DIP Episode 136 - Comprehensive USMLE Step 1 Immunology Review 1

Okay, welcome. My name is Divine. I am a resident and this is episode 136 of the Divine Intervention Podcast. In this podcast I'm going to be going over in Monology for the US and the SNP1. This will be the first part of this podcast. So just jump right into it. Really, Monology to be perfectly honest, the best we don't understand in Monology is to kind of get it as a story. If you're able to see how things, you know, all kind of like fit together, things get a lot more intuitive. And the problem is, Monology cuts across many, many, many different fields of medicine, right? So it's one of these things that it's almost like a subtle science, but again, if you buckle down and really learn it, it can be often speeds, especially when you're taking these USMLE exams, most especially USMLE step one. And as we're going along again, I'll try to introduce some clinical vignettes to sort of help you solidify things together. And I guess the well sort of talk about immunologies, I guess I'll maybe start by giving an overview of the immune system, right? So I mean, we know, obviously, the immune system helps you deal with infection, right? It also helps you deal with like cancer, for example, right? And I mean, there's like two big parts of your immune system. There's innate, there's adaptive. And I mean, it's essentially like multiple things kind of working in concert to protect your body as a cohesive as a cohesive home.

And the thing is, for your immune system to do its job, it kind of needs like some means of communication between the different players. These are the cytokines. Actually towards the end of these, this immunology review, I was playing sometime like really hammering all those cytokines so that you know the high old ones that you need to keep at the back of your mind for the exam. And then I mean, just some big groupings you want to be aware of with regards to your immune system, right? We have like the antigen presenting cells, right? There's a bunch of those, those include things like your macrophages, your B cells, your dendritic cells, those are those are your antigen presenting cells. And the big thing you want to know about those is that they all contain a MEC class too, right? And then we have some things that can help with like, opsonization, right? So things like your, you know, like your antibodies, your C3 B, C3 B is one of your complement proteins. Those things all kind of help with the phagocyteosis. Phagocyteosis is a process that already happens in and of itself, but the opsonants like these antibodies and the complement proteins, they kind of make that process a lot more efficient. So I guess with regards to differentiating between you and your adaptive immune systems, right? So big things you want to keep in mind. Your innate immune system, it's kind of, you're kind of like born with it, right? So it's kind of like hard wired into your germ line, right?

So for the most part, your innate immune system is heritable, right? So it's something that's transferred from father to son or mom to daughter or whatever. Basically it's transferred across generations. So it really doesn't change, doesn't change much. It gives you the same response every single time, right? But your adaptive immune system is actually not heritable, right? It's something that you build as you get exposed to antigen over the course of your life, right? So without exposure to antigen, your adaptive immune system essentially does not kick into gear, right? So it's not heritable for the most part. Again, that's a subtle point, but it's something that's very high yield to remember. And I mean, the thing is you need immune system right? It's almost kind of like non-specific. Although I mean, I guess if you really wanted to drill down, it's kind of specific for like some structures that are shared by like big groups of microbes, right? So those things are called like pamps. So pathogen associated molecular patterns. And those pamps, right, are things that you know, we find on like these foreign invaders that are not necessarily found on ourselves, right? So a classic one is for example, like a man nose, right? Man nose, the protein is generally not found on the surfaces of ourselves. So if you see man nose on the surface, something like, oh crap, this is bacteria, right?

So your in-eating immune system says, okay, I'm going to go ahead and attack this thing, because it has this pathogen associated molecular pattern. Another high yield one that is commonly tested on exam is a lipopolisaccharide, right? So like LPS. Remember LPS is found primarily on the surfaces of gram negatives, right? So because that LPS is found on the surfaces of gram negatives, it's something that again, your in-eating immune system recognizes and says, okay, it's time to go ahead and kill, kill this book, right? But again, the thing is your in-eating immune system kind of limited diversity. There's only so many things that can identify. And I mean, it doesn't have any memory. So again, it's because again, it's hardwired, right? It doesn't have like memory like you have for your for your adaptive immune system. There are actually many things that make up our in-eating immune system. So like all these physical barriers, right? So like your skin, your mucosal surfaces, all these chemicals you make like lysosine, for example, right? All these interferes, like interferon alpha, interferon beta, those are all examples of the of the barriers, right? That constitutes the in-eating immune system. And then all these cells like your basophales, your phsynafales, neutrophils, mass cells, those things are all part of your in-eating immune system.

