The Biology Blogger

In the intestines, there lurk these bacteria that aid in the digestion of different foods. In essence, they are a particular type of bacteria that is in a mutualistic relationship. Called commensals, there are typically anywhere from 300-500 of these bacteria in the intestines. The interesting thing is that despite the fact that they are bacteria, the immune system does not attack them. They live in our intestines and aid in a health digestive tract which seems almost contradictory because of the word bacteria going with them.

But, what a team of scientists have found is that these commensals do a lot more than just aid in the health of the digestive tract. Because the immune system has to deal with all different types of bacteria, it can have a hard time determining the difference between a commensal and an actual pathogen. In certain autoimmune diseases such as Crohn’s, the immune system attacks these commensal bacteria. So, how is it that the immune system knows typically not to attack the commensal bacteria?

By means of a certain interaction between the commensal bacteria and particular T-cells in the intestines, these commensals are able to stay alive. By binding with the receptor called Toll-like receptors (TLR), the commensal bacteria are given a means of survival. But, this doesn’t explain how they are able to help the immune system in fighting against pathogens.

The answer is in the immune cells called Tregs. They recognize the commensal bacteria and by recognizing them, help the immune system direct their attention to harmful pathogens. But, because of the existence of these Tregs, the other T-cells are kept at bay which is, in essence, a ‘weaker’ immune system. When a pathogen comes along, though, the DNA of these bacteria binds with TLR9, a receptor on the immune cells. By this occuring, Tregs are kept limited and other T-cells can come into being.

Since this happens, the T-cells can then go and attack the pathogen. But, because the commensal’s ‘aided’ in the attack, the T-cells don’t attack them; instead, they focus on the pathogens. It’s like the saying: ‘my enemies enemy is my ally.’

This leaves a lot of opportunities for certain therapies in oral and autoimmune diseases. But, the real question I have is: are we going to begin leaving antibiotics and perhaps using bacteria against themselves? It would be interesting to see what other kind of therapies can come from the research gained from this experiment.

Source.

When we hear a story about a gene variation that makes a person immune to malaria, people get excited. But, how excited would people be if that same gene that makes people immune to one disease left them more susceptible to another disease? I don’t know how excited we’d be. Unfortunately, that’s happened. According to an article I read at the New York Times, those in Africa that developed a gene that allowed for an immunity against an ancestor to the modern day malaria are more prone to get HIV.  Alone, this gene could be the cause of 11% of the cases of HIV.

The question people are asking is: why is it when one disease is protected against, the other becomes more likely to infect the person?  The answer to that lays on the receptors of the red blood cells and the white blood cells.  Malaria attaches to a receptor that is found on red blood cells.  This receptor is meant to attach to a hormone called CCL5.  About 10,000 years ago, humans in Africa stopped having those receptors and they suddenly stopped getting malaria.

Now that HIV is around, though, one scientist suddenly had a realization.  Robin Weiss is a biologist at University College of London.  He found that HIV was using red blood cells to get around the body in particular patients.  Instead of the malaria attaching to the receptor, the HIV attaches to the receptor.  And what you get is a case of increased HIV infections.  It sounds confusing?  It is.  Scientists realized that if there is a lack of this one receptor on the red blood cells, HIV increases.  If there is a lack of the receptor on the white blood cells, HIV goes away.  It’s confusing.

What does this all mean, though?  It explains why HIV is so dangerous in Africa.  More importantly, though, it gives more information into understanding about the biology behind HIV.  We don’t know much about HIV.  It’s relatively new so we can’t do genetic research.  That’s irritating for scientists because if we knew about the genome, we might be able to target it better.  This research, although very upsetting, could lead to more information on potentially finding a vaccine.  On an aside, a trial for a vaccine against HIV was just cancelled.

Hopefully we can find a cure for this virus.  But, right now, we just have more knowledge.  We are starting to understand more and more on how this virus works.  It’s not a lot, but it’s something.  Now all we need is to get a vaccine out, huh?

For those that know, a B-cell is a cell that is a part of the immune system that creates antibodies to give the body a sign when that antigen enters the body again. Basically, once you’re sick for a first time, it never happens again because your body has developed an immunity. That immunity comes from the antibody. Unfortunately, the B-cell isn’t all good. Research suggests that the receptor on the surface of the B cells actually cooperates with the MYC oncogene (a gene that regulates other genes and, when mutated, often causes cancer). This cooperation speeds up the development of lymphomas.

Cancer grows fast enough as we all know. However, the issue at hand is that with the increased speed of these lymphoma developments, it gives less time for doctors to essentially treat it. Studies show that Non-hodgkins lymphomas have become 85% more prevalent in the past twenty years. The unfortunate fact is that 90% of those are B-cell lymphomas. But, scientists do have hope. According to the lead research, Yosef Refaeli, PhD:

“Our findings have pointed to the B-cell receptor and its signaling pathways as very promising therapeutic targets for B-cell lymphomas.”

What does that mean? It means that they are looking to see if there is a way to treat lymphoma by working with the B-cell receptor. The study showed that with the B-cell receptor working, in essence, it was creating a autoimmune response with the tumor. So, the body began to destroy itself, but not the tumor. What they did was blocked the B-cell receptor with immunosuppressants. If the immune system is not beating itself up, then there’s nothing to worry about. The tumors were effectively destroyed.

Dr. Refaeli was thrilled and rightfully so. If this treatment does work then they can use this understanding to try and combat other cancers, lymphomas, but also autoimmune diseases. By understanding how the B-cell interacts with the MYC oncogene, scientists can find a way to hopefully limit its uses for the tumor. Survivability can increase tremendously with this research.

What does that mean for all of us though? I mean…How many people possibly die from autoimmune diseases alone? Here’s a number…Autoimmune disease death is the number eight cause of death among women aged 15-64. There are a lot of ways people can die and to be ranked number eight is definitely reason enough to be excited about this research. For more numbers, here’s this: 19,160 people have died from Non-hodgkins Lymphoma this year. So, when we look at these numbers and realize what this research could do, I have to say one thing: Hats off to Dr. Refaeli and his team.