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Related Experiment Videos

Systemic lupus erythematosus.

J M Jones, A J Martinez, V V Joshi

    Archives of Pathology
    |March 1, 1975
    PubMed
    Summary
    This summary is machine-generated.

    Systemic lupus erythematosus (SLE) may involve paramyxovirus-like structures and defective immunity. A child with SLE showed these findings, along with herpes simplex virus particles and thymic dysplasia, suggesting potential viral links in autoimmune disease.

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    Area of Science:

    • Immunology
    • Virology
    • Pathology

    Background:

    • Systemic lupus erythematosus (SLE) investigations reveal paramyxovirus-like nucleocapsids in renal endothelial cells.
    • SLE is associated with increasing evidence of defective cell-mediated immunity.
    • Previous studies have faced challenges in definitively identifying these structures as viruses.

    Purpose of the Study:

    • To investigate the presence of viral-like structures and immune defects in a pediatric case of SLE.
    • To correlate clinical findings of immune deficiency with postmortem pathological observations.

    Main Methods:

    • Clinical evaluation of a 3-year-old child with SLE and evidence of defective cellular immunity.
    • Postmortem examination of renal, neural, and thymic tissues.

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  • Morphological analysis of intracytoplasmic structures and cellular components.

    • Main Results:

    • Paramyxovirus-like tubular structures were identified in the kidneys of the SLE patient.
    • Intracytoplasmic viral particles resembling herpes simplex virus were found in neurons.
    • The patient's thymus gland showed lymphocyte depletion and absence of Hassall corpuscles, indicative of thymic dysplasia.

    Conclusions:

    • The findings suggest a potential association between viral-like particles, thymic dysplasia, and immune deficiency in SLE.
    • Further research is warranted to explore the role of viruses in the pathogenesis of SLE.
    • The observed 'nuclear bodies' may also be significant in the context of SLE pathology.