Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Visual representation of a dendritic cell presenting an antigen to T-lymphocytes. © Juan Gaertner/Shutterstock.com

A new study from the Ogg group published in Science Immunology demonstrates a previously unrecognised mechanism by which Group A Streptococcus (also known as Strep A) bacteria can cause skin damage. 

Group A Streptococcus, or Strep A, is a common bacterium, often found on the skin or in the throat. In the 1800s, Strep A infection was one of the most common causes of childhood mortality in the UK and, despite major medical advances, continues to cause serious medical problems. The mechanisms by which Strep A bacteria can cause damage to different parts of the body remain unclear in many cases.

In this study, the research team (which included researchers from the MRC Human Immunology Unit) discovered a hitherto unknown process linking Strep A infection and a form of skin damage called psoriasis. Psoriasis is a type of inflammation that affects many individuals and can have a significant impact on their quality of life. A variant of psoriasis, known as guttate psoriasis, was already known to be promoted by the immune response to Strep A throat infections. However, the underlying mechanisms of this were largely unexplained.

The first author Yi-Ling Chen and colleagues investigated how T cells, a type of white blood cell involved in the immune response, behave during a Strep A infection. By studying blood and skin samples, they identified a subset of T cells that were responsive to Strep A bacteria and accounted for up to 10 % of all human T cells.

The researchers found that lipids (or fats) produced in response to Strep A infection can activate these T cells, which then circulate through the body into other tissues. In the skin, these T cells become further activated by certain types of human skin lipids. Normally, T cells have mechanisms of self-control, but in some people this lipid activation can cause the T cells to produce excessive inflammatory proteins called cytokines, leading to psoriasis.  

Senior author Graham Ogg said, “Group A Strep has long been known to trigger different forms of psoriasis, but it has been unclear how this takes place. We hope that the new discoveries will provide insights which eventually lead to improvements in patient care.”

Having identified a route through which Strep A can induce psoriasis, the researchers are now trying to develop new ways to block the process in order to help patients with psoriasis and to reduce other consequences of Strep A infection.

Read the full paper