The Superhero Locksmith - EWTS #017

Joe: Hello and welcome to Enough with the Science. I'm Joe.

Senan: Yes, and I am Senan. And this is the show where we take simple scientific topics and we complicate them. No, that's wrong. We take complicated scientific topics and we oversimplify them.

Joe: Well no, you take complicated scientific topics and then you make them more complicated and then that's it. We just stop at that.

Senan: I'm confused. Look, we talk about science. That's it. So we take a different topic each week. And anyway, by way of introducing this week's topic, which by the way is Part 2 of something that we did last week, so if you haven't listened to last week's one it might be a good idea before you listen to this one.

Joe: There is a kind of foundation of knowledge that's sort of needed for this week's.

Senan: Anyway, by way of introducing this week's topic; Joe, what's your toolbox like?

Joe: Very underused. [laughter]

Senan: And do you have every tool for every job? The right tool for every job?

Joe: Absolutely not. No, I have a very limited experience in doing DIY and indeed in wanting to do DIY. So no, I have the bare fundamentals. I don't even know what most of them are called.

Senan: So you haven't just gone through that male rite of passage of tinkering in your garage for days on end to produce some ridiculous thing that doesn't work?

Joe: It would probably have to be in someone else's garage because I don't have a garage.

Senan: Anyway, imagine if you could have the right tool for every job; even jobs you've never anticipated that you might ever need to do.

Joe: That sounds like it might interest me.

Senan: So that is the topic of this week's show because we are going to be talking about the adaptive immune system, the human immune system, the adaptive part of it; and it tries to make a tool for every job before it even needs them.

Joe: Wow. Okay. That sounds like a busy week, I think.

Senan: Yeah, this is one of the most complicated topics we have ever approached so I apologise now.

Joe: He doesn't mean that. He means the most interesting. He always mixes those two words up.

Senan: It is interesting but by God it's complicated. Okay.

Joe: So essentially you're looking at how the body defends itself against sickness?

Senan: Well we kind of spoke about that last week but this week we're talking about how the body can anticipate what's coming down the line; things it never saw before. How it can target its response to exactly the right invader and how it can remember that it did that once before.

Joe: That sounds fairly simple.

Senan: So, you know, I'm going to be using extensively today an analogy of a lock and a key, right? So essentially our immune system, the cells of our immune system, are seeking out and trying to grab onto invaders. And the invader has a kind of a chemical signature on the surface which I'm going to call the lock. And we have like a chemical grapple that fits onto that particular chemical signature that I'm going to call the key. So you need a different key for each lock. So every invader has a unique lock on his surface and we're trying to find the key or trying to make the key for that.

Joe: So every dangerous pathogen, you taught me that last week...

Senan: A pathogen is anything that can make you sick, yes; any microorganism that can make you sick.

Joe: Okay, so any dangerous pathogen has a sort of a signature and the body is trying to anticipate what sort of pathogens are going to arrive in to annoy us.

Senan: See remember these pathogens are part of the natural world so they're evolving continuously. So just because we got the flu last year and dealt with it successfully, doesn't mean that we'll immediately be able to deal with the flu this year because it will have evolved into a new version. So that's why we need the ability to kind of deal with stuff we never saw before.

Joe: Okay, so basically our immune system has to evolve.

Senan: Yeah. So what our immune system is doing is it's trying to make every possible key that might ever be required for any lock that might ever occur, right?

Joe: That sounds very busy.

Senan: Yeah, I mean it's making millions of keys, all different. And how it's doing that of course is like the instructions for making those keys are a set of genes in our DNA. And it's just randomly shuffling that set of genes. Every time it makes a new key it shuffles the deck again, follows a new set of instructions, makes another key, shuffles the deck again and on it goes continuously.

Joe: And where is all this happening?

