Serum lymphocytotoxic antibodies and neurocognitive function in systemic lupus erythematosus.

Long, Aidan A.; Denburg, Susan D.; Carbotte, Ramona M.; Singal, D. P.; Denburg, Judah A.

doi:10.1136/ard.49.4.249

Cited by 82 publications

(46 citation statements)

References 34 publications

(10 reference statements)

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“…In the case of NP-SLE, it is hypothesized that disruption of the BBB and anti-neuronal autoantibodies account for CNS manifestations of disease (Rice et al, 2005;Hanly et al, 2006). Indeed, antibodies which react with neuronal cell lines and brain tissue have been reported in the sera and CSF of patients with CNS-lupus, but they are also found in lupus patients with no clinical evidence of CNS involvement (Long et al, 1990;Denburg et al, 1988;Bluestein et al, 1981;Kelly and Denburg, 1987).…”

Section: Prelude To Cns Damage: Disruption Of the Blood-brain Barriermentioning

confidence: 99%

Neuroimmunopathology in a murine model of neuropsychiatric lupus

Ballok

2007

Brain Research Reviews

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Animal models are extremely useful tools in defining pathogenesis and treatment of human disease. For many years researchers believed that structural damage to the brain of neuropsychiatric (NP) patients lead to abnormal mental function, but this possibility was not extensively explored until recently. Imaging studies of NP-systemic lupus erythematosus (SLE) support the notion that brain cell death accounts for the emergence of neurologic and psychiatric symptoms, and evidence suggests that it is an autoimmunity-induced brain disorder characterized by profound metabolic alterations and progressive neuronal loss. While there are a number of murine models of SLE, this article reviews recent literature on the immunological connections to neurodegeneration and behavioral dysfunction in the Fas-deficient MRL model of NP-SLE. Probable links between spontaneous peripheral immune activation, the subsequent central autoimmune/inflammatory responses in MRL/MpJ-Tnfrsf6 lpr (MRL-lpr) mice and the sequential mode of events leading to Fas-independent neurodegenerative autoimmune-induced encephalitis will be reviewed. The role of hormones, alternative mechanisms of cell death, the impact of central dopaminergic degeneration on behavior, and germinal layer lesions on developmental/regenerative capacity of MRL-lpr brains will also be explored. This model can provide direction for future therapeutic interventions in patients with this complex neuroimmunological syndrome.

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Section: Prelude To Cns Damage: Disruption Of the Blood-brain Barriermentioning

confidence: 99%

Neuroimmunopathology in a murine model of neuropsychiatric lupus

Ballok

2007

Brain Research Reviews

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“…We have also previously reported significant associations between both NA (14) and LCA (6) positivity and an overall designation of cognitive impairment, as well as an association between LCA positivity and specific visuospatial cognitive problems Precipitation of 50-52-KD bands by sera from 3 patients with neuropsychiatric systemic lupus erythematosus, studied using lysates from a CD4+ T cell line. All of these sera had lymphocytotoxic antibody activity, and none had neuronal antibody activity by mixed hemadsorption assay (13) or anti-Ro antibodies by enzymelinked immunosorbent assay.…”

mentioning

confidence: 99%

Lymphocyte Antigens in Neuropsychiatric Systemic Lupus Erythematosus

Denburg

Behmann

Carbotte

et al. 1994

Arthritis & Rheumatism

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Objective. To examine the relationships among specific lymphocyte antigenic reactivities of lupus sera and central nervous system complications of systemic lupus erythematosus (SLE), lymphocytotoxic antibody (LCA) positivity, and specific cognitive impairment.Methods. Sera from 115 patients with SLE were examined for the presence of IgM-and IgG-class autoantibodies binding to surface target antigens on lymphocytes, by immunoblotting and microdroplet lymphocytotoxicity studies. Seventy-three of these patients also underwent detailed neuropsychological testing within the same time period.Results. Significant associations were found between reactivities to several lymphocyte antigenic moieties and neuropsychiatric SLE (NPSLE) or cognitive impairment. Specifically, immunoblot reactivities to 31-32-kd, 50-52-kd, 54-56-kd, and 97-98-kd targets were associated with clinical NPSLE; there was a significant association between reactivity to the 50-52-kd moiety in particular and cognitive impairment. There were also associations between LCA and immunoblot reactivity. Furthermore, the previously reported association be-

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“…56 Recently, several potential lymphocyte/brain antigens have been studied by immunoprecipitation techniques.32'57-6' Many SLE patients have significant elevations of autoantibodies which bind to neuroblastoma cells,61'62 which are lymphocytotoxic in vitro.32'33'51'59 The nature of the surface antigens against which IgG class antibodies are directed in sera and in cerebrospinal fluid of SLE patients has also been explored.62'63 These include a 97 kD protein uniquely present on the surface of neuroblastoma cell linesW,6' and several determinants on the surface of peripheral blood lymphocytes or on CD4-positive lymphocytic cell lines 32,60,64 The most recent autoantibody candidates invoked in the causation of NP-SLE are the antibodies directed to anti-ribosomal P, mostly seen in association with psychosis and depression.65 67One patient with recurrent psychotic episodes studied recently was, however, negative for these antibodies in a prospective study.67 However, a second more recent case study tended to confirm the original observations.68 Since abnormalities of both cytokine and antibody production occur with lupus, future studies of the mechanisms of brain dysfunction should include both a study of cytokines as well as antibodies in the sera and cerebrospinal fluid of lupus patients.…”

Section: Pathologymentioning

confidence: 99%