title: Pathways leading to an immunological disease: systemic lupus erythematosus.
abstract: SLE is a chronic autoimmune disease caused by perturbations of the immune system. The clinical presentation is heterogeneous, largely because of the multiple genetic and environmental factors that contribute to disease initiation and progression. Over the last 60 years, there have been a number of significant leaps in our understanding of the immunological mechanisms driving disease processes. We now know that multiple leucocyte subsets, together with inflammatory cytokines, chemokines and regulatory mediators that are normally involved in host protection from invading pathogens, contribute to the inflammatory events leading to tissue destruction and organ failure. In this broad overview, we discuss the main pathways involved in SLE and highlight new findings. We describe the immunological changes that characterize this form of autoimmunity. The major leucocytes that are essential for disease progression are discussed, together with key mediators that propagate the immune response and drive the inflammatory response in SLE.
authors.affiliation: Singapore Immunology Network, 8A Biomedical Grove, Immunos.|School of Biological Sciences, Nanyang Technological University, Singapore.
authors.forename: Olga
authors.initials: O
authors.lastname: Zharkova
authors.affiliation: Singapore Immunology Network, 8A Biomedical Grove, Immunos.
authors.forename: Teja
authors.initials: T
authors.lastname: Celhar
authors.affiliation: Department of Neurology and Neurotherapeutics.
authors.forename: Petra D
authors.initials: PD
authors.lastname: Cravens
authors.affiliation: Department of Immunology.|The Rheumatic Diseases Division, Department of Internal Medicine, UT Southwestern Medical Center at Dallas, TX, USA.
authors.forename: Anne B
authors.initials: AB
authors.lastname: Satterthwaite
authors.affiliation: Singapore Immunology Network, 8A Biomedical Grove, Immunos.|School of Biological Sciences, Nanyang Technological University, Singapore.|Department of Immunology.
authors.forename: Anna-Marie
authors.initials: AM
authors.lastname: Fairhurst
authors.affiliation: The Rheumatic Diseases Division, Department of Internal Medicine, UT Southwestern Medical Center at Dallas, TX, USA.
authors.forename: Laurie S
authors.initials: LS
authors.lastname: Davis
mesh_terms: D015551:Autoimmunity / Q000235:genetics / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D016207:Cytokines / Q000276:immunology*; D004777:Environment; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology*; D017634:Self Tolerance / Q000235:genetics / Q000276:immunology
chemical_list: D016207:Cytokines
keywords: SLE; SLE pathogenesis; autoantibodies; immunology; inflammation; systemic lupus erythematosus; tissue destruction; tolerance