Senan: So it's all happening in the bone marrow. The bone marrow, like in the... it's like this stuff in the middle of your bones all over your body; it's like pulp flesh, I suppose you'd call it. And that's like the factory for all these. These guys that are the star of the show, they're called lymphocytes; these cells that have these keys on them. Most of these keys will never get used and after a couple of days they just melt away, you know, they disintegrate; but that's fine because we're continuously making millions of new ones.

Joe: But so they will make a new... so say we have Key Number 10 Million.

Senan: Yeah.

Joe: And they make Key Number 10 Million and after a few days Key Number 10 Million is gone. Do they make another Key Number 10 Million or do they keep a few?

Senan: No, so I mean there's so much; so many millions of these things being made that at any one time there might be a dozen different Key Number 10 Millions in our system.

Joe: Right.

Senan: Because randomly we just happen to make those in different, maybe one bone made one and a different bone made another one and so on.

Joe: Right.

Senan: And like so it's not that there's like only one single key somewhere in our body for a particular infection. Typically we will have several copies of that key that have been made randomly in different places.

Joe: Right.

Senan: So as I say they're called lymphocytes, these cells. Now the problem about making... I'm kind of going to give you an overview of how this thing works before we dive into the details, right? So these things are made in the bone marrow. The problem though is that because you're making all these random keys for invaders you've never seen before, some of those keys in fact quite a lot of them are going to fit a lock that's on our own healthy cells. So we don't want our immune system attacking our own healthy cells. So these things have to be rigorously tested before they're released out into the environment of your body because otherwise they might attack our own body. So we've got this really rigorous testing system. Some of that goes on in the bone marrow, some of it goes on in a gland called the thymus which is in your chest. And the ones that fail the tests are destroyed and that's a lot of; a lot of them get destroyed at that stage because they fail the tests. The ones that pass the test end up either in your lymph nodes or in some cases in your spleen as well and in there some training takes place. So they are; any fragments of invaders that are found around the body are brought there and they're exposed to these.

Joe: So you say fragments; this is after they've been dealt with?

Senan: Well no, I mean there are cells called dendritic cells, we'll come to later, that are extracting fragments of these invaders and bringing them to the lymph nodes. Well extracting fragments of anything that might maybe be an invader and bringing them.

Joe: You realise how violent that sounds? "Extracting fragments." I'm just going to take a leg. I'm not sure who you are. I'm just taking a leg; we just need to test it.

Senan: Yeah, now look they're not doing it to our own cells but they're doing it to what looks like an invader cell.

Joe: Oh that's okay then.

Senan: Yeah well look... ultimately we're planning to massacre the invaders so like, you know, it's okay. So they bring these fragments into the lymph nodes where the young new lymphocytes have collected and they see if any of them match the key.

Joe: Right. It's like a quiz game show. Who fits; I found this leg. Who fits?

Senan: So if they find a key, i.e. an immune cell that fits the lock, that means that we now know that there's an invader in the body. And the key cell, the lymphocyte that has the key, suddenly goes into overdrive manufacturing thousands of copies of itself to respond to that invader. And it's a targeted response. Every single one of those copies has a key for that particular invader. There's a few different roles; these copies that have these keys go on to play various different roles. We'll talk about that. Then after the battle is won most of them fade away and die off in a few days; all these, this army that we built up just to deal with that one invader. But crucially a few hang around and those are called Memory Cells. And those are the ones that the next time we get that infection they'll respond really quickly and deal with it before we even know we're sick. So that's the overview of how it works.

Joe: But there's a lot of complexity there.

Senan: Yeah, there's a lot of complexity.

Joe: So next week; what do we do next week?

Senan: I was hoping to save us. Next week is Part 3 of the Immune System! No, I think we'll leave it at two parts. Right so, these lymphocytes are the elite soldiers, they're the stars of the show and there's two types. The B Cells; B is for bone marrow by the way. They're born in the bone marrow, they're tested in the bone marrow and they mature, the ones that survive the tests, mature in the bone marrow. The T Cells also born in the bone marrow but they mature in the Thymus gland, which is why they're called T for Thymus, and the testing of those ones goes on in the Thymus gland.

