It’s unclear whether differing odds of dying between men and women reflect inherent differences between male and female immune systems or differences rooted in gender norms.

The temporary loss of olfaction stops the flies from eating any more of whatever it is that made them sick.

In rats, the spleen directs a cytokine surge that drives system-wide inflammation, but it is not, as once believed, the main producer of the chemical messenger.

Differences in the expression of genes associated with antiviral immunity and lung inflammation may contribute to a more serious COVID-19 infection.

A recent study elucidates some of the changes that occur in the body after inoculation with a tuberculosis vaccine.

Genetically engineered cells that overproduce ACE2, the receptor the novel coronavirus uses to enter cells, neutralize infection in vitro and mop up inflammatory cytokines in mice.

Conversations between the immune and central nervous systems are proving to be essential for the healthy social behavior, learning, and memory.

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.