Antibodies Against Neurons in a Patient With Systemic Lupus Erythematosus, Cerebral Palsy, and Epilepsy

Diederichsen, Hans; Pyndt, Ingeborg Cosmus

doi:10.1093/brain/93.2.407

Cited by 32 publications

(10 citation statements)

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“…Increased intrathecal synthesis (as revealed by an elevated IgG index and oligoclonal banding) in patients with CNS dysfunction (McLean et al, 1995;Hirohata et al, 1985;Winfield et al, 1983) and antigen-specific autoantibodies in the CSF (Yoshio et al, 2005) are associated with NP manifestations (Greenwood et al, 2002). For example, evidence suggests that neuronal antibodies are involved in the pathogenesis of psychiatric disease (Quismorio and Friou, 1972;Vincent et al, 2003;Diederichsen and Pyndt, 1970;Bluestein and Zvaifler, 1983), and parenchymal lesions associated with movement disorder have recently been documented in these patients (Rocca et al, 2006), supporting the link between autoimmunity, neuronal death, and neurologic manifestations. In many cases however, the correlational nature of clinical data has lead to the necessity for animal models.…”

Section: Introductionmentioning

confidence: 93%

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: Introductionmentioning

confidence: 93%

Neuroimmunopathology in a murine model of neuropsychiatric lupus

Ballok

2007

Brain Research Reviews

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“…[15] were unable to detect antibody in 18 patients. Recently, Diederichsen and Cosmos Pyndt [3] reported a patient with cerebral atrophy and epilepsy dating from birth who developed lupus-like syndrome at 7 years of age presumably associated with anti-convulsant medications, wherein antibodies specific for neurons were detected. In this patient, however, the neurological complaints were not due to SLE.…”

Section: Discussionmentioning

confidence: 99%

“…The re cent report of circulating antibodies reactive with neurons in a patient with cerebral palsy and epilepsy at birth who developed lupus-like syn drome presumably induced with anticonvulsants [3] have prompted us to investigate more fully the clinical significance of such antibodies.…”

Section: Introductionmentioning

confidence: 99%

Antibodies Reactive with Neurons in SLE Patients with Neuropsychiatric Manifestations

Quismorio

Friou²

1972

Int Arch Allergy Immunol

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Antibodies reactive with the cytoplasm of neurons were found in 41% of SLE patients with active neurologic disease (group I). In contrast, these antibodies were found in 24% of lupus patients with past history of neurologic disease (group II), in 9% in those without a history of neurologic involvement (group III) and 0.9% in non-SLE controls, Although reactive with neurons, these antibodies were non-organ specific since they reacted with cells of non-nervous origin. The incidence and titer of antibodies to DNA and DNA-protein were however the same in the three groups of SLE patients suggesting that the high incidence of anti-cytoplasmic antibodies in group I may be specifically related to neuropsychiatric involvement rather than an expression of increased serologic reactivity of acutely ill lupus patients.

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“…The criteria of diagnosis have been established previously [7], The pa tients were from 8 to 73 years of age (average age 32 years). Eleven patients, all females, had thyroid diseases with complement-fixing (CF) thyroid antibodies.…”

Section: Patientsmentioning

confidence: 99%

Anti-DNA Investigated by the DNA Bentonite Flocculation Technique

Diederichsen¹,

Nielsen²

1975

Int Arch Allergy Immunol

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The DNA bentonite flocculation test was used to investigate the presence of antibody to DNA. In most sera a prozone-like phenomenon was found, caused by a non-specific inhibition of serum. Anti-DNA was found with extreme frequency in patients with SLE, chronic liver disease, acute hepatitis, infectious mononucleosis, and blood donors over the age of 60, but was found rarely or not at all in patients with some other diseases or blood donors under 60 years of age.

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Antibodies Against Neurons in a Patient With Systemic Lupus Erythematosus, Cerebral Palsy, and Epilepsy

Cited by 32 publications

References 0 publications

Neuroimmunopathology in a murine model of neuropsychiatric lupus

Neuroimmunopathology in a murine model of neuropsychiatric lupus

Antibodies Reactive with Neurons in SLE Patients with Neuropsychiatric Manifestations

Anti-DNA Investigated by the DNA Bentonite Flocculation Technique

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