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Human leukocyte antigen (HLA) genes encode proteins found on the surface of cells, which help regulate our immune systems. These genes vary tremendously within the population, and such variations can lead to a high risk for, or protection from, autoimmune disorders. In a , a team led by Ó³»­´«Ã½ researcher Soumya Raychaudhuri and Paul de Bakker of University Medical Center Utrecht (Netherlands) showed evidence that two different versions of certain HLA genes may work together to heighten the risk of autoimmune conditions like rheumatoid arthritis, type 1 diabetes, and celiac disease — potentially explaining differences between individuals with these diseases.

Between 2013 and 2015, an outbreak of Ebola virus killed more than 11,000 people. Ó³»­´«Ã½ researchers quickly deployed real-time sequencing efforts that confirmed that the virus was primarily spreading through human-to-human contact rather than between animals and humans and that the viral genome was mutating. This work had a profound impact on how public health officials diagnosed the disease and developed strategies to contain it.

Human genetic studies have implicated the regulation of autophagy (the process by which cells break themselves down) in inflammation, neurodegeneration, infection, and autoimmunity. This has led scientists to search for small-molecules that might enhance autophagy in order to shed light on its role in disease. In the , Ó³»­´«Ã½ researchers described one such effort: the team screened nearly 60,000 small molecules and found one, BRD5631, that affects several cellular disease phenotypes linked to autophagy. The researchers believe that studying the molecule’s mechanism of action may reveal therapeutically beneficial ways to modulate autophagy in the context of disease.

Reprogramming adult cells to a stem cell-like state can provide researchers with tools to help illuminate the role genetic differences play in disease development and potentially regenerate tissue in the wake of injury. However, these induced pluripotent stem cells (iPSCs) are difficult to create. In a study published this week in , researchers, including Kevin Eggan, Alexander Tsankov, and Alexander Meissner of the Ó³»­´«Ã½ and Harvard Stem Cell Institute, describe an automated, robotic process that efficiently generates iPSC lines — a new approach that could facilitate studies with these cells.

The human body is governed by complex biochemical circuits. Chemical inputs spur chain reactions that generate new outputs. Understanding how these circuits work—how their components interact to enable life—is critical both to advancing basic biology and to identifying new treatments to disease, which arises when these circuits misfire. But getting to that understanding is no trivial task.