Cerebrospinal fluid and the choroid plexus during acute immune complex disease

Harbeck, Ronald J.; Hoffman, Andree A.; Hoffman, Steven A.; Shucard, David W.

doi:10.1016/0090-1229(79)90083-7

Cited by 51 publications

(13 citation statements)

References 28 publications

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“…These data suggest that this material represents in vivo formed IC A localization ofIC in the CNS has been suggested by the demonstration of electron-dense deposits in the basement membrane ofchoroid plexus in patients with systemic lupus erythematosus and in NZBxNZW mice (17). In addition, deposits of IgG, bovine serum albumin, and C3 were shown in the choroid plexus of rabbits undergoing an acute IC disease (18). The latter model was associated with a slight alteration in the blood CSF barrier permeability, but IC were usually not detectable in the CSF.…”

Section: Resultsmentioning

confidence: 87%

Immune Complexes in Serum and in Cerebrospinal Fluid in African Trypanosomiasis

Lambert¹,

Berney²,

Kazyumba³

1981

J. Clin. Invest.

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A B S T R A C T The possible occurrence of immune complexes (IC) in serum and in cerebrospinal fluid (CSF) has been studied in 36 patients with African trypanosomiasis (Trypanosoma brucei gambiense). In serum, very high levels of IC were detectable by the '25I-Clq-binding and by the conglutinin-binding assays with positive results in 94 and 87%, respectively, of untreated patients. Circulating IC were found in both early and late stages of the disease, without significant quantitative differences; their size was 15-25S. There was a significant negative correlation between C3 values and ClqBA. Our studies suggest that circulating IC occurring during trypanosomiasis may be the expression of a polyclonal B cell activation. Indeed, there was a significant correlation (P < 0.001) between the levels of circulating IC and either the levels of IgM (mean value 12.5±+7.2 mg/ml) or with the levels of rheumatoid factor-like antiimmunoglobulin antibodies that were detected by solid phase radioimmunoassay in 74% of the patients.IC were detected in 31 of 35 CSF samples, with a marked elevation in patients with definite involvement of the central nervous system as compared with earlier stages of sleeping sickness. The occurrence of IC in CSF was not related to an impairment of the blood-brain barrier as shown by analysis of CSF/serum albumin ratios.

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Section: Resultsmentioning

confidence: 87%

Immune Complexes in Serum and in Cerebrospinal Fluid in African Trypanosomiasis

Lambert¹,

Berney²,

Kazyumba³

1981

J. Clin. Invest.

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“…Choroid plexus is also a site of 746 ROJKO ET AL. TOXICOLOGIC PATHOLOGY predilection for vascular/perivascular IC deposition in human SLE patients, newborn Finnish-Landrace lambs with mesangiocapillary GN (interstitial IgG, IgM granular deposits), and New Zealand mice, and BSA-injected rabbits with acute ICD/serum sickness (Gardiner 1976;Harbeck et al 1979). FcgR for IgG- coated sheep erythrocytes have been described in human, rabbit, and monkey choroid plexus (Braathen et al 1979;Peress, Roxburgh, and Gelfand 1981).…”

Section: Localized Drug-ada Ic Formation and Localized Deposition In mentioning

confidence: 99%

Formation, Clearance, Deposition, Pathogenicity, and Identification of Biopharmaceutical-related Immune Complexes

et al. 2014

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Vascular inflammation, infusion reactions, glomerulopathies, and other potentially adverse effects may be observed in laboratory animals, including monkeys, on toxicity studies of therapeutic monoclonal antibodies and recombinant human protein drugs. Histopathologic and immunohistochemical (IHC) evaluation suggests these effects may be mediated by deposition of immune complexes (ICs) containing the drug, endogenous immunoglobulin, and/or complement components in the affected tissues. ICs may be observed in glomerulus, blood vessels, synovium, lung, liver, skin, eye, choroid plexus, or other tissues or bound to neutrophils, monocytes/macrophages, or platelets. IC deposition may activate complement, kinin, and/or coagulation/fibrinolytic pathways and result in a systemic proinflammatory response. IC clearance is biphasic in humans and monkeys (first from plasma to liver and/or spleen, second from liver or spleen). IC deposition/clearance is affected by IC composition, immunomodulation, and/or complement activation. Case studies are presented from toxicity study monkeys or rats and indicate IHC-IC deposition patterns similar to those predicted by experimental studies of IC-mediated reactions to heterologous protein administration to monkeys and other species. The IHC-staining patterns are consistent with findings associated with generalized and localized IC-associated pathology in humans. However, manifestations of immunogenicity in preclinical species are generally not considered predictive to humans.

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“…Albumin and IgG concentrations and their ratios to each other in CSF and serum were determined to detect perturbations in the blood-brain barrier (Harbeck et al, 1979;Tourtellotte, 1971). The samples assayed were those tested for antibodies to SRV-1 by ELISA.…”

Section: Albumin and Igg Levels In Csf And Serummentioning

confidence: 99%

Asymptomatic Infection of the Central Nervous System by the Macaque Immunosuppressive Type D Retrovirus, SRV-1

Lackner¹,

Marx

Lerche

et al. 1989

Journal of General Virology

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SUMMARYThe aetiological agent of spontaneously occurring simian acquired immune deficiency syndrome (SAIDS) in rhesus monkeys (Macaca mulatta) at the California Primate Research Center is a type D retrovirus designated SAIDS retrovirus serotype 1 (SRV-1). SRV-1 DNA and RNA have previously been detected in the brains of rhesus monkeys with SAIDS in the absence of viral antigen or neuropathological lesions. In this study we further define the relationship between SRV-1 and the central nervous system (CNS) in rhesus monkeys by examining the CNS for infectious SRV-1, viral antigen and anti-SRV-1 antibodies. In addition, cerebrospinal fluid (CSF) was assayed for alterations in IgG and albumin levels, IgG/albumin ratios and cell count in comparison to uninfected control animals. No differences in CSF parameters were detected between infected and uninfected animals except for the presence of infectious SRV-1 which was isolated from the CSF from 13 out of 19 (68%) viraemic rhesus monkeys. The probable source of this virus was the choroid plexus, where approximately 1 in 1000 surface epithelial cells were found to contain viral antigen by immunohistochemistry. Antibodies against SRV-1 were not detected in the CSF even when present in the serum. Neither infectious virus nor viral antigen were found in the brain parenchyma of any animal examined. Thus infection of the CNS by SRV-1 appears to be subclinical without an intrathecal immune response. This may be related to the apparent restriction of productive infection in the CNS to cells of the choroid plexus.

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Cerebrospinal fluid and the choroid plexus during acute immune complex disease

Cited by 51 publications

References 28 publications

Immune Complexes in Serum and in Cerebrospinal Fluid in African Trypanosomiasis

Immune Complexes in Serum and in Cerebrospinal Fluid in African Trypanosomiasis

Formation, Clearance, Deposition, Pathogenicity, and Identification of Biopharmaceutical-related Immune Complexes

Asymptomatic Infection of the Central Nervous System by the Macaque Immunosuppressive Type D Retrovirus, SRV-1

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