And also one of your lymphocyte derivatives, your natural killer cells, believe it or not, those are actually a part of your in-eating immune system. And then again, complement your complement proteins, the all-micop part of your in-eating immune system. And then if you jump into the adaptive immune system, right? Like your adaptive immune system is a lot more specific, right? Because again, your adaptive immune system is like a system that like you trained, right? So it learns what a specific pathogen looks like, right? Or you can force your immune system to learn, I mean like you can say, okay, you can either learn the hardware of the easy way, right? So the hard way is you get exposed to like a full-blown infection, you make an, you make like your adaptive immune system learns that infection and says, okay, come next time I'll deal with you, right? Or you can learn the easy way and get vaccinated, right? That's why I encourage people to get vaccinated, right? So you can learn the easy way, under like you know, like low stress conditions is kind of like being in residency as against being out in the real world. With a vaccine, your body learns those pathogenes on that low stress conditions, makes antibodies so that when you get a full-blown infection, you're better able and ready to deal deal with all those things. So the adaptive immune system, you know, it's super specific, right? It identifies unique pathogenes, right?

And it certainly has memory, which is something that is kind of different from your in-eating immune system. And again, remember your adaptive immune system, it is not hard wired into your, it's not hard wired into your genome. And then like some big parts of your adaptive immune system, right? For the most part, those are kind of like your being, your T lymphocytes, and all like, your in-eating immune system that you know, uses complement as it's like major protein, your adaptive immune system, the major protein that kind of like floats around in the serum, dealing with infection are your antibodies, right? Which ultimately produced by, produced by B cells. And again, remember your lymphocytes, right? Include B cells and T cells, natural killer cells are actually derived from lymphocytes as well. But your natural killer cells are considered to be a part of your in-eating immune system, they are not considered to be a part of your adaptive immune system. It's your B and your T lymphocytes that are set to be a part of the adaptive immune system. So let me, I guess, focus a little and talk about the in-eating immune system, right? So the thing is your in-eating immune system, again, like I said, right? You have like your phagocytes, like all these, like neutrophils, macrophages, and then all those, like all the little cells, their bisophils, eos, blah, blah, blah, mass cells, right?

And then again, like I said, your in-eating cells, which are again lymphocytes derivative, and then your complement proteins, they are all part of your in-eating immune system. So let's kind of talk about complement. Essentially complement, again, like I said, they're part of your in-eating immune system. They're essentially a bunch of proteins that help with the needy immune response. And the thing is, I guess the, I'll see, there are two big things you want to know with regards to the USML step one in relation to the complement, complement system. You want to know like the three systems, and you then want to make sure that you know the functions of the complement proteins. Trying to memorize like all the steps of each individual complement cascade makes no sense. I'll probably just spend like a minute or two on like two quick ones, or maybe even actually just one major one, just to kind of like, okay, make you see how it kind of works so that you can have like some understanding to be able to like build a foundation, I guess like a scaffold to memorize the concept. But basically, right, there are like three complement systems, right? There's like the classic one, there's the alternative pathway, and then there's like the manuals bind in a lectin pathway. Now, the thing is the classic complement pathway, right? That one essentially evolves antibodies.

