The researchers find that sera from lupus patients contains antibodies that bind to T cells and activate a complex cellular signaling cascade that ultimately results in decreased IL-2 production. This deficiency in IL-2 could result in the autoantibody production that occurs in lupus.
In an accompanying commentary, Gary Kammer of Arthritis Associates, Inc points out "the contribution by Tsokos and his colleagues…provides a new appreciation and insight into how the microenvironment in lupus can further impinge on a defective T cell to inhibit IL-2 production. From such studies will come the inspiration and novel approaches necessary to develop therapeutic tools to abate disease and improve the quality of life of our patients."
TITLE: Systemic lupus erythematosus serum IgG increases CREM binding to the IL-2 promoter and suppresses IL-2 production through CaMKIV
AUTHOR CONTACT:
George C. Tsokos
Walter Reed Army Institute of Research, Silver Spring, Maryland, USA.
Phone: (301) 319-9911; Fax: (301) 319-9133; E-mail: gtsokos@usuhs.mil
View the PDF of this article at: https://www.the-jci.org/article.php?id=22854
ACCOMPANYING COMMENTARY:
TITLE: Altered regulation of IL-2 production in systemic lupus erythematosus: an evolving paradigm
AUTHOR CONTACT:
Gary M. Kammer
Arthritis Associates Inc., Willoughby, Ohio, USA.
Phone: (440) 953-8700; Fax: (440) 953-8796; E-mail: gmkammer@hotmail.com
View the PDF of this article at: https://www.the-jci.org/article.php?id=24791
Journal of Clinical Investigation