposed to a particular antigen once again (like a second time), then those will
go on to produce plasma cells, which then produce antibodies, which then can help mount
that immune response. Okay, so that’s the overall picture of where we’re going with
this. So again, just to kind of give you this—the, the same idea again. When we talk about these
B cells, so let’s take a look at these B cells that are shown here in this top part
of the diagram. These are B cells that are specific to certain antigens. So if you notice
the one here that has the red antibodies, it’s very specific to these red antigens,
right? So when the red antigens bind—and do you remember what they’re binding to?
What’s the name of this receptor? This is called a membrane antibody receptor, or we
can call it a membrane immunoglobulin receptor.
Okay, so when this happens, then what your B cells are going to do is they’re going
to proliferate. So they can become plasma cells and memory cells, all right? So off
to the side let’s kind of diagram this big picture as we go. So here we have our B lymphocytes,
and they have to bind to an antigen. And remember that they’re binding to the antigen by using
the membrane antibody receptor. And once they bind to that antigen, then they can become
either plasma cells or they can become memory cells. Now, if they become plasma cells, plasma
cells will actually give rise to antibodies. So literally they produce antibodies. Memory
cells, when you’re exposed for the second time—so you have a second exposure to a
particular antigen—those will go on to make plasma cells, which will then make antibodies.
So it’s much faster when you’re exposed to an antigen for the second time, because
you have these memory cells that are hanging around waiting for that antigen to be—
waiting for your body to be exposed to that antigen once again. Now plasma cells are short lived.
These do not live for very long; so these are short lived. Memory cells are longer lived;
they’re long lived. Okay? So they survive for a much longer period of time.
So this is what we call the clonal selection theory. So what that means is you have these
B lymphocytes that give rise to a whole bunch of plasma cells that are all the same, and
those plasma cells all produce the same antibodies. And the B lymphocytes also give rise to memory
cells, a whole bunch of them. So they’re clones, right, and then those can ultimately give
rise to more plasma cells, which can give rise to antibodies.
All right, now even though we’re discussing these with respect to B lymphocytes, keep
in mind that T cells can also do this, but it’s not something that we’re emphasizing
in this course. Okay, so plasma cells, then, we know can produce antibodies as I just talked
to you about. And they will combine then—those antibodies then can combine with a specific
kind of antigen. So I’m going to show you here in just a few minutes how that will work.
Now when the antibodies enter the blood, they’re known as gamma globulins or immunoglobulins.
That’s where that term immunoglobulins comes from. So we have several different subclasses
of immunoglobulins. And here you’re just going to have to memorize these, because some
are found in different places. So we’ll use some of these as we go throughout the
next series of slides.
All right, so how does the antibody actually destroy the antigen? Remember that our bodies
produce antibodies because they want to destroy the antigen. So here are the methods that
they’re going to use: neutralization, agglutination, enhancement of phagocytosis,
activate the complement system, and they can stimulate killer cells.
So be sure you’ve watched the previous videos so that you understand phagocytosis and complement
and natural killer cells before you continue on here. Otherwise you won't quite understand
what’s going on. All right, so we’re going to cover each one of these. So remember the
big picture—we want the antibody to destroy the antigen. So, ways to do that? Let’s
start off with neutralization. So keep in mind that as we go throughout these slides,
when you see the term pathogen, the pathogen is the antigen, right? That’s the foreign
invader. So in neutralization, here you have your antibody, okay? And that antibody binds
to the pathogen. Notice how many antibodies are bound to this pathogen. There’s a whole
bunch. So because you have all of these antibodies bound to the pathogen, that’s going to block
the activity of the pathogen. And if you block the activity of the pathogen, what you’ve
essentially done is you’ve neutralized it. The antigen is unable to invade the tissues,
all right? So in this case, that antigen cannot invade that target tissue because it’s been
neutralized. It’s got all these antibodies that are bound to it. Now this isn’t going
to necessarily kill the pathogen. It could, because some pathogens if they can’t get
into a target tissue, can’t get the nutrients that they need to survive. So it might kill
them in that way, but it wouldn’t directly kill them. Later we’ll talk about how we
actually kill the antigen.
Now there’s also agglutination, and this is something that you should already be somewhat
familiar with when it comes to blood. When we talked about blood antibodies and blood antigens.
So in this case, we’re going to be dealing with two different types of antibodies. We’re
going to deal with IGM and IGA. So these are two different immunoglobulins, and what these
immunoglobulins do is literally they clump the antigens together, all right? So here
you see all of these pathogens, and that’s all clumped together and we’re using antigens
to clump them together. Because if you clump all these antigens together, then that
blocks the activity of your pathogen. So that pathogen, for example, couldn’t invade a
tissue, all right? Be sure you understand agglutination when it comes to blood types
as well. Okay, then there’s opsonization. So this is where we start off. Here’s your
macrophage, which is a type of phagocyte. So opsonization can occur with different types
of phagocytes. Here we’re focusing on a macrophage. So you have an antibody that binds
to the phagocyte. And when the antibody binds to the phagocyte, then the antibody binds
the antigen. And what that’s going to do then it’s going to trigger opsonization.
So in other words, this is triggering phagocytosis of the antigen, all right? And if you recall
from earlier, opsonization enhances the speed or it enhances phagocytosis, in other words.
So it’s a lot quicker. Makes sense if you want to phagocytose a pathogen, because you
want to start killing off those pathogens.
Now there’s also compliment activation. We talked about earlier, but this is a different
way to activate the compliment system. So we talked earlier about having a bacterial
cell that was our pathogen, and how there was a polysaccharide component on the cell
membrane and that activated the compliment. Here, however, we’re using different method.
We’re going to have an antibody that’s bound to the pathogen. So here you can see
the Y-shaped antibody, right? And it’s bound to the pathogen. So then very first compliment
protein recognizes that. And when it recognizes it, then it binds to the antibody. And then
that triggers the compliment system, and the end result of the compliment activation system
is that you develop this pore, which if you remember, is called a membrane attack complex.
So if you develop a membrane attack complex, in other words, a pore in the membrane, how
does that kill a pathogen? Remember that once you have a pore, that allows for increase
permeability. So you have flooding in of ions and water into the cell, and the cell is going
to lyse.
All right, antibodies can also enhance natural killer cells. And so if we look here, here’s
our natural killer cell up on the top left. Our abnormal body cell, maybe it’s a tumor
cell, is on the bottom right. So what we’re going to use, have here, we’re going to
take an antibody and it’s going to bind to the abnormal cell. So basically when it
binds to this abnormal cell, it’s marking the cell for death. So when it’s marking
it for death, what that means then is that the natural killer cell will release a chemical
that you’re very familiar with and those are called perforins. And when the natural
killer cell releases perforins that creates a pore or a hole in the membrane of the abnormal
cell. So we know from earlier that if you create a hole in the membrane, you have increased
permeability. In comes the ions, in comes water, in comes all sorts of goodies, and
the abnormal cell will lyse.