The alternative pathway is the one I think that's probably the one I'll maybe spend some time describing that one just kind of starts spontaneously. And then the manuals binding lectin pathway, the if you actually really think about it, it's a nice pathway because it's super specific and it's very good at targeting bacteria. And again, like I said, you do need to know the functions of the different complement proteins. That is floridly high you to know for exams. And the thing is these complement proteins, they're great, they're awesome for dealing with infection, but you also need to you know, kind of figure out a way to turn these things off because if they're running a mock, they can cause a lot of trouble in your body like very serious trouble in your body. So I guess let me pick one of the pathways and I think I probably won't let me just go ahead and use the alternative pathway and kind of describe how this complement system works. Again, just kind of like setting the stage. Again, you don't necessarily need to memorize every single step, probably like the next one or two minutes of what I see you probably don't need to memorize, but it sort of gives you an understanding of how this complement system kind of plays out. So the thing that happens is that, so say for example, you have like complement protein C3, okay? That's C3. Remember I told you that this alternative pathway is kind of spontaneous.

The thing is the C3 is kind of like spontaneously like broken down to like C3 A and C3 B. The thing is C3 B, remember it's a very good obscenity, that's a high-o thing you want to remember. And the thing is this C3 B once it's formed, it can actually bind to like an amino group or a hydroxy group on the surface of bacteria, right? And from there things then proceed further. But if for example like C, you form C3 B and there's no amino group, there's no hydroxy group on the surface of bacteria to bind to. The body immediately just quench is it by the C3 B like binding to water. But if let's say you know the C3 B, you know, finds a hydroxy group on the surface of bacteria, right? It binds, right? That C3 B there's something called factor B, now we'll come and bind to it. And then that C3 B that's bound to factor B, there's another thing called factor D. That factor D kind of throws along, right? And cleaves the C3 B, bound to factor B, complex to like C3 B BB, right? C3 B BB is known as a C3 convertis. And whenever you see the word convertis after something, it means it can cleave that thing, right? So like C3 convertis has the ability to cleave multiple C3s. C5 convertis has to the ability to cleave multiple C5s, right? So C3 B BB, right? Is C3 convertis? So you can kind of again cleave all the C3 groups like in a kind of like a continuous chain reaction. And then that C3 convertis, that C3 B BB, right? Can combine with another C3 B, right?

So I know you may be saying, oh, this is kind of ridiculous again, this is just for purposes of understanding, you can skip this part if you don't want to listen to it. But basically that C3 convertis combined with another C3 B, right? So you can have something like C3 B BB, which is the original C3 convertis. And then it joins with another C3 B. So it's almost like you have like C3 B squared BB, right? That's what's known as a C5 convertis. And then that C5 convertis, again, because it's a convertis for C5, that means you can cleave C5s. So that C5 convertis cleaves all the C5 groups to like C5 AC5 B. And then that C5 B joins up with a protein, a compliment proteins C629 to form something called the membrane attack complex, right? The membrane attack complex is essentially like forms like a hole and blows up the, blows up the bacterial cell. So that's kind of like the way the alternative compliment cascade works. And then the membrane attack complex C5, C5 B, C6 C7, C8 and C9, right? And again, you want to remember some high yield things there, right? So if you have a deficiency of these terminal compliment component proteins, right? You can get into some big trouble, right? Like you can have a recurrent like niacerele infections, but the infections with niacere meningitis and niacere amgonaria, right? Those are high yield things to know for tests.

So I kind of stated earlier that, you know, well, this compliment system is great, but it's not something, again, you want to work in all the time, right? So you kind of want to be able to turn it off. And at the end of this, I'll actually talk about a disorder where you don't turn off your compliment proteins as you shoot. And then you begin to get into a lot of trouble because compliments, they can destroy your own cells, they can destroy foreign cells, right? So your body has these mechanisms in place to prevent them from destroying your own cells for turning them off. So I'll give you some examples of this system. And again, these examples, again, are very high yield to know because they're actually clinically relevant, right? So there is this protein known as MCP, right? It's found on the surfaces of our cells. It essentially can activate enzymes that would convert C3 B, right? Remember, C3 B, I said that ultimately it constitutes a part of like a C3 convertase, right? So and remember that C3 B is also an obsceny. That C3 B, MCP can sort of like activate some enzymes, or even there's this thing called factor i that can convert that C3 B to like I C3 B. I C3 B is like the inactive C3 B. So again, by essentially taking C3 B out of commission, you have no, you know have no C3 convertase. And then probably the ones that are more clinically relevant, right? I think it's like CD55 and CD59, right? So the thing is CD55 is known as a decay accelerating factor or Daf.