Joe: Thymus is very unremarkable little gland, isn't it? You don't often hear of it. Not one of the big boys, not one of the big players.

Senan: You don't often hear of it. There's a great production line going on the whole time. Like in your bone marrow there are literally millions of these cells, these lymphocyte keys being created every day and they're all different random keys. And the same in the thymus; there's like thousands of them being tested continuously in the thymus and being matured if they fail.

Joe: Is that what the thymus does? Is that the job of the thymus?

Senan: Has it got other roles? I couldn't tell you. I'm sure it probably does 'cause generally speaking our body is multitasking; each part of our body does multiple things.

Joe: Yeah. I think the thymus is just a lazy gland. That's why we haven't heard of it. Just like; "What do you do?" "Well, I let these boys in, they do a bit of training."

Senan: Yeah. Well if I wasn't there see how you get on. So the testing that they do; there's basically two tests. The primary one is: Does this soldier mistakenly attack our own cells? So our own cells have certain chemical signatures, i.e. locks, on the outside of them. And the test exposes these young lymphocytes to typical locks, typical signatures that are found on our own cells. And any of them that react are instructed to kill themselves. So it's that...

Joe: That's my kind of school. That's where we've gone wrong with our education system. You don't agree with the system? You're out.

Senan: Yeah and it's that word we used last week: apoptosis. So it's like a nice, neat, programmed cell death. So it's an inbuilt mechanism in every cell how to kill itself in a nice neat way. So you just have to whisper the right secret phrase to tell it to kill itself.

Joe: Quietly in the corner. Don't annoy anybody.

Senan: And it'll do it. Afterwards there's a few bits of debris left over and our friends the macrophages will happily clean that up; will eat that up in the same way that they eat up viruses and bacteria.

Joe: It's amazing the difference in those two; like "Clean it up" / "Eat it up". It really changes your opinion of macrophages.

Senan: It does yeah. Well I mean generally they ingest stuff so eat is probably a reasonable way of putting it. But there's a second test. So last week we spoke about how the immune system has a radio. Now it doesn't really have a radio; it has a way of communicating using chemical signals. So certain immune cells release certain chemical signals that tell other immune cells to do certain things. So we'll call that a radio. And the second test is: Can the lymphocyte actually respond correctly to those radio messages? So those are the two tests. If it fails either of them it goes into programmed cell death and that's the end of that. And it's really severe. Like the T cells; about 95% of them fail the test and die off at that point.

Joe: So fail one or other of those two criteria?

Senan: Yeah, yeah. And there's only 5% of them go on to be released into the wild as it were. It's not quite as severe for the B cells but about half of them end up getting killed off and the other half go on to go into the wild. But the B cells have an interesting mechanism for checking to make sure they're not about to attack one of our own cells; we'll talk about that later on. Let's talk about the components of this training system that's teaching these lymphocytes, these B and T cells, how to identify invaders. You've got a thing called an Antigen. That's just a fancy word for the lock. So the chemical signature that is a part of the outside wall of an invader is... the bit that our immune system identifies as "That's the invader," we call that an Antigen. So each... it's the lock; and each invader has a different lock.

Joe: And antigens are only on invaders?

Senan: Well for the purpose of, yeah; it's just a name we have for the bit of an invader that our immune system identifies. The... you have these things called Dendritic cells. Now dendrite is just a fancy name for spiky. So these things look a bit like maybe starfish, these spiky things. And they use these spikes to essentially remove the piece of an invader that is the antigen.

Joe: Very violent world.

Senan: Yeah, they're collecting the bits of invaders that are antigens and they bring them back to the lymph nodes, which is where the training kind of takes place of the B and T cells. So after the B and T cells have passed the test and get released from either the thymus or the bone marrow, they go to the lymph nodes primarily. Some of them go to the spleen but the same thing happens in both places. These dendritic cells bring antigens, you know the locks from the invaders, and wave them around in the lymph nodes or in the spleen and say, "Hey has anybody got a key for this?" Right? So if somebody, i.e. a B or a T cell, has the right key, that's essentially the message that tells your immune system there's an invader here that we have identified that needs to be dealt with. So the B or T cell that has that key suddenly gets what they call 'activated'. Which essentially means he goes into overdrive and starts doing the thing he was born to do. We'll come back to that in a minute.

