Imperial College, London.

A crystallographer takes a jaunt into immunology.

Although I spend most of my time exploring a landscape formed by atoms and bonds, I know it is healthy to make occasional journeys into less familiar territories, and I was intrigued to spot a paper on the curious interplay between infection and immunity in cattle with foot-and-mouth disease virus (FMDV).

FMDV, a highly contagious pathogen that can cause lameness, low weight and decreased milk production, is a scourge of agricultural livestock around the world. Although the acute phase of infection is rarely fatal, infection may persist in animals that have apparently recovered, creating a viral reservoir that some fear could contribute to the spread of disease. Nicholas Juleff and colleagues, from the United Kingdom’s Institute for Animal Health, report a fascinating discovery that may have unlocked the secret of FMDV persistence.

They used an array of molecular techniques to search for traces of virus in tissues from the mouths and throats of infected cattle (N. Juleff et al. PLoS ONE 3, e3434; 2008). In a carefully controlled study, they found evidence of intact, non-replicating virus particles trapped by immune cells called follicular dendritic cells within the germinal centres of lymph nodes. Strikingly, virus was present for at least 38 days post infection, even though it was undetectable in surrounding tissues.

The retention of intact virus within germinal centres is likely to have a role in stimulating the long-lasting immune response of white blood cells that is characteristic of viral infections (but not current vaccine preparations) and echoes a pattern previously seen for HIV infection. The authors suggest that this capture may inadvertently also be responsible for preserving intact viruses capable of infecting susceptible cells as they come into contact with germinal centres. A causal relationship has yet to be firmly established but the paper illuminates a clear pathway by which to check this out.

Harvard Medical School, Boston, Massachusetts

An immunologist muses about inflammation through cell interactions.

I spend my lab hours trying to understand what prompts T cells — a type of white blood cell — to specialize. Some T cells produce soluble molecules that rattle the immune system into an inflamed state; other cells generate molecules that calm the system back down.

Upon infection, cells such as macrophages — another type of white blood cell — produce soluble molecules called interleukins that direct the fate of the responding T cells. An emerging curiosity in the field is which interleukins make certain T cells become pro-inflammatory, and which cause other T cells to become anti-inflammatory. This decision is crucial for determining whether an immune response induces or suppresses inflammation.

Recently, investigators have turned their attention towards an interleukin known as IL-27. This is produced by activated macrophages and was initially thought to induce IFN, a signalling molecule that activates macrophages even more.

But work by Nico Giraldi and his colleagues at Genentech in South San Francisco, and other groups, has recast IL-27 as a molecule that primarily directs T cells to suppress inflammation. In a paper published in March, Giraldi’s team confirmed that IL-27 acts in this way because it causes CD4+ and CD8+ T cells to make the anti-inflammatory IL-10, and does not work through an alternative pathway (M. Batten et al. J. Immunol. 180, 2752–2756; 2008). Mice with Listeria infections or autoimmune tissue inflammation in their brains and spinal cords generated fewer IL-10-producing T cells when they lacked an IL-27 receptor. Whether an analogous interaction occurs in humans is not known, but, if it does occur, this research could become medically useful.