Autoimmunity, neuroinflammation, pathogen load: A decisive crosstalk in neuropsychiatric SLE

• Published in: Journal of autoimmunity Vol. 74; pp. 13 - 26
• Main Authors: Jeltsch-David, Hélène, Muller, Sylviane
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-11-2016; Elsevier
• Subjects: Allergy and Immunology; Animals; Autoantibodies; Autoimmunity; Biomarkers; Blood-Brain Barrier - immunology; Blood-Brain Barrier - metabolism; Brain; Central Nervous System - cytology; Central Nervous System - immunology; Central Nervous System - metabolism; Central Nervous System - pathology; Humans; Immune System - cytology; Immune System - immunology; Immune System - metabolism; Immune System - pathology; Immunology; Infection; Life Sciences; Lupus; Lupus Vasculitis, Central Nervous System - etiology; Lupus Vasculitis, Central Nervous System - pathology; Lupus Vasculitis, Central Nervous System - psychology; Lupus Vasculitis, Central Nervous System - therapy; Neuroimmunology; Neuroimmunomodulation; Problem Behavior; Signal Transduction; Therapy; Brain; Therapy; BBB; neuropsychiatric systemic lupus erythematosus; MHC; major histocompatibility complex; SLE; TNF; PRR; pattern-recognition receptor; dendritic cells; ECs; CMA; damage-associated molecular pattern; ICs; O&NS; antibodies; AID; Toll-like receptor; Lupus; UV; chaperone-mediated autophagy; Autoantibodies; IL; N-methyl- D-aspartate receptor subtype 2; oxidative and nitrosative stress; autoimmune disease; immune complexes; central nervous system; Infection; cerebrospinal fluid; ROS; N-methyl-D-aspartate receptor; NMDAR; tumour necrosis factor; lipopolysaccharide; Ig; endothelial cells; CNS; LPS; IFN; NSPA; systemic lupus erythematosus; Abs; neuronal surface P antigen; DCs; CSF; reactive oxygen species; TLR; Neuroimmunology; interleukin; pathogen-associated molecular pattern; blood-brain barrier; immunoglobulin; interferon; NR2; PAMP; ultraviolet; NPSLE; DAMP
• ISSN: 0896-8411; 1095-9157
• DOI: 10.1016/j.jaut.2016.04.005

Abstract Depicting the cellular and molecular bases of the continuous dialogue existing between the peripheral immune and the central nervous systems, as in neurolupus, is fundamental to improve, and better apprehend the role played by immune cells and mediators in the initiation and progression of neurological and psychiatric diseases, which nowadays remain a major public health issue. The relative frequency of neurological symptoms occurring in systemic autoimmunity is particularly worrying as, for example, two-thirds of patients with lupus will eventually experience the disabling effects of neuropsychiatric lupus. Neurolupus is a particularly severe form of lupus with wide-ranging symptoms, which contribute to increased mortality and morbidity in patients. In this context, infections, which suddenly trigger exacerbations of the otherwise mild lupus disease, may drive the progression of neuroinflammation and neurodegeneration via different mechanisms involving a network of effector molecules and cells. The complex interaction of neuroimmunology and neuroinfectiology represents a genuine challenge for basic scientists and clinicians to understand the mechanisms that are implicated, and identify possible biomarkers of severity that might predict the development of this devastating form of lupus. The ultimate goal is to design appropriate, personalised therapeutic strategies to improve the outcome of the disease.