Complement System; Your Body's Powerful Defense Against Invaders

in StemSocial9 months ago

As humans, our bodies have evolved a remarkable defense system to combat harmful invaders and pathogens. One of the most powerful weapons in our immune arsenal is the complement system. Comprising over 30 serum proteins and regulatory cell membrane components, this complex system collaborates to neutralize intruders and protect our well-being. Activated by antibodies, the complement proteins play a crucial role in crippling invaders, activating the immune system, and perforating the cells of attacking organisms.

The complement proteins cripples invaders, activate the immune system and perforates the cells of the invading organisms. Remember that they are proteins, so their shapes are programmed to interact with certain things. Different proteins are able to perform differently to get the desired result. The complement system is made up of different pathways including the alternative pathways, classical pathway, lectin pathway, and, terminal pathway.

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Before an invasion occurs, the complement proteins remain inactive (zymogens). However, in the presence of an infection, the alternative pathway is the complement system's innate and initial line of defense. Proteins like C3 undergo a series of transformations, leading to the formation of C3a, C3b, C3bBb, C3 Convertase, and C5 Convertase, which sets the complement system into action.

In the case of a wound, for instance, C3 becomes the first triggered complement protein, breaking down into C3a and C3b. If C3b identifies an invading pathogen, it binds to it, initiating a cascade that shapes other proteins. This process allows for the binding of other proteins to form C3bBbP, then C3 Convertase, which further activates other C3 proteins and continues the cascade.

Eventually, the invading pathogen becomes coated with proteins, with C3a serving as an alert to the immune cells, summoning them to the site of infection. Part of the immune cells to arrive at the site are phagocytes which would engulf a pathogen with the help of the C3b receptors. The C3 convertase then binds with other proteins to become C5 convertase which would cause other proteins to become a membrane attack complex perforating the pathogen. With this, even without knowing, your body already fought a major pathogenic war to keep you safe.


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The Classical pathway begins with C1 with is made up of C1q, C1r, and C1s. The C1r and C1s are proteases and are inactive. When there is an invasion of a pathogen, the C1q binds to the bacterial surface, antibodies bound to the pathogen, or to C-reactive protein on bacterial surface. When C1q binds, it activates C1r, which also activates C1s.

C1s would cleave the protein C4, and C2 where C4b binds to the surface of the pathogen. It combines with C2a to become C4b2a complex which is the C3 convertase cleaving C3 into C3a and C3b. This would lead to potent inflammatory and destructive effects.

While complement systems are very good immune defence, there are still cases where the complement system is not able to function. A very good example is in the case of some viral infection such as Vaccinia virus where Complement control protein is released by the virus causing complement proteins to be inactive and not functional against fighting against the virus.

While the complement system is very good at keeping us safe, it also needs to work with other immune system defence such as neutrophils, natural killer cells, macrophages, virgin B-cells, B-cells, memory B-cells, killer T-cells, Virgin kille T-cells, memory killer T-cells, Dendritic cells, helper T-cells, Mast Cells, Eosinophils, Basophils, Monocytes, and many more.



Read More



https://www.ncbi.nlm.nih.gov/books/NBK27100/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097465/
https://www.sinobiological.com/research/complement-system/complement-activation-alternative-pathway
https://www.msdmanuals.com/professional/immunology-allergic-disorders/biology-of-the-immune-system/complement-system
https://www.physio-pedia.com/Complement_System
https://www.ncbi.nlm.nih.gov/books/NBK551511/

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