Let's just talk about the humoral response right now, that deals with B lymphocytes.
So B lymphocytes or B cells--let me do them in blue, B for blue
So let's say that that is a B lymphocyte.
It's a white blood cell, it's a subset of white blood cells called lymphocytes.
It comes from the bone marrow
and that's where the-- well, the B comes from
bursa of Fabricius, but we don't want to go into detail there.
But they have all of these proteins on their surface.
Actually, close to 10,000 of them.
I get very excited about B cells and I'll tell you why in a second
It has all of these proteins on them that look something like this.
I'll just draw a couple of them.
These are actually protein complexes, you can kind of view them.
They actually have four separate proteins on them and
we can call these proteins membrane bound antibodies.
And I'll talk a lot more about antibodies.
You've probably heard the word.
You have antibodies for such and such flu, or such and such virus
and we're going to talk more about that in the future,
but antibodies are just proteins.
They're often referred to as immunoglobulins.
These are essentially equivalent words.
Antibodies or immunoglobulins-- and they're really just proteins.
Now, B cells have these on the surface of their membranes.
These are membrane bound.
Usually when people talk about antibodies
they're talking about free antibodies that are going to just be floating around like that.
And I'm going to go into more detail on how those are produced
Now what's really, really, really, really, really interesting about these membrane bound antibodies
and these B cells in particular is
that a B cell has one type of membrane bound antibody on it .
It's going to also have antibodies, but those antibodies are going to be different.
So we'll focus on where they're different.
Let me just draw them the same color first and then we'll
focus on where they're different.
These are both B cells.
They both have these antibodies on them.
The interesting thing is that from one B cell to another B
cell, they have a variable part on this antibody that
could take on a bunch of different forms. So this one
might look like that and that.
So these long-- I'll go into more detail on that.
The fixed portion, you can imagine is green for any kind
of antibody, and then there's a variable portion.
So maybe this guy's variable portion is--
I'll do it in pink.
And every one of the antibodies bound to his
membrane are going to have that same variable portion.
This different B cell is going to have
different variable portions.
So I'll do that in a different color.
Maybe I'll do it in magenta.
So his variable portions are going to be different.
Now he has 10,000 of these on a surface and every one of
these have the same variable portions, but they're all
different from the variable portions on this B cell.
There's actually 10 billion different combinations of
So the first question-- and I haven't even told you what the
variable portions are good for-- is, how do that many
different combinations arise?
Obviously these proteins-- or maybe not so obviously-- all
these proteins that are part of most cells are produced by
the genes of that cell.
So if I draw-- this is the nucleus.
It's got DNA inside the nucleus.
This guy has a nucleus.
It's got DNA inside the nucleus.
If these guys are both B cells and they're both coming from
the same germ line, they're coming from the same, I guess,
ancestry of cells, shouldn't they have the same DNA?
If they do have the same DNA, why are the proteins that
they're constructing different?
How do they change?
And this is why I find B cells-- and you'll see this is
also true of T cells-- to be fascinating is, in their
development, in their hematopoiesis-- that's just
the development of these lymphocytes.
At one stage in their development, there's just a
lot of shuffling of the portion of their DNA that
codes for here, for these parts of the protein.
There's just a lot of shuffling that occurs.
Most of when we talk about DNA, we really want to
preserve the information, not have a lot of shuffling.
But when these lymphocytes, when these B cells are
maturing, at one stage of their maturation or their
development, there's intentional reshuffling of the
DNA that codes for this part and this part.
And that's what leads to all of the diversity in the
variable portions on these membrane bound
And we're about to find out why there's that diversity.
So there's tons of stuff that can infect your body.
Viruses are are mutating and evolving and so are bacteria.
You don't know what's going to enter your body.
So what the immune system has done through B cells-- and
we'll also see it through T cells-- it says, hey, let me
just make a bunch of combinations of these things
that can essentially bind to whatever I get to.
So let's say that there's just some new virus
that shows up, right?
The world has never seen this virus before this B cell,
it'll bump into this virus and this virus won't attach.
Another B cell will bump into this virus
and it won't attach.
And maybe several thousands of B cells will bump into this
virus and it won't attach, but since I have so many B cells
having so many different combinations of these variable
portions on these receptors, eventually one of these B
cells is going to bond.
Maybe it's this one.
He's going to bond to part of the surface of this virus.
It could also be to part of a surface of a new bacteria, or
part of a surface for some foreign protein.
