Helper T cells | Immune system physiology | NCLEX-RN | Khan Academy
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Helper T cells | Immune system physiology | NCLEX-RN | Khan Academy


In talking about the adaptive
immune system, we’ve already seen that there’s a
couple of actors. You have your humoral
response. So this is responding to things
that are floating around in the fluids of the
body and not necessarily things that have infiltrated
your body cells and then you have your cell mediated
response. And then in the humoral
response– and we’re talking about specific humoral
response– this is where the B cells, the B lymphocytes are
at their most active. And essentially what they do
is, you got a B cell here. It has a very specific antibody,
specific to just this B cell, not B
cells in general. If this happens to be the one
of the billions of B cells that happens to have the
matching key– or maybe I should say the matching lock
for the key that is the intruding pathogen–
that pathogen will bind to that B cell. Maybe it’s a virus, maybe
it’s a bacteria. And then the B cell will get
activated and we’ll talk about in this video that
the activation doesn’t always happen. In fact, it usually doesn’t
happen just from this, but so far we’ve said it gets
activated, it goes into memory B cells, which are essentially
multiple versions of this original B cell– just saying,
hey, let’s have multiple versions of this– because it
tends to recognize this virus. So in the future if we get this
virus, those multiple versions, those memory cells are
going to be there to have this interaction. This interaction’s going to be
more likely to happen in the future because I’m going
to have more of this variety of B cell. And then you have
effector cells. And these are essentially– so
both of these are B cells. So this guy, once he gets
activated, he proliferates, keeps dividing and
cloning himself. The memory cells just stick
around waiting to be activated in the future. And I’m only drawing one
of these membrane bound antibodies, but there are
actually 10,000 on them. I mean, I could draw
a bunch of these. I don’t have to just draw one. The memories just wade around
in the future, but there’s more of them now. So in the future, if we get
this virus again, this interaction’s going to happen
faster and so they’re going to get activated faster. And then the effector B
cells essentially turn into antibody factories. This antibody goes in and it
says, let me just produce– I’ve been activated. Let me produce many,
many more versions of that exact antibody. So they get spit out. I drew that one little wrong. So that exact antibody, that
can then be spit out to go disable or tag antigens– and
not just any antigen– this antigen right here. And we also saw that the other
thing that the B cell does is it becomes an antigen
presenting cell. So what it does is, as soon as
it recognizes this, it’s had this interaction with an antigen
that just matches the variable portion of its membrane
bound antibody. It endocytosizes that. It brings that into itself. It’s membrane facilitated so it
just kind of pulls it in, chunks it up, and then presents
a piece of that antibody on an MHC
II molecule. We saw that in the last video. So it cuts that up and presents
a piece of it right there and that’s why we call it
an antigen presenting cell. Now in this video, we’re going
to talk about why we even have these MHC II molecules. What are we presenting
these antigens to? So we’re going to start
talking about the cell mediated– and actually, even
more than the cell mediated, we’re going to talk
about T cells. And I said in the first video,
they’re called T cells because they mature in the thymus. And there are two types of
T cells and it’s all very confusing because you have B
cells and T cells, but then there are two types
of T cells. You have helper T cells– and
most people just write T with a lower-case or subscript
h there. And then you have cytotoxic T
cells– or T cells that kill other cells. Now just so that you have a big,
overarching impression of what does what– B cells. When they are activated, they
generate antibodies. At 30,000 feet, that’s the
best summary of what an activated B cell does. It actually generate
antibodies. Those antibodies attach to
viruses and bacteria and other types of pathogens and disables
them– either tags them so that macrophages can go
and eat them up or just by throwing all of those antibodies
on to the surface of the pathogen in question. It might disable the pathogens
or essentially bundle them altogether so that it’ll be
easier for macrophages to pick them up, but this is only
effective for things that are floating around. Free floating antibodies are
only effective for things that are floating around. Cytotoxic T cells, which I’ll
cover in more detail in a future video– these actually
attack cells that have been infiltrated. So this is attack, kill,
infiltrated cells– and when I say infiltrated, it could be a
cell that a virus has gone into or some bacteria
has penetrated it. And when I say infiltrated, it
doesn’t necessarily even mean something from the outside. It could even be a cancerous
cell that shows itself to be abnormal in some way and so the
cytotoxic T cells will at least attempt to kill them. But what I want to focus on–
out of the three types of lymphocytes– remember,
everything we’ve been talking about was leukocytes, white
blood cells, but lymphocytes are a subset of that and these
three are lymphocytes. And they’re called that because
they began their development in the
bone marrow. So this guy and this guy
actually do stuff. This guy generates antibodies
that attach to pathogens floating around. This guy directly attacks
cells that are broken in some way. They’ve either been infiltrated,
