title: Systems biology in systemic lupus erythematosus: integrating genes, biology and immune function.
abstract: Overactive B cells, abnormally activated T cells and inappropriate handling of cellular debris by the innate immune system are central in the pathogenesis of systemic lupus erythematosus (SLE). Genetic studies in SLE patients have unraveled allelic variations in genes encoding key molecules that control inter- and intra-cellular signaling and play a role in the abnormal handling of apoptotic material. Despite recent breakthroughs though, it is still unclear how exactly genes and environment interact to produce the characteristic immune dysregulation in SLE.
authors.affiliation: Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA. vkyttari@bidmc.harvard.edu
authors.forename: Vasileios C
authors.initials: VC
authors.lastname: Kyttaris
authors.forename: Sandeep
authors.initials: S
authors.lastname: Krishnan
authors.forename: George C
authors.initials: GC
authors.lastname: Tsokos
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000276:immunology; D001324:Autoantigens / Q000276:immunology; D020022:Genetic Predisposition to Disease; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000235:genetics* / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology*; D049490:Systems Biology
chemical_list: D001323:Autoantibodies; D001324:Autoantigens