Again, you also find it on the surfaces of our own cells. It essentially prevents the formation of the C3 convertase in all the in all the complement pathways, right? So it's pretty good for essentially making that C3 convertase not form, okay? You'll see why that's important in a second. Another protein that you may also see on exams is like CD59. Again, these are proteins that turn off the complement cascade. CD59, another new mission, the NBM is it's called a protecting, okay? It actually prevents C9. I remember I told you that the membrane attack complex includes C5 B, C6 C7 C8 and C9. The thing is all those things need to assemble together. I kind of think of it as like, or everyone needs to vote for a decision to be made. All those proteins need to come together for you to form the membrane attack complex. If one is missing, you will not form any membrane attack complex. So the thing is CD59 actually prevents C9 from being incorporated into the membrane attack complex. And when that happens, it essentially holds the formation of the membrane attack complex. So what's the clinical correlate here, right? They can give you a question about like a young guy, you know, that has like, you know, low hemoglobin, they tell you that he always has like, peace like blood in the morning and all that stuff. And he has like thrombosis of like weird arteries. And if you see that, you probably want to think about PNH, right? So like paroxysmal or nocturnal hemoglobin or yeah.

The thing about PNH is it effectively involves you having a mutation in a gene called a PGA. So PG like PIGA, like PGA. If you have the PGA mutation, then you'll have trouble with the GPI anchors, okay? GPI anchors. Now, what are those GPI anchors important? The thing is, I think of those GPI anchors as like sticks that put certain things on the surfaces of your cells, right? So like, for example, you need those GPI anchors to hoist like CD55 and CD59 on the surfaces of your cells, like your red blood cells, for example. So the thing is, if you have this PGA mutation, well, all the best with getting GPI anchors. If you don't have GPI anchors, you will not be able to hoist CD55, which is the care accelerating factor and CD59, which is a protecting on the surfaces of your cells. So the unfortunate thing that happens is because those things that turn off complement and not on your cells, complement can come and have a field day on the surfaces of your cells, right? So you may say, okay, so is this a death sentence? So thankfully, it's not, right? Because the thing is, there's a drug known as aculesumab, right? Aculesumab. It has a drug that was invented a couple of years ago. It's a monoclonal antibody against C5, right? And again, think about it. If you bind up C5, then you never form C5 B. And if C5 B is never formed, you can never form the membrane attack complex. And if you don't form the membrane attack complex, you don't blow holes in the walls of cells, okay?

And one of the usual, I guess, question that your friends at the NBM can throw on the USML exams is that, how do I put this? They can tell you that, oh, they can, essentially, give you a question about a patient that has P&H, and then they tell you that, oh, prior to studying drug therapy for bloody, bloody, bloody, blood, which of the following is the next best step in management, right? For those kinds of questions, you want to think about vaccinating those people against like NISERA meningelitis. Because remember, I said early in this podcast that whenever you have a deficiency of the terminal complement component proteins, you have a high risk of recurring NISERAL infections. So the thing is, when you give a patient aculesumab, you're essentially inducing a terminal complement component deficiency with pharmacology, right? Because you're essentially taking C5 out of commission. So those people in general actually need, before you start aculesumab, you would ideally want to, at least remember like, you know, like a few weeks before, you would ideally want to give the patient the NISERA meningelitis vaccine, right? Because again, by taking C5 out of commission, you can create serious NISERAL problems for patients that are on aculesumab. That's a very nice way your friends at the NBM can integrate, um, can integrate, um, immunology with a microbiology and the test. So those are, I think that's all I'm going to say about, um, like how the complement system works.