they’re abnormal, they’re cancerous–
who knows what. And I’ll do a whole video on
that, but that leads us to a very obvious question. What does this guy do? What does the helper T cell
do if he doesn’t directly interface either with pathogens
or produce things that interface with pathogens–
or if he himself doesn’t go and directly
kill cells? And the answer is that the
helper T cell’s kind of the alarm of the immune system. And on some level, it’s almost
the most important. So we talked already in the
last video about antigen presenting cells– that either
when a macrophage or a dendritic cell takes things
in, it cuts them up and presents it on its surface as
these MHC II proteins or in complex with these MHC II
complexes or proteins. And so do B cells. B cells are more specific. Now, once something is
presented, now the helper T cell can come into
the picture. So this is a– let me do a
dendritic cell– and I’m doing dendritic cells actually on
purpose because dendritic cells are actually
the best cells at activating helper T cells. We’re going to talk about in a
second what happens when a helper T cell gets activated. So let’s say I have this
dendritic cell. It’s called dendritic so
it looks like it has dendrites on it. So I have this dendritic
cell here. It’s a phagocyte. Let’s say it’s already consumed
some type of bacteria or virus and it’s cut it up and
now it’s presenting kind of the body parts of that virus
on the MHC II complex. It’s kind of its way of saying,
hey, I found this shady thing floating around
in the body’s tissues. Maybe someone ought
to raise an alarm. Maybe this is part of some type
of bigger thing going on and some type of alarm bell
has to be released. And that’s what the helper
T cell does. So let’s say this guy–
he’s presented it. He says, I found this thing. I killed it. Here’s a part of it. The helper T cell has a
T cell receptor on it. Let’s say this is the helper
T cell right here. And it has a T cell receptor on
it and the T cell receptors bond to– and I’ll be very
particular here. So this is the T
cell receptor. It’s just like a protein, but
like the membrane bound antibodies on B cells that every
B cell or almost every B cell has a different version,
different variable chain, that’s also true of helper T
cells– that just like the B cells, this has some variation
in where it binds. So this right here is going to
be variable from one helper T cell to another. For example, I might have
another helper T cell here. That also has a T cell receptor,
but the variable portion on that T cell receptor
is different than the variable portion on this
T cell receptor. So this helper T cell will not
bind to this dendritic cell or the MHC II complex of
this dendritic cell. Only this one would. And the mechanism of how you
get this variation is very similar to the mechanism in how
you get the variation on the antibodies and
the B cells. During these helper T cells’
development, at some point the genes that code for this part of
this receptor get shuffled around and they get shuffled
around intentionally so that each T cell has a certain
specificity to a combination of an MHC II complex and a
certain polypeptide, a certain part of a virus. So only this guy’s going to be
activated, not this guy. So this is why we call it the
specific immune system. Now we said, what does
that helper T cell do at that point? He said, hey, I happen to be the
one helper T cell that can bond to this guy, this antigen
that’s presented. It becomes activated. And I won’t go into the details,
but in general, dendritic cells are the best
ones at activating it, especially a naive T cell. In general, when we talk about
a naive B cell or a naive helper T cell, these are cells
that are non-memory, non-effector, that have never
been touched by– they’ve never been activated, in
the case of a B cell. They’ve never been activated by
something binding to their membrane bound antibody– or
a naive helper T cell is a non-effector, non-memory helper
T cell that’s never had anything bound to it. So if this guy is naive and then
he finally has a reaction with this antigen presenting
cell, he becomes non-naive. He becomes activated and when
activated, two things happen. Well, just like with B cells,
he proliferates many, many, many copies of himself and some
subset of those copies differentiate into
effector cells. And effector just means
it does something. It does something now instead
of saving the memory. And then some subset of them
become memory helper T cells after getting activated. Now the memory T cells, just
like memory B cells– now you have more copies of this. So in 10 years in the future,
if something like this happens, this interaction’s
going to be more likely to happen. These guys have the same T cell
receptor as their parent. It’s just that the memory T
cells– or actually even the memory B cells– they
last longer. They don’t kill themselves. They’ll last for years so that
if 10 years later, something like this starts presenting
itself, you’re going to have more of these guys around to
bump into this guy so that you can raise the alarm bells. This guy’s also going to have
the same chain right there. So you’re saying, fine. I have these memory cells. They’re going to stick around
so that this reaction can happen in the future, but I
still haven’t answered the question, what does the
effector T cell do? What the effector T cell does
is it raises the alarm. So there’s an effector T cell. It has been activated. Remember, this is
very particular. Only this version of T cells,
but once it got activated, it produced many copies of itself
because it says, hey, I’m responding to a particular
type of pathogen. So that this is a
helper T cell. This is an effector. And what these do is they
