Human Lupus Inclusions and Interferon

Rich, Steven A.

doi:10.1126/science.6166984

Cited by 151 publications

(45 citation statements)

References 27 publications

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“…In two of the ten cases, the endothelial cells and occasional epithelial cells showed abundant tubulo-reticular 'viral-like' inclusions of the type described in patients treated with interferon, HIV-associated nephropathy or lupus nephritis (23,24) (Figure 11). Virions, however, were not seen in endothelial cells in any instance.…”

Section: Vascular and Interstitial Changesmentioning

confidence: 90%

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

Drachenberg¹,

Papadimitriou²,

Wali³

et al. 2003

American Journal of Transplantation

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BK virions must enter the host cell and target their genome to the nucleus in order to complete their life cycle. The mechanisms by which the virions accomplish these tasks are not known. In this morphological study we found that BK virions localized beneath the host cell cytoplasmic membrane in 60-70-nm, smooth (non-coated) monopinocytotic vesicles similar to, or consistent with, caveolae. In the cytoplasm, the monopinocytotic vesicles carrying virions appeared to fuse with a system of smooth, vesicles and tubules that communicated with the rough endoplasmic reticulum and was continuous with the Golgi system. Membrane-bound single virions and large tubuloreticular complexes loaded with virions accumulated in paranuclear locations. Occasional nuclei displayed virions within the perinuclear cisterna in association to the perinuclear viral accumulations. Tubular cells with mature productive infection had large nuclei, distended by daughter virions, whereas they lacked significant numbers of cytoplasmic virions. In addition to virally induced cell necrosis, there was extensive tubular cell damage (apoptosis and necrosis) in morphologically non-infected tubules. The observed ultrastructural interactions between the BK virions and host cells are remarkably similar to viral cell entry and nuclear targeting described for SV40 virus.

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Section: Vascular and Interstitial Changesmentioning

confidence: 90%

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

Drachenberg¹,

Papadimitriou²,

Wali³

et al. 2003

American Journal of Transplantation

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“…TIs were described in patients with SLE and were called lupus inclusions 40 before their recognition in patients with DM. 41 TIs correlate with increased serum interferon-␣ levels in patients with SLE and other disorders, 42,43 and they are associated with interferon-␣ treatment. 44 TIs develop in vascular endothelial cells exposed to interferon-␣ in vitro.…”

Section: Fig 5 Plasmacytoid Dendritic Cells (Pdcs) In Dermatomyositimentioning

confidence: 93%

Interferon‐α/β–mediated innate immune mechanisms in dermatomyositis

Greenberg

Pinkus

et al. 2005

Annals of Neurology

527

480

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Dermatomyositis has been modeled as an autoimmune disease largely mediated by the adaptive immune system, including a local humorally mediated response with B and T helper cell muscle infiltration, antibody and complement-mediated injury of capillaries, and perifascicular atrophy of muscle fibers caused by ischemia. To further understand the pathophysiology of dermatomyositis, we used microarrays, computational methods, immunohistochemistry and electron microscopy to study muscle specimens from 67 patients, 54 with inflammatory myopathies, 14 with dermatomyositis. In dermatomyositis, genes induced by interferon-alpha/beta were highly overexpressed, and immunohistochemistry for the interferon-alpha/beta inducible protein MxA showed dense staining of perifascicular, and, sometimes all myofibers in 8/14 patients and on capillaries in 13/14 patients. Of 36 patients with other inflammatory myopathies, 1 patient had faint MxA staining of myofibers and 3 of capillaries. Plasmacytoid dendritic cells, potent CD4+ cellular sources of interferon-alpha, are present in substantial numbers in dermatomyositis and may account for most of the cells previously identified as T helper cells. In addition to an adaptive immune response, an innate immune response characterized by plasmacytoid dendritic cell infiltration and interferon-alpha/beta inducible gene and protein expression may be an important part of the pathogenesis of dermatomyositis, as it appears to be in systemic lupus erythematosus.

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“…Assuming a mean cell diameter of 16 pm, LI frequencies of 0.75% (6). Electron micrographs of sections from the interferon-treated samples confirmed the size estimate of the LI.…”

Section: Resultsmentioning

confidence: 57%

Human lupus‐type inclusions in umbilical cord blood mononuclear cells

Rich

Gibbons

1990

Arthritis & Rheumatism

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Mononuclear cells purified from umbilical cord blood activated oligoadenylate synthetase and formed human lupus-type inclusions (LI) when cultured with the purified recombinant human leukocyte interferon, IFLrA. LI frequencies increased from 0% to a low of 0.75% and a high of 6.25% in 4-day cultures with IFLrA (100 units/ml). These interferon-induced responses in the mononuclear cells of neonates indicate that LI are solely an intrinsic product of normal cells, and not an exogenous virus or some other environmental agent.

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Human Lupus Inclusions and Interferon

Cited by 151 publications

References 27 publications

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

Interferon‐α/β–mediated innate immune mechanisms in dermatomyositis

Human lupus‐type inclusions in umbilical cord blood mononuclear cells

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