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Scientists Discover New Link between Brain and Immune System

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The old immune system map of the lymphatic system (on the left), and the new map, reflecting the UVA discovery (on the right).

Nowadays it’s quite rare to make real groundbreaking discoveries in the areas of anatomy and physiology. Starting with the dissections done a few hundred years ago, to state-of-the art imaging in the 20th and 21st centuries, scientists have basically mapped out the human body. Recently, however, a team of researchers at the University of Virginia School of Medicine led by Professor Jonathan Kipnis have made a discovery which could, as one expert put it, “change the textbooks.”

How the immune system interacts with the brain is a poorly understood mechanism. One of the reasons for this is because it has been traditionally held that the brain wasn’t connected to the lymphatic system, or at least, no one had yet to discover any link between them. Which is what makes the finding of this link between the brain and the immune system, consisting of previously unknown lymphatic vessels, such a big deal.

We all know what the brain does and why it is important, but what about the lymphatic system? In a nutshell, it’s part of the circulatory system and it consists of a series of vessels which carry a clear fluid called rightlymph through the body. In addition to the removal of fluids from the various tissues and some transporting duties, it is a very important component of the immune system. That’s because lymphatic system is the home of the T cells and B cells (collectively known as lymphocites), two of the most important components of the adaptive immune system – basically our body’s elite enforcers.

While looking for T-cell gateways into and out of the meninges (the membranes which cover the brain), the researchers found functional lymphatic vessels between one of these membranes and the brain. These structures were incredibly hard to find. They were only detected after Antoine Louveau, a postdoctoral fellow in Kipnis’ lab, developed a technique to mount a mouse’s meninges on a single slide so that they could be examined in their entirety. Scientists then noticed vessel-like patterns in the distribution of immune cells on these slides, and when they tested to see if there were any lymphatic, sure enough they found them.

A discovery like this one is bound to have a huge impact in the medical field. For example, we know that Alzheimer’s disease is caused by the build-up of big proteins chunks in the brain. A reason they might be accumulating is that they’re not being removed by these vessels. This breakthrough could also have implications in the treatment of other neurological conditions, from autism to multiple sclerosis. When you discover new structures in the brain you previously didn’t know existed, things are certain to get interesting.

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Medicine and Health

There are signs of the COVID virus in the body years after the first infection

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COVID-19 used to mean coughing for two weeks and not being able to smell your new candle. Then we learned about Long COVID, which is a vague grouping of more than 200 symptoms that can be very bad months or even years after the main illness seems to have gone away.

We’re still not sure what’s causing the long-lasting condition four years after the pandemic began, but a new study that tracked 24 Covid patients for up to 900 days found a possible cause that hadn’t been seen before: your T cells.

This isn’t the first study to find a link between COVID-19 and these immune cells. Just last month, a study from Imperial College London suggested that targeted T cell therapies might be able to help fight the disease. But it has been going on for a long time—it was started in 2020, long before most people thought COVID-19 might stay in the body.

But that’s not the only thing that makes it unique. The people who worked on the study got ideas from studying HIV, a disease that is basically defined by its ability to kill T cells. Since they couldn’t keep an eye on antibodies so early in the pandemic, they used PET scans to look at how T cells behaved inside the body after infection.

A professor of immunology at Imperial College London and co-author of the Penguin Handbook of Long Covid and lead investigator of the NIHR WILCO LONG COVID Study, Danny Altmann, said, “It’s a new approach that lets them map activated T cells in the body.” Altmann was not involved in the study.

He said, “They find patterns of long-term T cell activation that may help to explain patterns of long-term Covid symptoms.” “For instance, people with breathing problems had activated T cells that stayed in the lungs for a long time.”

Activated T cells were seen flocking to the gut wall in other scans, which led the team to look at gut biopsies. As before, they found COVID-19 RNA, which Altmann called a “long-term virus reservoir.”

Six control samples were used to make the result even more clear. These were scans from before the pandemic, “before anyone on the planet could’ve possibly had this virus,” Michael Peluso, lead author of the paper and assistant professor of medicine at the University of California, San Francisco, told Stat. In these scans, T cells were activated, and they were mostly found in places that are known to help get rid of inflammation, like the liver and kidneys. People with Long Covid had them all over.

It’s very interesting, Peluso said. “This is happening in someone’s spinal cord, GI tract, heart wall, or lungs, my goodness!”

Unfortunately, the study isn’t a sure thing—the researchers aren’t sure what the T cells are reacting to and whether the scans are showing old infections or live virus particles—but it’s still interesting. “A lot of inferential data supports the idea that one of the main reasons for long-term Covid may be that some people don’t get rid of the virus properly and have SARS-CoV-2 reservoirs in their tissues,” Altmann said. “But it’s been hard to prove.”

“This study should be seen as a big step toward better understanding how this disease works,” he said. “This brings us closer to treatments that could give hope to the tens of millions of patients.”

It is very important to have new clinical trials right now, and studies like this help show the way.

The study is written up in the Science Translational Medicine journal.

