 Welcome back to our MedSmarter Lecture Series, where we're taking a smarter approach to preparing future physician. Before we get started, if you'll take just a quick minute and click that like button and also subscribe and turn the bell on so that you'll be notified when we post new videos. Finally, we have IgE. IgE is a monomer, once again. It binds the mast cells and the basophils, sometimes it will cross-link when exposed to allergens, specifically mediating the immediate type 1 hypersensitivity through the release of inflammatory mediators like histamine. And also it contributes to immunity to parasites by activating eosinophils. So we deal with allergies and parasites with IgE. One of the leading thoughts of why we're seeing so much increase in allergies lately is in the United States. We have decreased the parasites through treatment of water, treatment of food, better hygiene, all that kind of stuff. So the IgE is not dealing with parasites as much, and so it has more of an affinity to allergens increasing our risk of allergies. Let's talk about memory from antigens. So we have several different types, specifically the thymus-independent antigens. These are antigens that lack a peptide component, such as lipopolysaccharides from our gram-negative bacteria. It cannot be presented by MHC to our T-cells. These are weakly immunogenic, so what you're going to see here is we're often going to have to have boosters and adjuvants to our vaccines. So for example, the capsular polysaccharide subunit of streptococcus pneumonia is associated with the PPSV23 vaccine. We have thymant-dependent antigens, and these are antigens that contain a protein component. So strep pneumonia vaccine, the PCV13 vaccine. These are polysaccharides conjugated to the diphtheria toxin-like protein versus the capsular polysaccharide subunit in the PPSV23 vaccine. With these thymant-dependent antigens, class switching and immunologic memory occur as a result of the direct contact with the B-cells within our T-helper cells. And finally, let's talk a little bit about complement. And here is a system of hepatically synthesized plasma proteins, so they come from the liver, and they play a role in the innate immunity and inflammation. So we have max or membrane attack complexes that will defend against our gram-negative bacteria, and we can actually use the CH50 test to screen for activation of the classic component pathway. We'll talk about that pathway here in just a minute, but there are three different activation pathways. The two that we most often refer to, one that's a lot less common. But so we have our classic IgG or IgM mediated pathways. We have our alternative or microbe surface molecule pathway, and we have the lectin, which is a mannose or other sugar on the microbe activation of our complement pathways. One thing to remember here is that GM makes classic cars. So classic is GM mediated, IgG, IgM mediated. So let's look a little bit closer at these pathways. So we talked about the classic pathways, IgG or IgM mediated. And so we're talking about IgG, as you can see in this picture here, also can have lectin or other sugars on the microbe, so on the microbe binds that can also activate our classical pathway. And then we also said through our alternative pathway, it's actually going to be the microbe surface molecules that will activate that pathway. So let's talk a little more about the function of some of these complement that are produced. So C3B, C3B is functioning as an opsonization. What is opsonization? That's a process where we use opsonins to tag foreign pathogens for elimination by phagocytes, all right? So C3B, you can see this in this picture over here. You have C3, you have C3A break off, leave this with C3B that will then bind to that molecule which is targeting it for elimination by the phagocytes. If we don't have opsonin here, like the antibodies, then negatively charged cell walls of the pathogen and phagocytes will actually repeal each other. So we need that C3B opsonization to occur. C3A, C4A, C5A, these all are associated with anaphylaxis. So those binding can actually result in anaphylaxis in the host. C5A also does neutrophil chemotaxis. And C5A here is a result of the cleavage from C5 to C5A and C5B. And then our C5B9 or our membrane attack complex helps us undergo cytolysis. You can see those functions down here associated with the membrane attack complex. So one of the big keys that we need to take away from this here is that C3B through the process of opsonization will bind to lipopolysaccharides on the bacteria. So what are opsonins? C3B IgG are two of the primary opsonins in the bacterial defense that enhance phagocytosis. C3B also helps to clear those immune complexes. So like we said earlier, it is what is preparing these pathogens for phagocytosis. So think of the Greek form of opsonin, which means to prepare for eating. So we are preparing these molecules for phagocytosis. Here like decay accelerating factor, also known as CD55, and C1S8 will be an inhibitor to help prevent complement activation on self-cells. So we don't want to activate complement on cells that we want to keep like red blood cells. We don't want the phagocytes to come in, notice that complement has been activated on a red blood cell, and chew up the red blood cell and eliminate it because that's not the purpose there. If you found this material helpful for your studying, please like and consider subscribing to the channel. Also, share this video so that more people can benefit from it like you have.