start releasing these molecules called cytokines. So they start releasing
cytokines. There are many, many different
types of cytokines and I’m not going to go into detail on all
that, but what cytokines do is that they really raise
the alarm. So if you have other activated
lymphatic cells or other activated immunological cells–
when the cytokines enter those cells– remember,
cytokines are really just proteins. When the cytokines enter– or
polypeptides– when they enter those cells, it makes
them get in gear. It makes them multiply more
often or it makes them get more active in their
immune response. So what this does– these
cytokines you can view as chemical alarm bells chemical
or peptide alarm bells alarm bells it it tells everyone
to get in gear. So that’s one role, and so you
can see this is actually a very central role and it’ll tell
both activated cytotoxic T cells to get in gear, which
we haven’t talked about yet. And it’ll also tell B cells
to keep proliferating. So when an activated B cell gets
some of– so this is an activated B cell. When it gets some of these
cytokines, that maybe come from a local helper T cell,
it’ll tell it, hey no, divide more often. Divide more often. Only if you’ve been
activated already. And we’ll talk more about why
it has to be that case, because you don’t want all the
B cells to be activated. And the other thing that the
effector T cell does– in the B cell discussion, I said, OK,
if I have a B cell, and it has its membrane bound
antibody, has its membrane bound antibody. And remember, this is a
particular version, it has its particular variable
chain right here. And this guy binds
to a pathogen. So this binds to a pathogen. Maybe it’s a virus
right there. Up to now, I’ve been saying
that this guy’s activated. And he’s going to– well, when
he binds to the pathogen he’ll take this in and he’ll take part
of the pathogen and cut it up and place it on
an MHC II molecule. And we said, then he’ll
be activated. He’ll proliferate and he’ll
differentiate into memory and effector B cells– but that’s
not quite true. This first stage happens. This guy bonds. This B cell happened to be
specific to this virus. Cuts up the virus. Puts parts of the virus on its
surface and presents parts of the antigen. But in most cases, this B cell
isn’t yet activated. You can kind of view it as in
its resting state, ready to be activated, but it hasn’t started
proliferating and differentiating into effector
and memory molecules yet. And in order for that to happen,
an activated helper T cell that is also specific to
this very same virus– so you could imagine someplace else in
the cell– this virus was eaten by a dendritic cell. So this exact same virus, this
exact same species of virus, is eaten by that dendritic cell
and so the dendritic cell eats it up, it cuts it up, and
then it presents it– it’s antigen presenting so it
presents it just like that. Then this will activate
a very specific T cell, maybe that one. So a very specific T cell will
come and bump into it. Not just any T cell,
the one with the right variable portion. So think about what’s
happening. The variable portion for this
T cell, it connects to this part of the virus plus the MHC
II, but it’s really reacting to the same virus. It might be a different part. This little part that was cut
off might be someplace inside the virus while the epitope for
the B cell might be some place on the outside of the
virus, but they’re both specific to the same virus. Now once this guy gets activated
and he starts producing memory and effector
cells– or they’re descended from him, one of those effector
cells specific to this virus are needed to
come bind to this guy. So then this guy could then go
along and bump around and eventually end up here. And he is also specific
to this virus. So this binding site right
here is the same as this binding site. This combination of antigen
plus MHC II. And so when this guy binds–
and remember, this binding site is the same as this and
it only binds to this combination right here– this
is what activates the B cell in most cases. This is T-dependent
activation, which is usually the case. Sometimes all you need is this
first thing, but in general you need the first thing and
then you also need a T cell to come and activate it, and only
then will the B cell get activated and start
proliferating and dividing and differentiating itself and
producing– when its effector cells will produce a
lot of antibodies. And so there’s a natural
question. Why do biological systems–
or why do we have this double system? And at least my sense of it is,
it’s a failsafe mechanism. If every time a virus came and
attached this, this guy just started going crazy and
producing antibodies against this thing, there’s some
chance that maybe after development, this chain right
here or his genes for generating these chains become
specific, not for foreign pathogens, but maybe they
become specific for self molecules, molecules
that are naturally produced within the body. It’s just a random mutation, but
if he started going crazy for that, his antibodies will
start attacking molecules that are naturally in the body and
then that could really hurt. That what causes autoimmune
diseases, where your own immune cells start activating
yourself. But if you have this double
handshake system where this has to happen and this has to
happen, the likelihood of both of these guys after they leave
their development stage becoming specific to a self
protein or a self cell or a self molecule is
very unlikely. So it kind of inhibits this guy
from going wild, even if he has some type
of a mutation. Anyway, hopefully that explains
a little bit of what helper T cells do. We’ll talk a lot
more about it. I know it can be a little
bit confusing. In the next video, we’ll talk
about cytotoxic T cells.