Senan: The Lymph Nodes; this is where most of this training goes on. They are small reservoirs about the size of a big pea [laughter] and you have clusters of them in various parts of your body where lymph, this clear fluid called lymph, collects. And what a lot of people don't know is there's a complete separate plumbing system for lymph. So we know we have blood vessels, you know arteries and veins and that's the plumbing for the blood, but there's this other set of pipes going around our body for this clear lymph fluid that allows the immune system to circulate its components separate from the blood. And they connect up all these lymph nodes, these pipes, and that's kind of where the immune system training is taking place. Finally another component; a guy we spoke about last week and indeed we mentioned him earlier today: Macrophages. So those are like the Pac-Men of the innate immune system. They're going around eating as many invaders as they can find. They actually have a secondary role with the adaptive immune system. A bit like our friends the dendritic cells, the spiky guys we spoke about a minute ago, these macrophages will chop off the antigens—the locks, the identifying signatures off the invaders—display them on their back, on their outside...

Joe: Wow. Vikings. Look at my necklace of ears that I collected from these guys.

Senan: Yeah, and they're like as ferocious as Vikings too. It's a good analogy for them. And what that does is nearby lymphocytes; so these are lymphocytes like B and T cells that have now been released out into your general system, they latch onto this. Their key fits into that lock. And what that does two things: It confirms for the macrophage that yes, you really have found an invader, and it then provides assistance so the lymphocyte, the B or the T cell, will release some helpful chemicals that make the macrophage much more efficient at killing this invader. There's this whole over and back interaction between different components of the system. Now you've heard me talking at length about T and B cells and if you want to interject here at any point please do because I'm going to run dry here.

Joe: No, I've left. Sorry, I'm just back. [laughter]

Senan: So let's talk about what is the difference between these two different kinds of lymphocytes; the T cells and the B cells. So T cells need effectively to be taught in the lymph nodes and in the spleen about how to recognize an invader. B cells don't need any teaching; they can recognise the invader after they've matured themselves. However, they won't fully activate until a T cell comes over and confirms for them, "Yes you really have found an invader."

Joe: Oh yes, you're good to go here. Kill.

Senan: So the T cells can decide on their own because they've been properly trained. The B cells have not got much training; they can still identify the invader probably but they won't spring into action until a nearby T cell...

Joe: They're too dangerous to be allowed make their own decisions. I know a few people like that.

Senan: Yeah. Too naive. The T cells are kind of the command and control, the generals of the whole thing. There's a few different kinds, we'll talk about in a minute. But the B cells are the factories for antibodies. They also do a little bit of the teaching; a bit like the dendritic cells they help to teach other lymphocytes about invaders. But their primary thing is the B cells are basically churning out billions of antibodies. And we'll come to antibodies in a while; they're different from antigens that we mentioned a while ago, but antibodies are another part of the whole response.

Joe: This week's exit exam is going to be a doozy. [laughter]

Senan: What does this activation... you've heard me talking about T cells and B cells getting activated; that's when the key they have fits into a lock of an invader. It essentially means they go into overdrive and they start churning out thousands of copies of themselves. Like one T cell can literally make several thousand clones of itself in a matter of days. And of course there will be more than one of them getting activated for any one infection. And in the case of the T cells there are three different kinds of them, even though I'm using the word clones, but they have three different distinct roles. All of them will have the key that fits the lock of the invader so they can all target that specific invader. In the case of B cells, they mostly produce, when they start cloning themselves, they mostly produce something called Plasma cells. Got nothing to do with blood plasma.

Joe: That's what I thought now. I was going to jump in there. What's it to do with blood plasma?

