The life of many individuals with inflammatory diseases such as rheumatoid arthritis has been dramatically improved by treatment with drugs that target the protein TNF, so called anti-TNF therapies. However, anti-TNF therapies can decrease the ability of the immune system to fight infections and have been associated with an increased incidence of tuberculosis.
By studying the immune cells of patients before and after treatment with the anti-TNF therapy infliximab Steffen Stenger and colleagues, at the University Hospital of Ulm, Germany, have been able to identify a mechanism by which an anti-TNF therapy impairs host defense against tuberculosis.
In the study, a subset of CD8-expressing effector memory immune T cells characterized by expression of the proteins CD45RA and granulysin (which the authors termed CD45RA+ effector memory CD8+ T cells) were identified as having a major role in targeting the bacterium that causes tuberculosis (Mycobacterium tuberculosis). Furthermore, numbers of CD45RA+ effector memory CD8+ T cells were reduced in patients following treatment with infliximab.
As this correlated with a decreased ability of peripheral blood from the patients to kill M. tuberculosis, the authors conclude that the loss of this immune cell subset provides a mechanism to explain the reactivation of latent tuberculosis infection in some individuals being treated with infliximab.
In an accompanying commentary, Elizabeth Miller and Joel Ernst, at New York University School of Medicine, New York, discuss the clinical importance of these data and highlight some of the possibilities that they raise.
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