Autoimunitas (Pembelotan Imun)

Hello everyone, welcome to our discussion today. Have you ever thought about how our immune system, which is normally like an elite military bodyguard, suddenly suddenly collapses and attacks the ground itself? Yes, today we will discuss a story of betrayal at a very interesting microscopic level. Try to imagine for a moment, what will happen if the most powerful protector in your body suddenly turns into the most dangerous enemy?

Here, we're not just talking about clinical diseases, but we'll see how the actually the process of the injection from our most trained cellular troops.

How come they mispronounce their friends as enemies? To structure it, here are the five main points that we will discuss. First, definition and immune tolerance. Second, immune system inhibitors. Third, its damage mechanism. Fourth, five cases of its disease. And fifth, detection in the laboratory. Let's get started. Let's get to our first part, definition and immune tolerance.

The essence of it all is this: autoimmunity is basically a fatal damage, failure of the immune tolerance system.

In normal conditions, our immune system has an amazing balance keeper that makes them still not responsive or not attacking our own body cells. When this tolerance is destroyed, our system really loses its ability to distinguish between friends and enemies. So how does our body maintain this army discipline from the beginning? There are two main steps. The first step is central tolerance. This is very similar to super tight military training in the bones and spine.

Here, the water gene will display our body's antigens. If there are troops that appear to attack, they are immediately executed or eliminated.

But, yeah, there's no perfect system, right? There must be a passing transducer cell. That's the second step, peripheral tolerance. This is secondary safety on the field. Mechanisms such as energy will immediately turn them off. Or there is a special cell called the FOXOPT regulator T cell that will suppress and suppress the mutants that managed to escape earlier. Now we go to the second part, the immune mutation detector. What is the cause?

Speaking of the cause, this system rarely breaks down just because of one thing. It's like genetics is the one that sets the trap, through certain genetic variations such as HLA-DR4 or HLA-DR3, which makes someone more vulnerable than before.

Then, the environmental factors are what attracts the plague. How? It can be through molecular mimicry. So viruses like Epstein-Barr or Koksaki are prone to being similar to our body cells. As a result, antibodies that intend to attack viruses, instead attack the body's network. In addition, other environmental predators such as UV rays or even certain drugs such as hydralazine can also trigger this autoimmune syndrome. Now, let's see this one fact that really surprises.

When it comes to systemic lupus erythematosus or lupus, the ratio is very tight, 9:1 between women and men. This explains very clearly how sex hormones, especially estrogen, plus the presence of two X chromosomes in women, really has a big impact on immune dysregulation. Estrogen can change the gene expression and reduce the immune tolerance regulation we discussed earlier. That's why women are much more prone to this disease.

Okay, let's continue to the third part, the network damage mechanism.

Autoimmune damage is often operated by hypersensitivity reactions. Let's compare two types first. Type 2 is like a direct sniper attack. The autoantibody specifically locks and attacks the receptor on the surface of our body cells. It's different from type 3. If this type 3 creates a different mess, it doesn't attack one point, but the antibody and antigen form a lump called the immune complex.

This lump is walking on the blood, then clogging the areas with high pressure, such as kidneys or kidneys. As a result, they activate the protein complement that massively destroys the blood vessels.

And then there's another one called Type 4 hypersensitivity. Well, if the previous types used antibodies, aka long-range weapons, Type 4 is really a very brutal close-range battle. Here, T lymphocytes, especially the CD8+ cytotoxic T cell, directly go down to kill and destroy the body network using their own hands. Then there is the CD4+ helper cell, which calls other radon cells to make the mess worse. This is really an infantry attack directly to our own network. Entering the fourth part.

5 cases of autoimmune diseases. Look at how each of these diseases has its own target organ and main weapon. In lupus, the attack spreads, aka systemic, through the third type of immune complex. Calorematoid arthritis, which is attacked, is senile, until it makes a panus network that breaks the bone. Interestingly, try to see thyroid gland. Hashimoto thyroiditis, breaks the thyroid through the T-cell attack type.

This is a classic example where pancreas is destroyed by T-cell type 4. The initial concept is the same, the failure of immune tolerance, but the clinical reality in the patient can be really different 180 degrees.

We are now at the fifth part, as well as the last one: Detection through laboratory testing. If Dr. Curiga has systemic autoimmune rheumatic disease, the first and most important post-test to be performed is the antibody-antinuclear test or ANA. This is the standard of the MAS. The patient should have a minimum ANA of 1/80 to be able to be classified more consistently.

The higher the titer, the higher the possibility of the disease being active. So this is our main diagnostic gate. To detect a fire in the body, we often use these two tests, LED and CRP. Both of these are brilliant for describing different body kinetics. LED is like smoke that is still left after a week of burning. Slow and slow too normally. On the other hand, CRP is the alarm of the fire.

Once there is a presence of the IL-6 cytokine, CRP can rise drastically or drop sharply only in the hour count. Then, to know for sure what kind of conflict is happening, we need a more specific tracker. The presence of anti-DSDNA antibodies, for example, is really specific and confirms the presence of lupus. Well, when it comes to AIDS, the presence of rheumatoid factor and anti-CCP is like a red flag.

With a specificity of up to 95%, anti-CCP can not only diagnose rheumatoid arthritis, but also predict if the patient's kidney will experience damage or very aggressive erosions in the future.

Not only early detection, we also have to regularly monitor their condition. For example, in lupus patients, if the amount of C3 and C4 complement protein they drop, it is actually a bad sign. It means that the presence is still active and it is still very hard to consume the protective protein. It's different if the specific organ is like pancreas. We will look for presence of symptoms such as anti-GAD-65. This is the most dominant symptom at the beginning of the appearance of type 1 autoimmune diabetes.

Wow, we've seen how complicated and amazing this autoimmune disease is. Until now, our main treatment is to kill the entire body's immune system so that the attacker stops attacking, which clearly makes the patient prone to other infections. So, I want to close this explanation with one question for us to think about together. With the progress of therapy that is now targeting the T-cell regulator specifically,

Will in the future, precision immunology no longer focus on crumbling all the troops in our bodies, but purely re-educate and restore their immune tolerance? Imagine how cool that is. Thank you very much for joining us in our discussion this time. Stay curious and see you soon!