Please forward this error screen to 104. These lecture notes accompany my lectures in immunology in the study module “Infection, immunology and allergology” dc generator lecture notes pdf Innsbruck Medical University. Every multicellular organism, including our own, constantly has to be on guard not to be gobbled up by others, as it constitutes a potential source of valuable organic molecules. The ability to resist being used as “food” automatically confers a selective advantage.
Over the course of evolution, this has led to the development of highly sophisticated defense systems in multicellular organisms. THE BASIC PROBLEM: COMBATING WHAT, EXACTLY? Early in evolution, simple multicellular organisms developed a defense system activated by sensing typical molecular patterns associated with pathogens or distressed cells. This system is conserved and also works in humans. This innate, prefabricated, one-size-fits-all immune system is immediately available. Our most efficient defense mechanisms mount a custom-made counter-attack against the specific infectious agent invading our organism. We call this an adaptive immune response.
Bespoke work takes time, meaning the system is simply not ready for use during the first days of an infection. These immune mechanisms fight “foreign” organic material that has entered our body. Several of these cell types share molecular systems that are necessary for their defense functions. Collectively, these are designated “mediators of inflammation”. They are either preformed or newly synthesized on demand. While these molecules in fact cause inflammation, their ultimate goal is of course not inflammation, but defense. Inflammation is a transitory state that makes it easier to combat infectious agents.
The drawback: if we would like to inhibit unwanted inflammation, we are usually able to alleviate it, but not to suppress it completely. The complement system primarily serves to fight bacterial infections. It has a basic recognition function for many bacteria, can alert and recruit phagocytes, enhance visibility of bacteria to phagocytes and sometimes even lyse bacteria. The complement system can be activated by at least three separate pathways. The two evolutionary older pathways are the so-called “alternative” and the lectin pathways. Both are activated on many bacterial surfaces, contributing to innate immunity.
The third pathway, which is mainly antibody-activated and hence part of the adaptive immune system, developed much later, but was identified first. B which is in turn cleaved into fragments Ba and Bb by the plasma protease factor D. C3a and a larger fragment, C3b, which normally is rapidly inactivated. In case C3b is generated near a bacterial or cellular surface, it binds covalently to this surface. The process just described now repeats on the membrane: factor B attaches, to be cleaved by factor D. The further development depends on the nature of the surface in question.
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The smaller cleavage products C3a, C4a, C5a, sometimes called “anaphylatoxins”, have additional functions in their own right: apart from attracting phagocytes, they cause mast cell degranulation and enhance vessel permeability, thereby facilitating access of plasma proteins and leukocytes to the site of infection. The lectin pathway of complement activation exploits the fact that many bacterial surfaces contain mannose sugar molecules in a characteristic spacing. The classical pathway usually starts with antigen-bound antibodies recruiting the C1q component, followed by binding and sequential activation of C1r and C1s serine proteases. C4 and C2, with C4b and C2b forming the C3 convertase of the classical pathway. Pharmacology cross reference: humanized monoclonal antibody Eculizumab binds to complement component C5, inhibiting its cleavage and preventing activation of the lytic pathway.
This is desirable when unwanted complement activation causes hemolysis, as in paroxysmal nocturnal hemoglobinuria or in some forms of hemolytic uremic syndrome. Factor XII is activated by contact with the negatively charged surface, starting the entire coagulation cascade. In addition, factor XII cleaves prekallikrein, releasing the active protease kallikrein that in turn releases the nonapeptide bradykinin from HMWK. The upshot of these plasma protein cascades is the start of an inflammatory reaction, and the blocking of small venules by coagulation, which is useful to prevent spreading of an infection via the blood. Driven by blood pressure, plasma is filtrated out of the vessels showing enhanced permeability, forming tissue lymph. Activation of the plasma protein cascades is in many regards a precondition for the next step, the activation of cellular systems at the infection site.