Well, let me kind of talk about, like, some of the complement proteins and their key functions, right? So like C3 AC5 A, right? Those are high, you know, because they're anaphyla toxins, right? So you may say, okay, divide. What do you mean by the term anaphyla toxin? Well, the thing I mean is that, um, C3 and C5 AD can like, non-specifically, kind of like bind to mass cells and make them degranulate, right? And that can trigger an anaphylactic reaction, like a hypersensitivity, star reaction, right? So, um, that's why they're called anaphyla toxins. Now, C5 A, you want to remember that it's a powerful like hemotactic factor for neutrophils, and all the inflammatory cells. This thing is floridly high yield to know for the USML Es. Now, C5 A, it attracts, it attracts neutrophils and other inflammatory cells. The thing is, there are also some other things that actually pretty good hemotactic factors for neutrophils. And you want to, again, commit them to memory for the USMLE Step 1. C5 A is the first one, but other ones you want to keep in mind are things like interlooking eight, okay? And you could try B4, okay? So, C5 A, IL8, and LTB4 are all powerful hemotactic factors for neutrophils, and actually all their immune system cells. And then C3 B, it's very good for the purposes of opsonization, okay? And C3 B, I mean, like, if you remember earlier, I said something about like C3 B being converted by like factor I to inactive C3 B or IC3 B.

The thing is, IC3 B actually has the ability to do something called ADCC. ADCC is like antibody, dependent cellular cytotoxicity. I will talk about that in a later podcast. So, those are kind of like, again, some big things you want to know. I already talked about like C5, BC6, C7, C8, C9, that are all kind of involved in the formation of the membrane attack complex. So, again, those are big things you want to commit to memory for your exam. So now, I'm going to, I guess go ahead and talk about the adaptive immune system, right? Your adaptive immune system, again, like I said, it's mostly your bees and your teas, your bees and your tea cells. And the thing is, all your adaptive immune system cells, they're actually born in the bone marrow, okay? They're actually born in the bone marrow. But the thing is, they complete the amat... Like, most of those cells complete the amatrician elsewhere, like the postures child is the tea cell. The tea cell is born in the bone marrow, but it kind of like finishes up its livelihood, like kind of finishes up its maturation essentially in the in the thymus, okay? Remember the team team deep foresight for team thymus. And the thing is, all these like the stem cell that ultimately forms like many of these bees and tea cells and all these neutrophils and all that stuff, the thing is that stem cell can actually go down to pathways. It can either go down a myeloid pathway or it can go down a go down a lymphoid pathway, right?

It kind of just kind of depends on the kinds of signals you get. And again, like I said, tea cells, they complete the amatrician in the thymus, bee cells, they actually do complete the amatrician in the bone marrow. So let's, I guess, kind of talk about some of these high yield um... Let's talk about some of these are high yield cytokines that you want to keep at the back of your mind, for example, right? So if for example you want to proceed down the pathway of um... Down the pathway of um... Like the lymphoid pathway, the thing you actually need for that process to happen is something called interleukin seven. IL-7 actually helps you go from like the pluripotent stem cell down the lymphoid pathway, right? And then obviously from that lymphoid pathway, you can form a lateral killer cell, you can form a tea cell, remember tea cells in general all have CD3, right? And then if you're a helper tea cell, you have CD4, if you're a cytotoxic tea cell, you have CD8. And then those are your lymphoid cells can also form bee cells, right? Remember bee cells, um... They give birth, they give rise, uh... They give rise to plasma cells, right? Remember bee cells have things like, you know, like CD19, CD20, CD21 kind of deal. Um... But if that's your lymphoid lineage, right? If you want to really go down like the um... the myeloid lineage, you need things like uh... like GMCFF, right? So like a granulocyte macrophage conoli... granulocyte macrophage colonist immolidine factor.