Senan: They are essentially biological 3D printers. They start churning out antibodies; which antibodies are not cells, they're proteins; but they start churning out antibodies at a rate of thousands of them every second. One of these plasma cells can create thousands of antibodies every second and every single one of those antibodies has the same key that allows it to identify that specific invader. So suddenly you've got this huge army all focused on one invader. So it's this massively active system all of a sudden as soon as the key fits into the lock; the first time the key fits into the lock. As I said, three different kinds of T cells. Helper T cells: these are kind of the generals. These are the boys that are directing traffic...

Joe: Whispering at the B.

Senan: That are directing the whole battle. They don't kill anything directly themselves; they're above all that.

Joe: They're sitting at home drinking tea.

Senan: They coordinate the whole response. So one thing they do is they release chemical we mentioned last week was Cytokines. This is part of the radio signaling system. So the cytokines wake up a lot of the other cells in the immune system. So that's one of the things they do. They release Interferons, another thing we mentioned last week, which is a chemical that interferes with viruses. What it actually does is it causes cells nearby an infected area to toughen themselves up so it's harder for the invader to invade them. Right. The next type of T cell: these are the elite soldiers. The Cytotoxic T cells. So cyto means cell, toxic means well, poison. So they're poisonous to cells. So they are the ones that actually hunt down and kill the enemy. So these guys have specifically targeting one particular kind of enemy and they're hunting them down in their thousands.

Joe: I'm glad to see they put some thought into this name though. Not like the Natural Killer cells. Natural Killer cells was just like "Wow, where'd you get that name from?" But Cytotoxic...

Senan: Well it's wonderfully descriptive isn't it though? Natural Killer.

Joe: Natural Killer cell; I think if you typed that into Google though that might attract the attention of the NSA or a drone would be over your house.

Senan: Perhaps.

Joe: Cytotoxic T cells though does sound like a punk band.

Senan: You know actually I can even imagine the dendritic spiky hair.

Joe: Yes.

Senan: So the cytotoxic T cells have... so their main function is to kill invading cells but they can also do another interesting thing. So as we mentioned last week how viruses operate is they inject their own DNA into your cells and then they convert your cell into a factory to make more viruses.

Joe: The devils.

Senan: The cytotoxic T cells can actually identify one of your own cells that has been invaded by a virus and it can kill that cell to stop it from churning out more viruses. So they're pretty efficient at handling invaders, these cytotoxic T cells.

Joe: Although if they ever wanted to go bad they could use that as an excuse to kill your own cells, couldn't they?

Senan: Well as long as all your own cells are virus infected cause they're only doing it to virus infected cells.

Joe: Oh yeah. But I mean if they decided suddenly just to go rogue and kill healthy cells they could go "Oh no, he had a virus."

Senan: Well I suppose any of these cells are capable of doing that if their instructions go a bit awry. So yeah, but yeah, maybe.

Joe: I just can't... I'm at the point now where I can't believe someone hasn't kind of animated this.

Senan: It probably has been animated.

Joe: Would be some sort of Japanese anime sort of ultra-violent type of cartoon.

Senan: Finally the third and final kind of T cell; they're known as the Regulatory T cells. So they kind of keep a lid on the frenzy because once this frenzy of your immune system response gets going it has the potential to go overboard and start damaging your own healthy cells or just generally interfering with the healthy operation of your body. So these guys they're trying to keep a lid on it, stop it going overboard. And then when the battle is over; assuming you have survived; they calm everything down afterwards and try and damp down. They basically tell...

Joe: Right that's enough lads. That's enough now. Let's go back. Let's go home.