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Medicine and Health

Not many people know what a QR code stands for yet

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During the COVID-19 pandemic, QR codes made a surprising comeback as a “touchless” way to send information. Some restaurants and bars still ask customers to scan a QR code to see the menu, which makes people unhappy. This is a holdover from lockdowns. But surprisingly, few people know the long and interesting history of QR codes. In fact, not many people even know what the initials stand for.

“Quick Response” is what QR stands for. Masahiro Hara and his team at DENSO, a Japanese company that worked on the development of barcode technology, came up with the code system in 1994.

Automobile factories called the company and said that barcodes were no longer working because each one could only hold about 20 characters of information. As car companies’ inventory grew, their boxes needed more and more barcodes, which was very inefficient for their workers.

Hara, who is now the chief engineer at DENSO, had an “aha!” moment when he looked at the board of the strategic game Go and realized how much data it could store.

“We knew what we were doing because we had been making barcode readers for ten years.” Hara told The Guardian in 2020, “I was looking at the board and thought that the way the stones were lined up along the grids… could be a good way to get a lot of information across at once.”

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QR codes were a huge hit in Japanese auto factories, but Hara was surprised at how many other uses people found for them, like making payments and keeping track of infections during the COVID-19 pandemic.

The fact that it was used to make people safer makes me very happy. In 1994, we were interested in how it could be used in the economy. “We had no idea it would be used for this,” Hara said.

A normal QR code can hold up to 7,089 numbers, 4,296 letters and numbers, 2,953 bytes of data, or 1,817 kanji characters. This is a lot more data than a simple barcode can hold. Scanners can still read the code, even if it is messed up or hard to see. This is very useful in the real world, where things can change quickly.

Hara wants to make his masterpiece even better, though. During Ahmedabad Design Week 4.0 in January 2023, he gave a hint that he was working on the QR Code 2.0.

“I am coming up with a new QR code right now.” But it will take some time. “The new code system will have colors and may be rectangular instead of square like the current one,” the inverter was said to have said at the event.

“The new QR (quick response) code will be made so that it can hold more data than the current design,” he said.

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A new immune pathway discovery points to a “possible cure” for lupus in the future

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Finding a pathway in the immune system that seems to be a main cause of lupus could lead to the creation of more targeted treatments for this autoimmune disease. This new study is good news for a lot of people who have been living with this long-term condition. In the US alone, 1.5 million people are affected.

People with systemic lupus erythematosus, or SLE, or just “lupus,” have a long-term autoimmune disease that shows up in many ways. Some of the most common are joint and muscle pain, extreme tiredness, and a rash that looks like a sunburn on the face. Other symptoms include headaches, fevers, hair loss, and swollen glands.

It may take some time to figure out if someone has lupus because their symptoms are so different and can look like other health problems. If you catch the disease early, you may be able to get better. Moderate to severe forms of the disease can damage organs like the heart and kidneys and, in some cases, even kill you.

Lupus affects millions of people around the world, mostly women and people who were assigned female at birth, but no one knows what causes it.

There is some evidence that it results from issues between the T cells and B cells, two different types of immune cells. Patients usually have a lot of T follicular helper cells and T peripheral helper cells. These cells make CXCL13, an inflammatory molecule that attracts B cells. It’s less clear why this happens, though.

The main goal of treatment is to weaken the immune system so that it doesn’t attack the body’s own tissues. However, this method doesn’t always work and can cause a number of side effects. “Ever since the beginning, all lupus treatment has been rough.” “It’s a broad immunosuppression,” dermatologist and co-corresponding author of the new study, Dr. Jaehyuk Choi, said in a statement.

Choi and his colleagues have now found a pathway in the immune system that seems to be responsible for the disease process in lupus. More importantly, they think they know how to fix it.

Co-corresponding author Dr. Deepak Rao said, “We’ve found a fundamental imbalance in the immune responses that people with lupus make, and we’ve identified specific mediators that can correct this imbalance to dampen the pathologic autoimmune response.”

The aryl hydrocarbon receptor (AHR) controls the pathway in question. Its main job is to help cells deal with things that stress them out, like bacteria and pollution. If the AHR pathway isn’t activated enough, too many T peripheral helper cells are made. This leads to more autoantibodies, which are what make people with lupus have so many problems.

They put their theory to the test by adding AHR activators to blood samples from people with lupus. The researchers saw that the T cells changed into the Th22 subtype, which might help the body heal itself instead of making it inflamed and sick.

We learned that we can lower the number of these disease-causing cells by either using small-molecule activators to turn on the AHR pathway or limiting the amount of interferon that is too high in the blood. It might be possible to cure this if the effects last, Choi said.

People who have an autoimmune disease would love to hear those two words: “potential cure.” However, more research needs to be done before these results can be turned into clinical therapies that could help patients. The writers have already started this project and are looking into how AHR activators can be used in a treatment in a safe and effective way.

Still, these results are a big step toward finding better ways to treat a disease whose causes are still not well understood.

The study was written up in Nature.

 

 

 

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