The reason you have those names, right? It's like macrophage, right? Your macrophage is a part of your myeloid cell line. Well granulocyte, right? Remember your granulocyte, you can remember that one, the numonic bend, right? So like bisophiles, your synophiles, neutrophiles. So those are bend cells, if you may. Um... Um... You can form them by again, like by having like GMCFF. Another thing that actually kind of helps in that process is like interlooking three. It helps you again go down the myeloid lineage. And some key things I guess you want to keep at the back of your mind here is, if for example, a person you know gets chemotherapy for like some bad malignancy and the white blood cell count is like knocked down, right? So they become like profoundly nontropinic. You can actually treat that by giving a drug, right? That again will promote differentiation down this myeloid uh... myeloid lineage, right? So you can give like a GMCFF analog like sagramostim, right? So like I think that's spelled like S-A-R-G-R-A-M-O-S-T-I-M. So you can give a sagramostim. Or alternatively you can give a G-C-S-F analog. So G-C-S-F is just like a granulocyte colonist immolating factor analog, right? A drug like a fielgrass stem. And then um... Again, that myeloid stem, like you can go from purported stem cell with like again, like I said, IL3, GMCFF, G-C-S-F, you form the myeloid stem cell, and then the myeloid stem cell can become like...

It can become an Eocenophil, usually you kind of need like interlooking five for that to happen. Or you can expose that myeloid stem cell to a erythropoetin. Remember, Epo comes from the kidneys, right? That's why for person has a chronic kidney disease, they can get like a normal psiliconemia with that, right? So erythropoetin from the kidneys, right? The goal and convert that myeloid stem cell to like erythrocytes, like red blood cells ultimately. And remember, for person again has CKD, you can give them an Epo analog, right? So like, you can give them things like um... Darbe poitin, right? Darbe poitin is an Epo analog, you can use it to treat normal psiliconemia in patients that have CKD. And then if a person has like a tumor, right? That secretion, a ton of Epo, right? Like a renal cell, carcinoma, right? Those things can all give... Those things can make those people have like high hematocrit because again, they are producing a ton of red blood cells because that myeloid stem cell is being exposed to all this Epo. So all these cells are differentiating down the lineage of becoming... becoming red blood cells, right? Another classic Epo secretion tumor in MDM is a humangeoblastoma. Remember, that has an association with a VHL for hipo lendout, right? So if a person has VHL, they'll con... they'll secret a ton of Epo. I mean, the hematocrit, the hematocrit, usually it's in the it's in the posterior force cell like right around the cerebellum.

Secret's a ton of Epo, and that ultimately gives rise to polypsychemia. Okay, so in all those processes again, you ultimately end up forming like your red blood cells. If you say, okay, you know what, how about I want to form platelets, right? Remember, platelets come from mega-carrier sites. So the thing is, if you actually want to form mega-carrier sites in the first place, kind of like we used a rethropoetin for red blood cells, you use thrombopoetin for platelets, right? So if you want to go down the mega-carrier site or out, you need thrombopoetin, and then those mega-carrier sites, you can convert them to platelets, right? With like inter-looking 11, right? Inter-looking 11 helps you convert like mega-carrier sites to to platelets. So if they need like higher pharmacology here, well of course there is. If you go back to one of my earliest podcasts that I meet on the website, I call it like, I think it's like immunopharmacology and the monoclonal alphabet. I talk about some of this pharmacology that I'm gonna, I guess sort of mention in passing here, right? So like, if for example a person has like a disorder where, you know, they don't have like many platelets like ITP, right?

