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
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
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
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
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.
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
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
antigen and MHC II.
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 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
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.
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