About James Carlton

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100 thoughts on “Helper T cells | Immune system physiology | NCLEX-RN | Khan Academy

  1. Hi there. Nice job on your ed videos. I am wondering if you can tell me what kind of tablet you use to draw on. It has a nice effect.

  2. Thank you so such for all this work. My daughter is lucky she can understand English, because her classes in our country (France) are so badly taught not all but this year the biology one is particularly bad that she learns things on YouTube. The difference between these cells was so poorly explained that she was all confused and now she's fine.

  3. Does T helper cells circulate like the cytotoxic T cells in blood  or it just remains in lymph nodes . i am so much confused.

  4. half a million views in 5 years. Taylor Swift gets that many in 5 days. Imagine if it were the other way around. 

  5. nice video could have done without all the repetition I swear it could have drove me insane. "This piece right here, this piece right here ya this piece right here it bind to and it binds, this right here it binds to the b-cell…"

  6. Thank you for the videos! I am learning a ton of stuff, this explains better than my college because you show pictures and actually explain it! I LOVE IT LOVE IT LOVE IT THANKS A TON XOXO KHAN ACADEMY

  7. Does it mean that when the pathogen attacks the body, both B cell and dendritic go to interact with that pathogen? I'm able to follow the story that the dendritic cell eats the pathogen ,cut it up and presents the antigen for T helper cells to attach to it and raises alarm. However, I'm lost at how does the B cell get involved and represents the antigen of this pathogen ??  Can you help me understand it please. Thank you!

  8. i love your existence KHAN! YOU ARE THE MOST AMAZING TEACHER IN THE WORLD ! Thank you for everything you have done for us college students !!!!

  9. So is dendritric cell has antigen receptor on its surface?? or it just engulf directly??without antigen receptor??…and After helper T cells get activated, only the effector helper T cells will bind to B cells?? the memory helper T cell just stay there for recognition for year?

  10. What is the function of Helper T cells in cell mediated immunity. Cytotoxic cells kill the infected cells and is there any involvement of Helper T cells? Tx

  11. Great video! this isn't easy to understand, I enjoy the redundant information since introducing this subject once into the mind doesn't cut it. Keep up the videos!

  12. Does the The mannose receptor (MR) that is a PRR bind the T helper cell to the antigen? Or would it just be stated the PRR binds the T helper cell to antigen. I have researched this and read binding is do to antigen processing. I would think there would be more to it then. "antigen processing"?