So like a immune thrombocide-opening paper, one way you can actually treat that is you can give like thrombopoetin analog, and there's this drug that occasionally pops up on the, on the USML Step 1, it's known as Romyplostim, Romyplostim is a thrombopoetin analog that can be used to treat like ITP. Remember, again in ITP, the thing that happens is that you make auto-antibodies against GP2 B3 A, right? That aggregation step of primary hemostasis doesn't work out so well. And when you form those antibodies, that also clubbers down your, your platelet population, right? So it will be a person that, you know, presents on an NBME, they'd be having like nosebleeds and bleeding gums and all that crap that kind of studied like, you know, like a week or two ago, and then they will give you like a CBC, and you notice that everything is fine, but you have an isolated, profound thrombocide-opening. If you see that, think about ITP, especially in the patient that has a, has a history of lupus. Alternatively, instead of you say, okay, you know what I don't want to give a thrombopoetin analog, how about I go ahead and give you something that activates thrombopoetin receptors? There's this drug known as L-thrombopag, so ELTROM, L-thrombobopag, PH. Again, I talk about all this from Acology, and the immunofomacology and podcast, but L-thrombopag is a thrombopoetin receptor agonist that you can use to treat, you can use to treat ITP.

So again, these are essentially the different ways you go down these different cell lines and form these stents, right? So again, ultimately like these o-fails, they're part of your myeloid lineage, your eocenophils, they're part of your myeloid lineage. Again, remember, you need them to look in fight for that to happen. And then like your macrophages, your dendritic cells, all those things, again, they are all part of your lymphoid lineage. So what are some, I guess, other things, because I really want to try to keep these podcasts short. I'll just make them like a multiple series in like rather quick succession, but I only need to be something and say, okay, let me just take a 30-minute study break and study. In fact, you know what, maybe let me go ahead and pause here. I will go ahead and continue this in the next series of this, but again, as I do at the end of every single podcast, I do offer one or one tutoring for all the USMLA exams. Step one, two CK, two CS, step three, the preclinical exams, you're taking med school 30-ish off exams, I tutor for all those stents. And then if you're medicine resident and you're a brain for like the intruding exam or the IBI-M board exam, I tutor to all those stents. If you're a college student and you need tutoring for like physics, Gen-CAM, O-CAM, physiology, biochemistry, histology, I tutor for all those stents, right?

And then I offer this thing, I call like longitudinal tutoring, where I work with people for like a year, leading up to like a big exam, right? So, classically, like I work with like first and second year medical students, I tutor them like for all their like class exams, leading up to step one, but the thing is, as I tutor them for those class exams, I also infuse step one knowledge along the way longitudinally. So, it's almost like studying for your classes and studying for step one at the same time, right? I also do kind of like the same thing with 30 year med students, like again, I start with 30 with them, and then I tutor them for all their shelf exams, I tailor my tutoring specifically to like their shelf exams and also for step two. So, when those people hear the dedicated periods for those respective exams, they feel so much better prepared and again, I've had like wildly successful results with this. And then I guess the other thing I also offer is I do like one on one, like consulting or coaching for like applications, so like the ERS application, if you're applying to residency or the AMCA's application, if you're applying to med school, right? So, like things like personal statement editing, personal statement writing, editing applications, mocking reviews, all those things I've done that with like just tons and tons and tons of students.

So, if you need help with any of those things, reach out to me through the website, or you can send me an email at divineinterventionpodcasts with an SADN at gmail.com. So, have a wonderful rest of your day, I'll see you in the next podcast, God bless you. Thank you.

Innate and Adaptive.

The innate immune system.

Lipopolysaccharide (LPS).

GM-CSF, IL-3, and G-CSF.

CD59.

Opsonization (marking pathogens for phagocytosis).

Classic, Alternative, and Lectin.

Natural Killer (NK) cells.

Anaphylatoxins (e.g., C3a, C5a).

Deficiency in terminal complement components (C5b-9).

Decay Accelerating Factor (DAF); prevents the formation of the C3 convertase.

Thrombopoietin (TPO).

B cells complete maturation in the bone marrow; T cells complete maturation in the thymus.

Natural Killer (NK) cells.

Anaphylatoxins (e.g., C3a, C5a).

Deficiency in terminal complement components (C5b-9).

Decay Accelerating Factor (DAF); prevents the formation of the C3 convertase.

Thrombopoietin (TPO).

B cells complete maturation in the bone marrow; T cells complete maturation in the thymus.