Discover the crucial role of antigen presenting cells (APCs) in immunity. Learn about their types, functions, and importance in health and disease.

Unlike traditional islet transplants — which are expensive, donor-limited, and prone to rejection — these 3D-printed islets are designed for better integration into the body. Implanted under the skin, the new islets respond to glucose fluctuations and begin producing insulin in real time, offering a more natural and automated regulation process.
Early tests revealed that the printed islets remained viable and fully functional for at least three weeks, a major improvement over past transplantation methods that often fail due to tissue damage and immune response.
Researchers at MIT and other institutions have identified compounds that can fight off viral infection by activating a defense pathway inside host cells. These compounds, they believe, could be used as antiviral drugs that work against not just one but any kind of virus.
The researchers identified these compounds, which activate a host cell defense system known as the integrated stress response pathway, in a screen of nearly 400,000 molecules. In tests in human cells, the researchers showed that the compounds help cells fend off infection from RSV, herpes virus, and Zika virus. They also proved effective in combating herpes infection in a mouse model.
The research team now plans to test the compounds against additional viruses, in hopes of developing them for eventual clinical trials.
In Alzheimer’s disease, proteins like amyloid beta form clumps, known as plaques, that damage the brain.
But in some people, immune cells called microglia break down these proteins before they can cause harm. This leads to fewer and smaller clumps—and much milder symptoms.
Researchers at UC San Francisco identified a molecular receptor that enables microglia to gobble up and digest amyloid beta plaques. The findings are published in the journal Neuron.
University of Kentucky Markey Cancer Center researchers have discovered a genetic biomarker that could help identify patients with glioblastoma most likely to benefit from the cancer drug bevacizumab.
The study, published in JCO Precision Oncology, found that brain tumors from patients treated with bevacizumab who lived longer were more likely to have a genetic change called CDK4 amplification. This suggests that testing for the molecular marker could help oncologists identify patients most likely to respond well to bevacizumab treatment.
“The findings could help oncologists make more informed treatment decisions for glioblastoma patients, potentially sparing those unlikely to benefit from unnecessary side effects while ensuring those who might respond get access to the drug,” said John Villano, M.D., Ph.D., the study’s lead author and professor in the UK College of Medicine.
The researchers identified three key factors involved in controlling the invasion routes. The gene ANXA1 was linked to invasion along blood vessels while HOPX and RFX4 was associated with diffuse infiltration in the brain. To evaluate the role of the genes, the researchers tested to knock them out in preclinical models, which resulted in a shift in the tumor’s invasion pattern. In several cases, the survival of the experimental animals was also prolonged.
The researchers also discovered proteins encoded by the identified genes in tissue samples from patients. In addition, they found that the presence of the ANXA1 and RFX4 correlated with poor survival. This indicates that these proteins could have a value as prognostic biomarkers.
An international research team has identified new mechanisms behind how the aggressive brain tumor glioblastoma spreads in the brain. Targeting the identified connection between the tumor invasion routes and the tumor cell states could be a potential new treatment strategy.
Glioblastoma is the most common and most lethal primary brain cancer in adults, known for its capacity to spread locally in the brain rather than forming distant metastases. The locally infiltrating cells are largely out of reach for current therapies and it is therefore crucial to determine how the spread in the brain is controlled.
In the current study, which was recently published in the journal Nature Communications, the researchers found that some tumor cells choose to grow along blood vessels in the brain whereas others spread diffusely in the brain tissue. This choice is controlled by the tumor cell states.
The Argentine microbiologist Federico Rey and Indian pathologist Vaibhav Vemuganti applaud the “exciting opportunities” that the new study opens for the prevention and treatment of cardiovascular disease. In a commentary also published Wednesday in Nature, the two experts emphasize that exposure to imidazole propionate worsens plaque formation in the arteries of mice. “This effect occurs independently of changes in cholesterol levels, a surprising result given the central role of cholesterol in the development of atherosclerosis,” note the two specialists, from the University of Wisconsin-Madison. “This discovery offers an interesting clue about a possible new factor involved in the origin of atherosclerosis. This is very relevant because, although lowering cholesterol — through drugs called statins, for example — can effectively reduce the risk of cardiovascular disease, a considerable proportion of people still experience adverse cardiovascular events, such as myocardial infarctions or strokes,” they warn. The CNIC itself said in a statement that the new study “could revolutionize” the diagnosis and treatment of atherosclerosis.
Sancho stresses that the work has been made possible thanks to the collaboration of thousands of volunteer employees of Banco Santander in Madrid, but also thanks to grants of €1 million from the “la Caixa” Foundation, €150,000 from the European Research Council and €100,000 from the State Research Agency.
The discovery of the decisive effect of imidazole propionate on atherosclerosis takes place against a backdrop in which the scientific community is revealing the unknown role of intestinal microbes in some human diseases. The biotechnologist Cayetano Pleguezuelos and his colleagues at the Hubrecht Institute (The Netherlands) demonstrated in February 2020 that a strain of the bacterium Escherichia coli produces a toxic molecule, called colibactin, which damages the DNA of human cells and causes malignant tumors.