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  • It is time!

  • We have arrived at the final conflict.

  • The battle royale.

  • A fight to thewell, hopefully not death, but a big fight anyway.

  • It only seems fitting that we spend this, our last episode of anatomy and physiology,

  • talking about one of your body’s last-ditch efforts to defend itself, at all costs.

  • This is what happens when all the other failsafes have failed.

  • Your skin and mucous membranes did what they could, as physical barriers against infection. And

  • your humoral immune response cranked out antibodies, in an effort to keep your interstitial spaces healthy.

  • But when those systems weren’t enough, your cells themselves were breached. And pathogens

  • and abnormalities began to run amok where antibodies could not get to them.

  • Now, it becomes the business of your cell-mediated, or cellular immune response.

  • And that’s where stuff gets real. Where cell fights cell.

  • And where the heroes look like T lymphocytes.

  • These lymphocytes, known on the streets as T cells, go after body cells that have been

  • hijacked by things like viruses, or bacteria, or become cancerous.

  • T cells cause inflammation, activate macrophages, get other T cells fired up, and generally

  • regulate much of the immune response.

  • Which is important, because -- of all the ways in this course that we have described

  • how you could die -- two that weve neglected to mention are what happens if your body completely

  • fails to protect itself, and what happens if your immune system goes rogue, and attacks

  • your own, healthy cells.

  • But even when theyre functioning well, some of your immune cells are careening around

  • your body like miniature, biological versions of Mad Max war boys.

  • Amped up on signaling chemicals, scouring the terrain for hostiles, and covered from

  • top to bottom in the dismembered parts of the enemies that they have vanquished.

  • Theyre out to protect all of the tissues and organs and systems that weve been talking

  • about for the past 46 weeks.

  • And these guys play for keeps.

  • If there are cells in your body that look and act like theyre from some post-apocalyptic

  • hellscape, it’s gotta be the cells in your immune system.

  • Aside from the fact that they go around literally eating their enemies, and have names like

  • natural killers,” some of these cells are dressed for the part, too.

  • Specifically, they go around wearing parts of the organisms that theyve killed, so

  • others can see them.

  • Sounds a little bit messed up, but were talking life and death here. The stakes are high.

  • And this kind of behavior occurs both in your innate immune response and your acquired response.

  • Weve already talked about how, in the innate response, when a phagocyte sees a suspicious

  • character, it engulfs it, and kills it, right?

  • But what we didn’t get into before is that, during its attack, the phagocyte actually

  • breaks the pathogen into tons of tiny molecules, and then proudly displays those broken bits

  • in grooved proteins on its outer membrane.

  • These proteins are called major histocompatibility complexes, or MHCs. And theyre a lot like

  • how Vlad the Impaler decorated his front yard with the bodies of his skewered enemies ... or

  • how a battle-crazed warrior might show off a necklace made of knucklebones.

  • Because cells from both your innate and adaptive branches do this grisly accessorizing like

  • it’s their job, they are referred to as professional antigen presenting cells.

  • Which might make you think, “Is there an amateur version of an antigen presenting cell?”

  • and yeah, there kind of is.

  • Every nucleated cell in your body -- which means all of your cells except for your red

  • blood cells -- have one kind of MHC protein on their surface, called class 1 MHC.

  • MHC 1 proteins present short chains of amino acids that are based on endogenous proteins

  • -- that is, proteins synthesized inside that cell.

  • So if a particular cell is healthy, the antigens on its MHC 1 tell roving immune cells that

  • everything’s ok inside, nothing to see here.

  • But if the cell is, say, cancerous and it’s making abnormal proteins, then itll fix

  • bits of those proteins to its MHC, which alerts immune cells that there’s a problem inside,

  • and basically asks to be killed.

  • Now: your immune-related cells -- like macrophages, dendritic cells, and B cells -- wear class

  • 2 MHC proteins on their outsides.

  • These are the professionals.

  • Class 2 MHC proteins bind to fragments of exogenous antigens, like a virus that’s

  • been engulfed, broken up, and displayed to get the attention of other cells.

  • And this is how MHCs are totally essential to the cellular immune response.

  • Because, the heroes of your cellular defenses, the T cells, can’t actually detect whole antigens --

  • they can only recognize them when theyre all diced up and decorating an antigen-presenting cell.

  • T cells are made in the bone marrow, but they mature in the thymus, the lymphoid gland that

  • sits on top your heart, and which is actually what the “T” in “T cellstands for.

  • And you have several different kinds of T cells, but the two you really have to know

  • about are the helper Ts and the cytotoxic cells.

  • Helper Ts themselves can’t kill, but they can activate cells that do, and they help

  • call the shots for the whole adaptive immune response.

  • Meanwhile, cytotoxic cells are the ones that actually do the killing of the cells gone bad.

  • Now, much like how a naive B-cell carries antibodies for one specific antigen, a naive

  • helper T cell has receptors that will only bind to one specific combination of a class

  • 2 MHC and a particular antigen.

  • If that match is right, the Helper T bonds to the MHC-antigen bit and it gets activated.

  • Then, just like with the B cells we talked about last time, the Helper T starts copying

  • itself like crazy, making a few memory T cells as well, which remember that particular antigen

  • should it meet one again in the future.

