B lymphocytes (B cells) | Immune system physiology | NCLEX-RN | Khan Academy

B lymphocytes (B cells) | Immune system physiology | NCLEX-RN | Khan Academy

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. So let’s say that that
is a B lymphocyte. 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 variable portions. 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 immunoglobulins. 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 an epitope. 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 weeded out. 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 cloning himself. 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 do something. 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 membrane bound. 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 antibodies. 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?

100 Replies to “B lymphocytes (B cells) | Immune system physiology | NCLEX-RN | Khan Academy”

  1. I don't know how to explain how much I appreciate and respect what u do…. thank you very much …. u r rely helping us,,,pllllllz keep it up

  2. amazing how you make it so easy to undestand thank you, it really shows you're very passionate about your work/job

  3. I'm taking micro now. This what I was learned. It's different in the way of an invader presenting itself so to speak.

    B cells see Ag. The Ag attaches to the immunoglobulin binding site & processed inside the B cell making Ag fragments (epitopes). MHC2 attaches to the Ag making MHC2-Ag complex. It will then go to the surface of the B cell to display itself for the TH cell to recognize it. TH cell attaches it to the MHC2-Ag which will release cytokines to activate the B cell to Clonal expand. The clonal expansion will make some B cell, memory B cell & developing into antibody producing plasma cells.

  4. Thank you for this video and others you have created. I have even seen some of your chemistry videos. You truly have a gift for teaching.  Very clear and concise!

  5. your videos are very helpful! i think a bit of restructuring the organization of material presented could be helpful as well as numbering your videos in the order they should be viewed. THANKS!

  6. Mr. Khan, I've been watching your videos since grade 8… now im in medical school still watching ur videos. Thank you so much for your time and spreading your great talent of teaching to the world

  7. I swear I would never understand any concepts taught in my lectures if it weren't for you teaching them in much better depth and explanation

  8. 'Immunoglulobing' 'Teaching biology really stresses my perspelling part of my brain' Laughing my ass off hahaha!!

  9. I like to think of opsinization as "honey" that makes the target pathogen more delicious to phagocytes. Visual: bees to honey. "Bee"-cells respond, make honey, to attract "b"ears to eat them.

  10. Listening to your explanations is the glue in my studying regimen. Thank you SO MUCH for these videos. I know I'm not only speaking for myself when I say that your videos are life savers.

  11. I go to an elite Australian dental school and haven't gotten any sense of understanding until these videos. THANK YOU!

  12. THANK YOU! I have an anatomy and physiology test tomorrow and no matter how many times I read the text I couldn't comprehend this information. This is SOOOOO helpful!

  13. Listening to you being excited about protein diversity (I actually went to ask a professor to confirm if I got the information right from the textbook, so I understand you completley) and struggling with big science words makes me wanna marry you. :'). Thank you for this, breaking this down made it way more easier to understand and comprehend. 😀

  14. so what's the problem with HIV virus.. Why its difficult to eradicate the virus… and why our immune system is unable to tackle it

  15. Fantastic, love the video! 🙂

    Two questions.

    First, can an IgG really bind two viral particles simultaneously (see at ~13:30)?

    An IgG is about 150 kDa in size (source: https://en.wikipedia.org/wiki/Immunoglobulin_G).

    A polio virus is abouth 2.6 X 10^6 daltons (source: http://jvi.asm.org/content/4/4/475.full.pdf)

    So IgG is orders of magnitude smaller than the virus- could two viruses fit in the small space between the two arms of a single IgG?

    Secondly Question: How are antibodies against none-protein (e.g. sugars) epitopes formed? (Is there a video on this?)

  16. So, do I understand it right if I summarize that a naive B-cell actually needs 3 stimuli:
    1) Binding the antigen to its BCR,
    2) Binding cytokins produced by T-helper cells
    3) Binding a TCR from a T-helper cel to its own MHC2-antigen complex

    I wonder if #3 is always necessary. Can a B-cell also be stimulated by only the first two stimuli?
    And: is this true for both naive B-cells and memory B-cells?

    And: does the clone of effector B-cells stay in the 2nd lympoid tissues (while producing antibodies) of do they travel to the site of infection?

    Thanks for helping me!

  17. I'm currently taking immunology this Semester and this Video helped me a lot!
    Textbooks couldnt help me comprehend these concepts but right after watching this video? I am ready for tomorrow's lecture 😀 Thank you! 😀

  18. since the variable regions of B-cells are assembled randomly, there is a chance they can become autoreactive, or react against healthy antigens within the body. Just like T cell receptors, B cells must be tested and autoreactive cells must be eliminated. The mechanisms controlling T cell "training" have been elucidated, but the mechanism for B cell training has yet to be discovered. Maybe it will be you, I'm sure there is a Nobel prize in it for ya for added incentive

  19. so helping videos…i really really really really like the way you said really really really sir…love your way of teaching ;D…great JoB <3

  20. I dont undertstand when you say that if a virus enter in which the body has never encountered before and no B cells can recognize it, how come later one B cell eventually recognizes it? Vid Ref 7:00–7:08.

  21. very well explained. can u pls discuss also about stemcell transplant. how the new stemcell destroys the old immune system and the graft vs host disease. why after yrs of fully engrafted (100% donor chimerism) still the old stemcell suddenly goes back again and destroys the new stemcell.

  22. In short, before 5:50 the B cell was drawn with antibodies attached. Interestingly, individual B cell produces different antibodies. The antibodies are different due to their difference on the variation part, the (pink and orange colored part)

  23. how does Class Switching come into play. Do the effector cells essentially keep the variable portion from the original IgMs but attach them to IgAs, IgG, etc.? Thanks for any help!

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