When we learned about antigen
presenting cells, we learned that they can first digest
something-- let me draw a dendritic cell right here--
my best version of a dendritic cell. Maybe I should draw them
simpler than that. A dendritic cell is a phagocyte
and it is an antigen presenting cell. So after phagocytoses some type
of a pathogen, it'll cut it all up, and then it'll
display-- it'll present the antigen on its surface on a
protein complex here and the part of the pathogen that
it cut up, it'll put up right here. And we learned on the antigen
presenting cell video that this complex right here was an
MHC type II complex, where MHC stands for major
histocompatibility complex. Where histocompatibility just
means tissue compatibility. And this was the case on antigen
presenting cells. So even B cells did this. Let me draw a B cell. So a B cell-- it has
its membrane bound antibody, just like that. It actually has many, many
thousands of these. I could keep drawing a bunch of
them, but just so you know there's more than one. Maybe one of these get triggered
or get attached to some type of virus or protein
or bacteria floating around. And what it'll do is it'll take
this in and cut it up again and do the same thing as
what the dendritic cell did. It'll cut up a part of this and
present it on its surface in conjunction with
an MHC II complex. So once again, this is
an MHC II complex. So these professional antigen
presenting cells that go out and take things out of the
fluid, out of the humoral parts of our body, things
just floating around. They'll take them in, they'll
say, this is bad, cut them up, and then present them
on these MHC II. That's why we call them
professional antigen presenting cells. Now, it turns out that pretty
much all cells in our bodies-- when I say almost all
cells, it's actually all nucleated cells. So all cells that have a nucleus
in the human body-- so the only cells in our human body
that don't have nucleuses are red blood cells, which I
find fascinating-- so that they can have more space
for storing hemoglobin. But all nucleated cells in our
bodies have another major histocompatibility complex on it
and it's called an MHC I-- major histocompatibility
type I. And just so you know, these
are also nucleated cells. So they're also going to have an
MHC type I complex on them right here. Now the interesting thing about
the MHC type I complex is because it's on every cell in
our human body-- so pretty much everything but the red
blood cells have an MHC I-- this is where if anything
wacky is going on inside the cell. Maybe the cell is cancerous and
producing crazy proteins. Maybe it's been infected
with a virus. Maybe some type of bacteria or
some type of weird protein has gotten in here-- any cell in the
human body can cut those up, even if it's malfunctioning,
and it will present them. So let's say the cell
is cancerous. So this cell's cancerous and
it has all these wacky proteins that only cancer cells
present that is not normal for a normal cell--
that will be presented on the MHC I. Let's say that I have some other
cell in my body that's a different type of cell. It's nucleated. Let's say it's been infected
with a virus. So it's turning into
this virus factory. Same thing-- there are
mechanisms in a cell that will take some of the proteins that
make up those viruses and present them on the
MHC I complex. So in the case of MHC II, this
is what triggered helper T cells to say, hey,
you know what? I found something floating
out here. Here's a little piece of
it, Mr. Helper T cell. Why don't you bond to this and
raise the alarm system? Now the MHC I system
says, this isn't stuff floating around. I've been infected. I am cancerous. I'm going nuts. You better kill me. I'm a virus, I'm a virus-making
machine. You better kill me. And that message goes to the
cytotoxic T cells and that's really the topic
of this video. So just to make sure
you understand the difference-- so T cells. They both have T cell receptors,
but the helper T cells bond to MHC
II complexes. Let's say that this is a helper
T cell right here. It would want to-- not all
helper T cells will. Only the ones that have the
right combination, the right variable portion right here that
just perfectly bonds to this combination of an antigen
and the MHC II complex-- this type of helper T cell will bond
here, get activated, and start differentiating. And the effector versions of
them will start raising the alarms and the memory versions
of them will stick around in case this type of thing
needs to happen again. With MHC I, instead of
attracting a helper T cell, it will attract a cytotoxic
T cell. So like helper T cells, the
T cell receptor has a non-variable portion, but it
also has a variable portion that is specific to this
combination of antigens and MHC I. So maybe this cytotoxic T cell
will be involved when this cell goes cancerous. This cytotoxic T cell would be
of no use-- or it won't bond to this one that was attracted
to a virus. It's going to have to be
another cytotoxic T cell that does that. And the mechanism where we get
this variability in the helper T cells or the cytotoxic T
cells or you saw in the B cells on their membrane bound
antibodies, that all comes from when-- in their development
stage or in the maturation process, the DNA that
codes for these variable portions gets shuffled
around intentionally. So normally, we're always
trying to preserve DNA information, here it gets
shuffled around. But anyway, once a cytotoxic T
cell finds one of these guys on an MHC I-- remember, every
nucleated cell in the body has an MHC I-- then what it does
is, it gets activated. So let's say this guy says,
hey, that looks shady. You need to die. So this guy gets activated and
just like all other activated cells, he starts to divide and
divide and divide and divide and differentiate. And he divides and he
differentiates into memory, just in case you're going to
need me again, just in case this type of cancer
shows up again. And then also into effector T
cells, which are the ones that do the killing. So this is an effector. So let's say one of these
effectors-- they'll also bind to cancerous molecules,
cancerous cells, just like this one. So let's say this cell has
split and there's another version of it right here. That's what cancer does. It divides aggressively. It's producing wacky proteins. It presents the wacky proteins
on its MCH-- major histocompatibility type I
complex-- it displays the wacky proteins and then one of
these effector cytotoxic T cells will be attracted
to it just like that. And I'm not going into details
on what necessarily does the attractions and all the membrane
bound proteins. If you take an immunology
class, you'll see more on that. So this is a cytotoxic T cell
and it essentially forces this cell to kill itself in a couple
of different ways. One, it actually can exocytose
a bunch of proteins. They're call perforins-- that
make little holes in the membrane of the cell. And it has other proteins that
it releases called granzymes that go in here and essentially
start mechanisms that make this cell want
to kill itself. So the big picture is, if you
want to just take 20,000 feet, these cells are very effective
at produces-- so when a B cell gets activated, it produces
antibodies that kill things that are floating
around, right? Once a B cell gets activated, it
starts producing a bunch of antibodies. These antibodies float around
and then they can bond up to viruses, make them ineffective,
or essentially tag them for pickup from
macrophages or dendritic cells, or other types of
phagocytes-- while cytotoxic T cells-- these are used to
essentially kill cells that have gone awry. For example, a cancer cell
that's presenting weird proteins or once the virus has
entered the cell, then the antibodies are really
of no use. The antibodies aren't
going to be able to get into those cells. In that case, instead of
cleaning up the virus itself, a cytotoxic T cell will come
here and just kill this cell because this cell is
a virus factory. So you have to get it
out of the way.