An unexpected aspect of the immune response to TB may lead to better treatments – for cancer as well as TB.

The body's immune response needs to control an infection but not be so powerful that it damages host tissue in the process. A Mycobacterium tuberculosis heat shock protein (Hsp70) is known to influence the strength of the immune response to this bacterium, but quite how has been unclear. Now, an international team led by Professor Paul Lehner from the University of Cambridge has identified how Hsp70 acts – a finding that could benefit cancer therapies as well as TB treatments.

Like other heat shock proteins, M. tuberculosis Hsp70 stimulates dendritic cells, which are important for controlling T-cell responses to invading organisms by passing on short bacterial peptides. But in addition to this role, Hsp70 was also found to signal directly through the CCR5 receptor on dendritic cells, causing them to aggregate together and with T cells.

As well as highlighting a possible route to enhance the immune responses to M. tuberculosis, the research may also lead to improved cancer therapies. Hsp70 is being used to deliver peptides specific to cancer cells to dendritic cells, to provoke stronger cancer cell-specific immune responses. Understanding how Hsp70 stimulates dendritic cells opens up the possibility of further boosting immunity by targeting the CCR5 receptor.

• This research was supported by the Wellcome Trust and a range of other funders.

External links

• Floto RA et al. Dendritic cell stimulation by mycobacterial Hsp70 is mediated through CCR5. Science 2006;314(5798):454–8.