Senan: Tell the soldiers to go off and have a smoke or whatever it is that they don't need to fight anymore. So basically those guys are preventing friendly fire from happening. Right, I mentioned antibodies a while ago. What are they? So they're not cells as I said; they are proteins. Now a protein is essentially a long complicated bio-molecule and typically they are folded up in very complicated structures and part of their functionality depends on them being folded up the exact right way. Anyway that's a bit of a digression. These antibodies are Y-shaped proteins and one end of the Y has the key to fit into the lock that is the invader. And they operate in typically four different ways. And remember we said that your B cells that have become Plasma cells are churning these guys out at a rate of thousands every second. So the system has been flooded at this stage by antibodies which all have a key for the invader. They have four key operations. First one is called Neutralization. So in the case of a virus; a virus has its own key that it's trying to use to find a lock to get into one of your cells. What these antibodies will do is they will actually stick to the virus and block its key from activating. So they physically get in the way of the virus from invading a cell. A word from last week: Opsonization. Which is an awfully complicated word for tagging.

Joe: They give them a giant coloured hat.

Senan: So what they do is they latch on to the lock; the key that the antibody has latches onto the lock. Doesn't actually kill the invader but it acts as a tag now. It's now; the invader is now walking around with this thing flapping around attached to it. And that calls in other like macrophages or neutrophils or other elements of the immune system who recognize that tag and latch onto it and kill that invader. Another; the words here are fantastic. Agglutination. So this is basically the sticky ball technique.

Joe: We're going to have a spelling test next week. I'm going to take all this down. We're going to do a spelling test.

Senan: So what it does is it kind of; the antibody barrels into a place where there's a load of viruses and it's like a big lump of glue and it sticks a bunch of them together into a bundle, right? And again that physically stops those viruses from invading our cells, from doing what they want to do. And finally then the antibodies help to activate the Complement system we spoke about that last week too. That's a set of about 30 different proteins that are floating around in our blood that are normally dormant. 30 different types of proteins that are normally dormant. But when they're triggered they assist with the response to an invader. So for example they punch holes in the walls of bacteria; that kind of thing. So yeah, the antibodies are a key part of the whole thing even though they don't directly kill cells themselves. Right. How long does it take for this adaptive response to happen?

Joe: Because there's a lot going on.

Senan: There's an awful lot going on. And the training; there's several stages to the maturity and testing and training of the cells so it's a slow enough process. It takes seven to ten days for the adaptive immune system to ramp up to full speed. And that's often why you will feel sick for maybe a week or a week and a half with a cold or a flu before you start to get better because your innate system is trying to fight it off and it's not really doing a fantastic job; it's kind of keeping it at bay but you're feeling sick all the same. But all the time your adaptive system is getting ready for action and then suddenly it has the right tool for the job...

Joe: Like, "Woohoo! We found the key! We found the key! New! Come on! Let's go!"

Senan: And it's able to just kill off the infection in a day or two once it does ramp up. So that's kind of... very serious illnesses typically are ones which get serious enough before our adaptive system gets into gear. So in that first 7 to 10 days they really make us very sick and maybe might make us too sick to recover from. Now wouldn't it be fantastic; all of this training, all of this adaptation to a particular enemy to have a real strong response against one particular invader; wouldn't it be amazing if we could remember that for the next time? Like if we didn't have that seven to ten days delay at the start...

Joe: Well I was just thinking there because it's horrible; I was kind of going "Oh seven to ten days that's atrocious." But like when you hear everything that's going on...

Senan: Yeah. It's amazing.

Joe: You're like: "Holy moly." They're not sitting around these guys.

Senan: Yeah, yeah. And that's exactly what happens because after the battle is over a hardy few, a very small percentage of that big army that was built up for the battle, stick around. They continue to live on. They're called Memory cells; the B cells and T cells that have kind of transformed themselves into these memory cells. Some of them are in the bloodstream, some of them are hiding in special places in the bone marrow or in other tissues around our body. And they live on for years in some cases; some last longer than others, we'll talk about the effectiveness of it in a while. But the important thing about it is that the next time that particular invader comes to your body, they react with lightning speed. Like they ramp up in a matter of hours. The response is typically stronger than it was the first time you had that illness even though it took seven to ten days to build up the response the first time; the new instant response is actually stronger. In almost every case you're unaware you ever got sick. Like they just deal with it in a matter of hours. You've no symptoms of being sick and it's dealt with.

