T lymphocytes in systemic lupus erythematosus: an update

T cells from patients with systemic lupus erythematosus have been shown to be activated in vivo and provide cognate and noncognate help to autoreactive B cells. In particular, T cells exhibit aberrant responses to stimuli with increased calcium influx and decreased production of interferon-gamma and interleukin-2. An imbalance in the proapoptotic/antiapoptotic mechanisms also seems to contribute to the persistence of autoreactive clones and the lack of productive immune responses. The purpose of this review is to discuss recent studies that shed light into the pathogenetic mechanisms underlying T-cell dysfunction in systemic lupus erythematosus.

Significant progress has been made in understanding the causes of the abnormal T-cell receptor and other surface molecule-mediated signaling. Furthermore, investigators have characterized better the intracellular and nuclear signaling pathways that lead to abnormal cytokine production in lupus. Finally, efforts to correct these abnormalities in vitro have yielded promising results.

New findings in the pathophysiology of T cells in lupus and especially the application of novel techniques to correct immune cell aberrations on the transcriptional and translational levels give hope for the development of rational treatments in systemic lupus erythematosus.