Proinflammatory lytic cell death releases cytosolic TRIM21, which binds to circulating antibodies and is internalized by macrophages, stimulating cross-antigen presentation and inflammation in Sjögren’s disease.
Learn more in Science Immunology.
TRIM21/Ro52 assembles proinflammatory immune complexes.
In Stroke due to medium or distal vessel occlusion, endovascular treatment plus best medical treatment preserved more brain tissue and was linked to improved imaging outcomes and better clinical recovery compared with medical treatment alone.
Interventions EVT plus BMT compared with BMT alone.
Main Outcomes and Measures Primary outcome was calculated as the difference in volume of tissue at risk and the final infarct volume divided by the tissue at risk (change in Vrel). We defined a Vrel of 0.8 or greater as a good imaging outcome, meaning that at least 80% of the brain tissue initially at risk was not infarcted at 24 hours. Additionally, the association between brain tissue preserved and clinical outcome at 90 days was investigated.
Results From the 447 patients (252 [56.4%] male; median [IQR] age, 77.0 [68.0–84.0] years) included in this secondary analysis, 226 received EVT plus BMT and 221 received BMT alone. Median (IQR) time of the follow-up imaging was 22.9 (19.2−25.5) hours. Median (IQR) Time to maximum less than 6 seconds (Tmax6) volume was 34.0 (20.0−50.0) mL. Median follow-up infarct volume was 7.0 (1.0−22.9) mL. The median (IQR) change in absolute volume in the EVT plus BMT group was 23.6 (5.7−38.9) mL and 14.8 (0−30.3) mL in the BMT group. Median (IQR) change in Vrel was 0.8 (0.2−1.0) in the EVT plus BMT group and 0.6 (0−0.9) in the BMT group. Odds for reaching a change in Vrel of 0.8 or greater were higher in the EVT plus BMT group compared with BMT (adjusted odds ratio [aOR], 1.6; 95% CI, 1.1−2.3) and with successful reperfusion compared with no successful reperfusion (aOR, 2.5; 95% CI, 1.3−4.8). Patients with a change in Vrel of 0.8 or greater had a better clinical outcome at 90 days.
A popular Korean skincare ingredient may be far more powerful than anyone realized. Scientists have discovered that madecassic acid—derived from the herb Centella asiatica—can stop antibiotic-resistant bacteria in their tracks, including dangerous strains of E. coli. By targeting a bacterial protein that humans don’t have, the compound disrupts the microbes’ ability to survive, making it a promising new type of antibiotic.
It is not yet known how the immune system’s discovery of the pathogens leads to a change in behavior. “As this learned food avoidance can be found in all species, we investigated this question in a model organism – the fruit fly Drosophila,” explains the senior author. “Within this model, we can clarify how the brain and body interact with each other to trigger an avoidance reaction that is vital for survival.”
In the current study, the group had their test animals choose between two food sources. One of them was contaminated with the pathogenic bacterium Pseudomonas entomophila. The other contained a harmless Pseudomonas strain. The two food sources were otherwise completely identical.
Flies that have not yet had any bad experiences with the pathogen prefer the harmful food because they find its odor attractive. “As this is life-threatening for the animals, we wondered how animals that have consumed these bacteria with their food behave,” explains the scientist.
The pathogens did not remain undiscovered among the flies for long: The animals’ innate immune system has sensors that raise the alarm in cases such as this. “In our experiment, receptors were activated in them that respond to components of the bacterial cell wall,” explains another author.
These sensors mainly respond to the harmful Pseudomonas strain, but hardly respond at all to the harmless strain. Many of them sit on the surface of special neurons located near the fly’s throat. Via their branches, these neurons are connected not only to the fly’s brain but also to a fat store in the fly’s head. If the receptors raise the alarm in the presence of harmful microorganisms, this leads to the release of the neurotransmitter octopamine in the neurons, which is closely related to adrenaline. This travels through the neuronal branches to the fat store.
“The octopamine then triggers the formation of another neurotransmitter, dopamine, in the fat cells,” says the author. “The dopamine, in turn, is transported into the fly’s brain, where it causes the continuous, increased activation of neuronal networks that are important for learning and trigger an avoidance response.” The animals then tend to be deterred by the odor of pathogenic bacteria. “We were able to show that the flies chose the food source with the harmless germs following their experience with the spoiled food,” explains the scientist.
The adipose tissue is significantly involved in this learned behavioral change. But why is that so? “We still do not have a definitive answer,” says the author. “However, the flies’ decision may be linked to their nutritional status.”
Moving from the Big Bang and the discovery of cosmic beginnings, to the fine-tuning of the physical constants that make life possible, to the extraordinary complexity and information embedded in DNA, mathematician John Lennox, philosopher of science Stephen Meyer, and chemist James Tour, explores whether these developments point to blind, undirected processes—or to the activity of an intelligent mind. The trio challenges long-held materialist assumptions, revisits classic scientific debates, and reflects on what these questions mean not only for science but also for our understanding of human existence and purpose.
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UniQure’s highly promising Huntington’s disease gene therapy BLA (biologics license application) was rejected by the FDA — because UniQure used an external control rather than a surgical sham control. Yet the latter would put control group patients at additional risk, making it ethically problematic. Hopefully some agreement will be reached which circumvents these issues! For now, it is an educational story to watch unfold.
Abi-Saab said during uniQure’s earnings call that he wouldn’t count on the four-year data altering the FDA’s decision.
“We don’t believe that there’s any reason we have today to believe that this will change the FDA’s position regarding the Phase 1/2 trials,” he told investors.
H.C. Wainwright struck a different tone, however, in the Monday note. “While the FDA appears to be enforcing a full sham surgery-controlled Phase 3 trial in Huntington’s, we believe an alternative path forward may be negotiated given the strong AMT-130 data generated to-date,” the analysts wrote. The 4-year data “should further inform the durability and magnitude of effect observed to date.”
As a proof of concept, the team used CRISPR gene-editing tools to insert the genetic blueprint for producing rare, protective antibodies directly into hematopoietic stem and progenitor cells of mice. Once transplanted back into mice, the edited stem cells gave rise to B cells programmed to produce the engineered antibody. A conventional vaccination would then serve as the trigger.
It worked. Even when only a few dozen stem cells were edited, vaccination triggered rare cells to expand, mature into plasma cells, and produce large amounts of antibodies that persisted long-term and could be boosted if necessary. The engineered B cells behaved just like normal immune cells, and even provided protection from disease. Mice engineered to produce a broadly neutralizing influenza antibody were spared from an otherwise lethal influenza infection.
The team went on to demonstrate their novel platform’s versatility. Engineered B cells were able to secrete non-antibody proteins, pointing to potential applications in treating genetic diseases caused by missing enzymes or other essential proteins.
The researchers also showed that stem cells carrying different antibody instructions could be combined, enabling a single immune system to produce multiple antibodies at once—an approach that could limit viral escape and ultimately lead to functional cures for rapidly mutating pathogens such as HIV.
And the team showed that human stem cells edited using the same approach gave rise to functional immune cells, providing a key proof of feasibility that the platform could one day work in humans, as well. Science Mission sciencenewshighlights.
An innovative gene-editing strategy could establish a new way for the body to manufacture therapeutic proteins—including certain kinds of highly potent antibodies the are naturally difficult to produce—by reprogramming the immune system itself.