cytokines

Some viruses, possibly even SARS-CoV-2, can sneak into the brain through the nose. Recent studies show that microglia are ready for them when they do.

Several routes exist for immune cells to communicate with neurons in the central nervous system, though T cells rarely come in direct contact with neural tissue.

Researchers are trying to make sense of immune systems gone haywire and develop biomarkers to predict who will become the sickest from a coronavirus infection.

Gamma delta T cells in the meninges of the brain release a cell signaling molecule that does more than protect mice from microbial pathogens.

When mice that had suffered a stroke were given blood from a healthy donor, they experienced less tissue and neurological damage.

Excess of the inflammatory molecule bradykinin may explain the fluid build-up in the lungs of patients with coronavirus infections. Clinical trials of inhibitors are putting this hypothesis to the test.

The leaky blood vessels and lung fluid build-up in some COVID-19 patients might be explained by the virus’s corruption of an inflammation safeguard.

Increases in the levels of three cytokines are among the features linked to poor outcomes.

These antiviral proteins are produced by the body as a natural defense against viral infections and synthetic interferons might help prevent or treat the beginning stages of SARS-CoV-2 infection.

The cholesterol-lowering drugs quell inflammation and reverse endothelial tissue damage, hints that they might curb the body’s excessive immune response to SARS-CoV-2 infection.

Drugs targeting patients’ immune systems, rather than the virus itself, could be key to recovery from severe cases of the disease, some researchers suggest.

By studying influenza in mice and cells, researchers identify a glucose metabolism pathway critical to the dysregulated immune response that kills many infectious disease patients, including those with COVID-19.

Oligomannate, recently approved in China, is being met with some skepticism from researchers.

A specific type of lung cell withstands flu infection by doubling down on DNA repair.

Patients with the rare autoimmune condition, highlighted in the Oscar-nominated film The Big Sick, currently have limited treatment options.