  13. Dude please give a lecture about advanced immunology – B and TCR formation, complement system, cytokines, etc. I am studying medicine and you normally have enough substance to achieve greater levels of education but the immunology is under-developed 🙁

  14. Hold on, do the cytokines cause the B cells to divide, or does the T helper cell binding to the B cell cause it to divide into active and memory B cells? or both? If both, then how does that work?

  15. I'm a bit confused !! Here B cell need effector Th and antigen to really get activated (double handshake) . By the way B cell is an APC so NaiveTh thus can get activated by B cell too. B cell can activate Th and Th can activate B cell ?

  16. Nice video, especially for beginners. However, It can also help you gloss over your knowledge for more advanced viewers too! Congrats for your efforts and keep up!

  17. Es poco entendible la traducción al español, el ingles o español médico no cualquier traductor logra plasmar lo que se esta diciendo, la Fundación Slim debe tomar eso en cuenta, hay una máxima más vale no hacer las cosas, que hacerlas mal, disculpen pero así lo percibo

  18. what's the chance of a B cell to meet his corresponding particular antigen??
    I mean there are thousands of B cells in your body which are different right?

  19. Isn't the main difference between B and T cells is that B-cell receptors bind and recognize carbohydrates, and T-cells recognize peptides? And only peptides can be loaded on MHC receptors.

  20. How can the effector-TCell bind to the MHCII+Anitgen-complex of the B-Cell if the Antigen presented on the MHCII of the dendritic cell is not the same? (At 17:20 until 18:23)

  21. Hey Sal? You mentioned 3 types of lymphocytes at 6:00 but you only mentioned 2 of them – B cells and T cells. Did you also mean to include the Natural Killer cells?

  22. So the B cell is activated when a helper T cell binds and a helper T cell is activated once it binds to its specific antigen?

  23. I have a question that keeps bugging me because I cant find any answer to this. From what I understand T helper cell gets activated when its receptors recognize antigens presented by MHC II on some APCs. What's not clear to me is that when the activated T helper cell move on to activate B cells, does it require the B cells to have the same antigen presented on its surface just like the APC has presented in order for the B cell to produce antibodies against that specific antigen? If not, how would the T helper cell instruct the B cells what antibody to make? If yes, the chance for all events to happen seems to be very very small to me. Can someone please answer my questions? It would be a great help to me. Thanks

  24. Had the dean of the auckland med school try to explain this to my class of pre med kids and it was so bloody difficult to comprehend.
    However this video was my personal saviour for understanding adaptive immunity… ABSOLUTE LEGEND

  25. better than how my bio teacher explains this. THANK U SO MUCH YOU ARE A LIFE SAVER. YOU REVIVED MY SUFFERING GRADES

  26. If the T lymphocytes become mature in the thymus and the thymus becomes very small by adolescence does that mean that the number of t lymphocytes which mature are reduced?

  27. cytotoxic are also called killer t cells right?!?!? ive been trying 2 figure this out for like years!!! please tell me someone!!!

  28. my question- can one of the helper t cell specific to the virus bond with B lymphocytes activate it??? without involving dendrite of the non specific immune system?? or its only affector helper t cell produced by dendrite or other microphage etc???

  29. after searching all over the internet for a good explanation about this subject, in english and portuguese(my first language), I could FINALLY understand!!! Thank you so much!

  30. how can you increase your t helper cells. after stemcell transplant my sons b cells and nk cells goes up more than the normal levels but his t cells remain low as in below the half range of the normal range.

  31. Autoimmune pathology is the wreckage of the Immune System as Nature Intended (Normal Anatomy and Physiology).  Nothing of the normal physiology of Lymph Nodes, the active Cellular Player (Neutrophils and Lymphocytes) or simply stated Leukocytes, are any longer present.  Of course, I am talking about the Most Proliferating Disease (MPD) in Mankind's Brief History.  Although, there is Neoplasia (Abnormal Cell Growth, Cancer) and Prions, but if there is an Idiopathic and Profitable Failure of the Immune System, Then Save ALL because that is PATHOLOGY as never seen before….

  32. Sal, aren't we assuming that a membrane-bound antibody specific to a particular pathogen already exists to bond to that unwanted body? What happens if a pathogen for which there is no antibody becomes present in our body? Do we call the undertaker?

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