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This case study introduces students to the complex field of immunology and the wide variety of host-pathogen interactions that drive evolutionary change.  The case begins with a basic overview of the phases of the immune response and how each contributes to host defense against an invading pathogen.  In order to delve deeper into each phase, students explore the metaphor of a battle in which a host and pathogen are locked in combat in order to understand the individual components of the immune response.  Once students successfully understand how the immune system works in general, they are then asked to think creatively about how a pathogen that wants to survive could evolve to evade the immune response, and to find concrete examples in the literature.  The overall goal is for students to gain a deeper understanding of the immune response and how host-pathogen interactions drive coevolution of both host immune components and the pathogen itself. The case was originally designed for an introductory biology course, but can easily be adapted for use in a variety of different courses and levels.

Why did you get the flu this winter, but your co-workers didn't? The answer, according to a new study of twins, may have less to do with your genes and more to do with your environment-including your past exposure to pathogens and vaccines. Our immune system is incredibly complex, with diverse armies of white blood cells and signal-sending proteins coursing through our veins, ready to mount an attack on would-be invaders. Everyone's immune system is slightly different-a unique mixture of hundreds of these cells and proteins. But the main driver of this variation is unclear. Although scientists know that our immune system can adapt to our environment-that's why vaccines work, for instance-it is also built by our genes.

Quintana-Murci and his colleagues also took advantage of a previously published map of areas of the human genome where Neanderthal genes are present, showing that innate immune genes are generally more likely to have been borrowed from Neanderthals than genes coding other types of proteins. Specifically, they noted that 126 innate immune genes in present-day Europeans, Asians, or both groups were among the top 5 percent of genes in the genome of each population most likely to have originated in Neanderthals. The cluster of toll-like receptor genes, encoding TLR 1, TLR 6, and TLR 10, both showed signs of having been borrowed from Neanderthals and having picked up adaptive mutations at various points in history. Meanwhile, a group led by Janet Kelso of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, used both the same previously published Neanderthal introgression map that Quintana-Murci used and a second introgression map. The researchers searched for borrowed regions of the genome that were especially long and common in present-day humans, eventually zeroing in TLR6, TLR10, and TLR1. These receptors, which detect conserved microbial proteins such as flagellin, are all encoded along the same segment of DNA on chromosome four.

An overview of the immune system, concentrating on the roles played by B and T lymphocytes, and the antigen-presentation system.

Lessons on the immune systems and disease. Print and go!

Some of the anti-glutenists argue that we haven't eaten wheat for long enough to adapt to it as a species. Agriculture began just 12,000 years ago, not enough time for our bodies, which evolved over millions of years, primarily in Africa, to adjust. According to this theory, we're intrinsically hunter-gatherers, not bread-eaters. If exposed to gluten, some of us will develop celiac disease or gluten intolerance, or we'll simply feel lousy. Most of these assertions, however, are contradicted by significant evidence, and distract us from our actual problem: an immune system that has become overly sensitive.