Joe: And it lasts; it depends on the illness how long that store lasts.

Senan: Yeah so I mean there's a couple of reasons why different ones last for different amounts of time. There's a couple of reasons because of that. You're probably aware for example COVID vaccinations typically are only expected to last for maybe six months or so.

Joe: What?

Senan: Yeah. Which is why you were getting a booster shot every now and again. And it's also why there's a different flu vaccine every year. So some viruses and bacteria evolve at a really fast rate. They're constantly changing. So although you might have memory cells for last year's flu still in your body this year, the flu you get this year looks... has a different lock. It looks different to the one that you got last year so it doesn't trigger the memory cells from last year's one. Same with the common cold. That's why the cold makes us sick every time we get it. Well at least... we probably get it more often than we think we do and the adaptive system deals with it sometimes but sometimes it has evolved so different from the last time you had it that your memory cells don't get triggered. On the other side of that coin, there are certain viruses; say the Polio virus. That one hardly evolves at all and as a result a vaccination... oh yeah we'll talk about vaccines in a minute but they use this memory system. But as a result a vaccination you had, you know, when you were a child still lasts into your adult years. And another one is the Spanish Flu which happened there about 100 years ago. There was people tested like, you know, people who maybe were children when the Spanish Flu was around and who maybe lived to be in their 80s, and their immune system was tested and they were found to still have viable memory antibodies and memory cells.

Joe: And is it linked to the severity of the virus? You know like Spanish Flu killed...

Senan: Amount of people?

Joe: Amount of people.

Senan: I don't think so because look at COVID. I mean COVID we don't retain the immunity for. So like and that was a pretty severe virus for a lot of people too. So yeah look it varies from virus to another. But yeah I touched on the whole thing of vaccines. And vaccines only work because of the memory cells; because these memory B and T cells. We're basically piggybacking on that system with vaccines. So what happens is you get injected with a weakened form of whatever the invader is, whatever the disease is. It's too weak to actually make you sick; or it might make you feel a bit off for a couple of days in some cases; in others you mightn't feel anything at all; but it's enough to trigger our adaptive immune system to ramp up, start the battle. Then the battle is kind of over pretty quick and we don't really feel sick. But we now have the memory cells because the battle created a few of these memory cells and they are now going to hang around and the next time, like if we get that illness for real as opposed to the weak version we got out of the syringe, the next time they're going to immediately spring into action and deal with it. So that's basically what vaccines are doing. Yeah, so that is the story of our immune system.

Joe: Lazy, lazy system isn't it? Doesn't do very much. Sits around all day.

Senan: It's amazing when you consider all the things we have spoken about this week and last week. It's like a phenomenal amount.

Joe: But it's doing that all the time. Like for example bone marrow... like your bones are just sitting there and they do lots of amazing things to help you function as a standy-uppy person.

Senan: They're basically scaffolding. And yet they have this...

Joe: In the middle of them are these factories that are working day and night.

Senan: Yeah, yeah. It's phenomenal. I mean and there are so many dangerous bugs that we can't see floating around in the environment. I mean if we didn't have this fantastic system we wouldn't... none of us would be alive. You know? It's pretty thought-provoking stuff.

Joe: Well I'm sure everybody who's listening to the programme is glad they're alive this week because now they know so much more about like why you're alive. And you should go out and appreciate it even more.

Senan: Absolutely. Enjoy your life while you have it because you've got this massive army working away silently to allow you have a nice fun life so...

Joe: It is amazing all the millions and millions of things that have to go right to make you feel good today.

Senan: Yeah, yeah. That's before we even start about psychology.

Joe: Yes. That's next week. We get back to depressing, depressing topics.

Senan: Anyway before we go, don't forget you can find full transcript of this and every other episode on our website enoughwiththescience.com. And yeah, that's the end of this week's show.

Joe: Brilliant. Thanks very much. Good luck from me.

Senan: Yes, and goodbye from Senan too.