Nature Immunology pp 1309 - 1316

A protein expressed in developing embryos may protect mothers against immune-mediated attack by fetal cells, according to a study to be published in the December issue of Nature Immunology. This protein, called Zfp608, appears to function by switching off the expression of Rag genes, which are involved in the development and function of fetal immune cells.

Thomas Aune and colleagues identified Zfp608 by honing in on a genetic defect exhibited by a strain of mice called ZORI, which have a compromised immune system. These mice have reduced numbers of T lymphocytes, immune cells that develop in the thymus. Normally mice express Zfp608 during embryonic development but stop its expression soon after birth. In contrast, ZORI mice continue to express Zfp608 in their thymus well beyond birth; continued Zfp608 expression is therefore linked to lack of thymic immune cell development.

The authors show that Zfp608 inhibits Rag gene expression in thymic cells, which explains the defect in T lymphocyte development observed in ZORI mice. They speculate that the timing of Zfp608 expression in embryos might play a protective role by preventing the development of fetal immune cells that could potentially recognize and attack maternal tissues, thereby harming both mother and her unborn offspring.

Nature Immunology pp 1299 - 1308

Developing a fever gives the immune system a boost, according to a study in the December issue of Nature Immunology. Sharon Evans and colleagues show elevating the internal temperature in mice, mimicking the fever response to infection, increases the number of immune cells that are recruited to the lymph nodes where these cells are educated and armed to seek out and destroy the offending pathogen.

Lymph nodes act as the powerhouse of the immune system. Cells and particles from nearby tissues drain into lymph nodes and alert lymphocytes, immune cells that enter nodes via the bloodstream, to the presence of foreign intruders.

Evans' group reports that fever acts on cells called 'high endothelial venule cells' (HEVs), which function as gatekeepers between blood-borne cells and lymph nodes. Fever triggers HEVs to produce more CCL21, a molecule that recruits lymphocytes to the lymph node from the blood. Fever also increases the number of adhesion molecules on the surface of HEVs, resulting in more efficient lymphocyte entry into the nodes. Indeed, lymph nodes swollen by increased numbers of immune cells, as seen with mumps disease, are commonly recognized as a sign of infection.

So when suffering with a cold if you consider reaching drugs to reduce your temperature, remember that fever can actually be good for you.