Short interfering RNAs that were directed against a conserved region of flaviviruses, when delivered to the brain, enabled mice to fight off West Nile virus (WNV) in both the brain and the body, and develop a durable immune response. Researchers from Yale University reported those findings in the March 29, 2018, issue of Cell Host & Microbe.

Immune responses to gut bacteria may initiate systemic lupus erythematosus (lupus) in susceptible individuals. Individuals who go on to develop lupus have autoantibodies years before the onset of symptoms, and the earliest detectable antibodies are often those to the RNA-binding protein Ro60. Scientists from Yale University and the NIH investigated potential sources of Ro60 antigen, and they showed that several species of commensal bacteria express bacterial versions of Ro60. 

As antibody developers can attest, many antibodies can bind to cells. But most of them don't do anything of therapeutic value after they do.

Physiologically, antibodies are one of the major weapons the body deploys against infection. And the very first Nobel Prize in Physiology or Medicine, in 1901, was awarded to Emil Adolf von Behring for antibodies (in the form of serum therapy) against the diphtheria-causing Corynebacterium diphtheriae. So it is perhaps surprising that in the 117 years since, as far as antibiotic therapeutics go, small molecules have largely been the name of the game.

Type I diabetes (T1D) is an autoimmune disease that results in the destruction of insulin-producing pancreatic beta cells by killer T cells. However, most of the killer T cells that patrol the pancreas during diabetes do not recognize any pancreatic antigens. The assumption has been that even the nonspecific T cells contribute to disease progression by contributing to tissue damage. Researchers from the La Jolla Institute of Allergy and Immunology have reported that the opposite is true. 

The threat of drug-resistant superbugs is no secret, and neither is the fact that the development of new antibiotics faces commercialization challenges as well as scientific ones.

A significant fraction of knockout genes are embryonic lethal – that is, knocking them out causes mouse embryos to die before birth. Research into the function of those genes has focused on the embryos themselves, but researchers from the British Babraham Institute have shown that the majority of embryonic lethal genes affect the placenta.

Romidepsin, a histone deacetylase (HDAC) inhibitor and FDA-approved lymphoma drug, reversed the social deficits of autism spectrum disorder (ASD) in a mouse model of the condition.