And part of the surface that it binds on the bacteria-- so
maybe it binds on that part of the bacteria-- this is called
So once this guy binds to some foreign pathogen-- and
remember, the other B cells won't-- only the particular
one that had the particular combination, one of
the 10 to the 10th.
And actually, there aren't 10 to the 10th combinations.
During their development, they weed out all of the
combinations that would bind to things that are essentially
you, that there shouldn't be an immune response to.
So we could say self-responding combinations
So there actually aren't 10 to the 10th, 10 billion
combinations of these-- something smaller than that.
You have to take out all the combinations that would have
bound to your own cells, but there's still a super huge
number of combinations that are very likely to bond, at
least to some part of some pathogen of some
virus or some bacteria.
And as soon as one of these B cells binds, it says, hey
guys, I'm the lucky guy who happens to fit exactly this
brand new pathogen.
He becomes activated after binding to the new pathogen.
And I'm going to go into more detail in the future.
In order to really become activated, you normally need
help from helper T cells, but I don't want to
confuse you in the video.
So in this case, I'm going to assume that activation can
only occur-- or that it just needs to respond, it just
needs to essentially be triggered by
binding with the pathogen.
In most cases, you actually need the
helper T cells as well.
And we'll discuss why that's important.
It's kind of a fail safe mechanism
for your immune system.
But once this guy gets activated, he's going to start
He's going to say, look, I'm the guy that can match this
virus here-- and so he's going to start cloning himself.
He's going to start dividing and repeating himself.
So there's just going to be multiple versions of this guy.
So they all start to replicate and they also differentiate--
differentiate means they start taking particular roles.
So there's two forms of differentiation.
So many, many, many hundreds or thousands of these are
going to be produced.
And then some are going to become memory cells, which are
essentially just B cells that stick around a long time with
the perfect receptor on them, with the perfect variable
portion of their receptor on them.
So some will be memory cells and they're going to be in
higher quantities than they were originally.
So if if this guy invades our bodies 10 years in the future,
they're going to have more of these guys around that are
more likely to bump into them and start and get activated
and then some of them are going to turn
into effector cells.
And effector cells are generally cells that actually
What the effector cells do is, they turn into antibody-- they
turn into these effector B cells-- or sometimes they're
called plasma cells.
They're going to turn into antibody factories.
And the antibodies they're going to produce are exactly
this combination, the date that they originally had being
So they're just going to start producing these antibodies
that we talk about with the exact-- they're going to start
spitting out these antibodies.
They're going to start spitting out tons and tons of
these proteins that are uniquely able to bind to the
new pathogen, this new thing in question.
So an activated effector cell will actually produce 2,000
antibodies a second.
So you can imagine, if you have a lot of these, you're
going to have all of a sudden a lot of antibodies floating
around in your body and going into the body tissues.
And the value of that and why this is the humoral system is,
all of a sudden, you have all of these viruses that are
infecting your system, but now you're producing all of these
The effector cells are these factories and so these
specific antibodies will start bonding.
So let me draw it like this.
The specific antibodies will start bonding to these viruses
and that has a couple of values to it.
One is, it essentially tags them for pick up.
Now phagocytosis-- this is called opsonization.
When you tag molecules for pickup and you make them
easier for phagocytes to eat them up, this is what--
antibodies are attaching and say, hey phagocytes, this is
going to make it easier.
You should pick up these guys in particular.
It also might make these viruses hard to function.
I have this big thing hanging off the side of it.
It might be harder for them to infiltrate cells and the other
thing is, on each of these antibodies you have two
identical heavy chains and then two
identical light chains.
And then they have a very specific variable portion on
each one and each of these branches can bond to the
epitope on a virus.
So you can imagine, what happens if this guy bonds to
one epitope and this guy bonds to another virus?
Then all of a sudden, these viruses are kind of glued
together and that's even more efficient.
They're not going to be able to do what they normally do.
They're not going to be able to enter cell membranes and
they're perfectly tagged.
They've been opsonized so that phagocytes can come
and eat them up.
So we'll talk more about B cells in the future, but I
just find it fascinating that there are that many
combinations and they have enough combinations to really
recognize almost anything that can exist in the fluids of our
body, but we haven't solved all of the problems yet.
We haven't solved the problem of what happens when things
actually infiltrate cells or we have cancer cells?
How do we kill cells that have clearly gone astray?
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