The adaptive immune system

This is our second episode on the epic saga that is the immune system. Last week, we talked about the innate immune system, or the rapid way our body answers to a threat. Today, we will talk about the adaptive immune system, a response much slower than the innate one but more deadly. It has evolved to be specific to the threat that is presented, allowing it to hone in on the flaws of the pathogen and remove it very fast.

Where we left of, everything was wrong for our body: our skin fortress was down and compromised, and the leukocytes were not able to kill the pathogens. That’s when our messenger the dendritic cell left, but not without taking the antigen. The dendritic cell left to special immune hubs named lymph nodes. These structures are located all around your body and only contain a special kind of leukocyte: the lymphocytes. These lymphocytes are the heavy hitters in the immune system. But first, they need to be activated. Once the dendritic cell arrives at the lymph node closest to the site of infection, it will present its antigen to every lymphocyte present. Many of them will not do anything because they do not have the receptor that recognizes the antigen. However, once a lymphocyte has recognized the antigen, it will get activated and multiply in great number, causing the expansion of the lymph node. This is why for example when you have a sore throat the doctor is touching the side of your throat: we can feel the lymph node expanding, which indicates that there is an infection. Once ready, it will leave the lymph node and prepare for the attack. To better understand the adaptive immune system, I will go through different kind of lymphocytes one by one and present their functions [source / source / source].

The B lymphocytes: the snipers of the immune system

The first lymphocyte is called a B cell. It possesses a receptor conveniently called the B cell receptor (BCR), which recognizes the antigen. Once at the site of infection, it can do two things: first, it can phagocytose a pathogen and act like a dendritic cell, to activate other lymph nodes if needed, but more importantly, it becomes a plasma cell, and produces antibodies. Antibodies (also called immunoglobulins if you want to shine at parties) are proteins that have the same specificity as the BCR, which means that they can bind the pathogen. The plasma cell will produce many antibodies, which will trap the pathogen, preventing it to move. It is then easier for macrophages to phagocytose it and destroy it. Antibodies and plasma cells are key parts of what is called the humoral immunity: they protect the blood and other tissues from pathogens that do not enter cells, the extracellular pathogens [source / source / source].

The CD8 T lymphocytes: the brawlers of the immune system

Other that the B cells, the other type of lymphocytes are the T cells. These have another conveniently named receptor, the T cell receptor (TCR), which recognizes the antigen and allows for activation and multiplication. But T cells also have another receptor, either CD4 or CD8. We will start by talking about CD8 T cells, also called cytotoxic T cells. Once at the site of infection, CD8 T cell will focus on infected cells: they will bind them and either kill them by creating holes through the membrane, just like NK cells, or force a mechanism called apoptosis, a form of programmed cell suicide. We will talk more about apoptosis in upcoming articles, but it overall causes the cell to implode on itself and die. T cells are part of what’s called the cellular immunity: their aim is to protect non-infected cells from infection by targeting infected cells. They work best against pathogens that lives inside cells, the intracellular pathogens [source / source].

The CD4 T lymphocytes: the master tacticians

CD4 T cells, also called helper T cells, are activated the same way as CD8 T cells. However, their function is very different: they act as immune regulator. Upon being activated and by seeing the pathogen in action, the CD4 T cell will be able to determine what is the best attack against the pathogen. For instance, if we are attacked by a virus, the CD4 T cells will see the presence of intracellular pathogens and make the CD8 T cells more active and stronger, while B cells will stay a bit less active. The opposite is true if we encounter an extracellular pathogen: B cells will be stronger and the CD8 T cells will be a bit weaker. They work by first maturing into a specific CD4 subset. In the presence of extracellular pathogens, they become CD4 Th2 cells. In the presence of intracellular pathogens, they become CD4 Th1 cells. Each subset will release specific cytokines that will help overcome the threat. Many other subset exists, one of which we will discover next week, and several subsets can exist simultaneously depending on the pathogen. CD4 T cells are what makes the adaptive immune system so strong: they make the body adapt and evolve directly based on the threat to better fight it [source / source].

The innate and adaptive immune system are the core of any immune response, and each have a very specific role: the former is very fast and stereotypical, acting the same way every time, allowing for a quick removal of weak threat. The latter is slower but very specific. If a threat is strong, it will adapt to its flaws and remove the threat more efficiently. But both immune responses are interconnected: the adaptive response cannot start without the innate, and during an adaptive response, innate players such as macrophages are still actively working to remove the threat. Once again however, this system is not as perfect as it seems, otherwise we would never get very sick. Many pathogens have evolved to use the adaptive immune response to their advantage, and we will see one example in a few weeks. Next week, we will look at the aftermath of an immune response: the body won and the pathogen is destroyed; how do we calm the immune system down to prevent damages? And more importantly, how can we make sure that the next time we encounter this pathogen, it will be destroyed faster?