  • And it also produces a whole mess of effector T cells -- mostly more Helper Ts, but also

  • some regulatory T cells that I will get to in a minute.

  • But the main thing the helper T cells do is raise the alarm that tells other immune cells

  • that there is a problem.

  • And they do this by releasing a cocktail of chemical messengers called cytokines.

  • When a cytokine enters another Helper T, that cell usually starts dividing, making more

  • memory T cells and more Helper Ts, which release more cytokines that keep boosting the signal.

  • And some of those cytokines also go on to help activate the cytotoxic T cells.

  • You know that macrophages from the innate system just sort of roll up and swallow pathogens

  • whole…. but cytotoxic T cells do their killing a little differently.

  • They roam the blood and lymph, looking for hijacked amateur body cells that are asking to be killed.

  • Basically, these infected cells are already dying, so theyve digested some of their

  • invader’s proteins, and stuck them on some of their class one MHCs, effectively waving

  • a surrender flag made of fragments of the very virus or cancer that is destroying them.

  • If a cytotoxic T cell with the right receptor floats by, it binds to the antigen-MHC combination,

  • and moves in for a mercy killing.

  • It does this by releasing special enzymes that punch holes in the cell’s membrane

  • or otherwise trigger apoptosis, killing both the cell and whatever is inside of it.

  • Then the cytotoxic cell just detaches and continues to run down other prey.

  • So by now it should be pretty obvious that without T cells, there basically is no adaptive

  • immune response. And it really all comes back to the Helper Ts.

  • Which is why immunodeficiencies can be so deadly.

  • AIDS, for example, is caused by the human immunodeficiency virus that specifically attacks

  • Helper T cells. And without the Helper T’s, there wouldn’t be much of a humoral response, either.

  • Because the cytokines that come screaming out of the helpers not only activate other

  • T cells, but they also finish the training of the B cells.

  • The fact is, most of your so-called naive B cells don’t get fully activated -- and

  • become memory or effector cells -- when they first bind to an antigen.

  • And there’s a good reason for that.

  • Since antibody receptors are generated randomly, you might wind up with B cells that could

  • bind to your own, healthy proteins, like, say, your growth hormone.

  • So, once a B cell interacts with a substance -- whether it’s growth hormone or some dangerous

  • bacterium -- it still needs to bind to it, engulf it, and present some fragments of it on its surface.

  • But then, itll stop, to await inspection.

  • It pauses until the right Helper T cell comes by to check out its presentation. If the T

  • cell binds to the presented fragment, then it releases cytokines, which fully activate

  • the B-cell and suddenly youve got antibodies going everywhere.

  • But if it doesn’t, then the B-cell just goes about its business and doesn’t trigger an immune response.

  • This check and balance between Bs and Ts is an important safeguard against your immune

  • system becoming too good at its job.

  • Which is a very real risk.

  • A hyperactive immune system can cause mayhem by losing its ability to distinguish enemy

  • from self, as it turns on your own body.

  • Your regulatory T cells -- another type of effector -- help prevent this by releasing

  • inhibiting cytokines that tell other immune cells to stand down once the initial threat has been handled.

  • Without that regulation, the body might start cranking out too many antibodies and cytotoxic

  • cells that could damage or destroy its own tissues.

  • This dangerous confusion is what causes many autoimmune diseases -- like multiple sclerosis,

  • which eats away at the myelin sheaths around neurons, or Type One Diabetes which

  • tears up the pancreatic cells that make insulin.

  • So the takeaway here is that your immune system is usually really good at its job, which is

  • to kill stuff in the name of keeping you alive.

  • And you really don’t want it to go rogue on you, because if there’s one thing you

  • should have learned in the past year with us, it’s that your body is both resilient

  • and fragile, and it survives only when the sum of its many complicated parts

  • stays balanced and works together.

  • And that is the glorious wonder of you.

  • As we wrapped up our tour of the immune system today you learned how the cellular immune

  • response uses helper, cytotoxic, and regulatory T cells to attack body cells compromised by

  • pathogens. We looked how cytokines activate B and T cells, and what happens if your immune

  • system goes rogue and starts causing autoimmune trouble.

  • Thank you to our Headmaster of Learning, Linnea Boyev, and thank you to all of our Patreon

  • patrons whose monthly contributions help make Crash Course possible, not only for themselves,

  • but for everybody, everywhere. If you like Crash Course and want to help us keep making

  • videos like this one, and teaching courses like Anatomy & Physiology, visit patreon.com/crashcourse.

  • This episode was filmed in the Doctor Cheryl C. Kinney Crash Course Studio, it was written

  • by Kathleen Yale, the script was edited by Blake de Pastino, and our consultant is Dr.

  • Brandon Jackson. It was directed by Nicholas Jenkins, edited by Nicole Sweeney, our sound

  • designer is Michael Aranda, and the Graphics team is Thought Cafe.

It is time!

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免疫系、パート3:クラッシュコースA&P #47 (Immune System, part 3: Crash Course A&P #47)

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    羅紹桀 に公開 2021 年 01 月 14 日
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