Novel molecular targets in the treatment of systemic lupus erythematosus.
T cells from patients with systemic lupus erythematosus (SLE) display a number of biochemical abnormalities which include altered expression of key signaling molecules, heightened calcium responses, and skewed expression of transcription factors. These defects are involved in the altered behavior of SLE T cells and are probably central in the disease pathogenesis. The aim of this communication is to review the defects that have been consistently documented in SLE T cells, highlighting molecules and pathways that represent therapeutic targets.
Crispín
José C
JC
Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 4 Blackfan Circle, HIM-244, Boston, MA 02115, USA.
Tsokos
George C
GC
D017252:CD3 Complex / Q000187:drug effects / Q000378:metabolism; D016503:Drug Delivery Systems; D006801:Humans; D018960:Hyaluronan Receptors / Q000187:drug effects / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000503:physiopathology* / Q000628:therapy*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
D017252:CD3 Complex; D018960:Hyaluronan Receptors