Human lupus‐type inclusions in umbilical cord blood mononuclear cells

Rich, Steven A.; Gibbons, William E.

doi:10.1002/art.1780330915

Cited by 7 publications

(4 citation statements)

References 28 publications

(15 reference statements)

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“…The unusual acid-labile IFN-␣ in sera from individuals with SLE and AIDS has an extraordinary ability to induce LI (24,30). LI are known to be products of normal cells abnormally stimulated with IFN-␣ because peripheral blood mononuclear cells from healthy adult Red Cross blood donors (31) and umbilical-cord bloods from routine births (32) form LI when cultured with IFN-␣.…”

Section: Interferons (Ifns)mentioning

confidence: 99%

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Purification, Microsequencing, and Immunolocalization of p36, a New Interferon-α-induced Protein That Is Associated with Human Lupus Inclusions

Rich

Bose

Tempst

et al. 1996

Journal of Biological Chemistry

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The trace interferon-␣-induced protein, p36, was induced in Raji cells in association with lupus inclusions. It was solubilized in a nonionic detergent buffer, enriched by differential centrifugation and by preparative isoelectric focusing, and purified to homogeneity on two-dimensional protein gels. Failure to obtain N-terminal amino acid sequence, however, suggested a blocked ␣-amino group. Sequences of six tryptic peptides, 13-19 amino acids in length, were obtained after digestion, microbore-high performance liquid chromotography purification, and chemical sequence analysis. None of the six sequences, which represented approximately 25% of the entire protein, shared any meaningful homologies with entries in protein sequence repositories. Rajicell p36 was shown in Western blots with antipeptide antibodies to be induced at least 400-fold and by immunofluorescence microscopy to co-localize with the endoplasmic reticulum resident protein, protein disulfide isomerase. These results show that p36 is a new interferon-␣-induced protein that localizes in the endoplasmic reticulum, the cell region in which the lupus inclusions form, and that p36 is probably physically associated with the lupus inclusions.

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Section: Interferons (Ifns)mentioning

confidence: 99%

“…2b). The SDS-buffer system had to be modified for use with Rotofor fractionation to enrich p36 (32) (Fig. 2c) prior to purification to homogeneity.…”

Section: P36 a New Ifn-␣-induced Protein Associated With LImentioning

confidence: 99%

Purification, Microsequencing, and Immunolocalization of p36, a New Interferon-α-induced Protein That Is Associated with Human Lupus Inclusions

Rich

Bose

Tempst

et al. 1996

Journal of Biological Chemistry

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“…These inclusions are induced both in vitro and in vivo by type I (a and /; 1) but not type 1 (y) IFN (4). The inclusions are known to be products of normal cells abnormally stimulated with a-IFN as shown by their induction in peripheral blood mononuclear cells prepared from adult Red Cross blood donors (4), and from umbilical cord bloods from routine deliveries (5).…”

Section: Introductionmentioning

confidence: 97%

“…Cell pellets washed in PBS were overlaid with 500 Ml of Triton X-100 lysis buffer (0.5% wt/vol Triton X-100, 20 mM Hepes, 120 mM KC1, 5 mM magnesium acetate, 7 mM,6-mercaptoethanol, 10% wt/vol glycerol) and vortexed (5,21).…”

Section: Introductionmentioning

confidence: 99%

De novo synthesis and secretion of a 36-kD protein by cells that form lupus inclusions in response to alpha-interferon.

Rich¹

1995

J. Clin. Invest.

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In response to the pure recombinant human a-IFN, IFLrA, Raji and Daudi were the only two cell lines among 19 human lymphoblastoid cell lines tested that formed the human lupus inclusions (LI) to a high frequency. Raji, Daudi, and five other cell lines were examined for protein changes that might accompany LI formation. Their selection was based upon T or B origin, association with Epstein-Barr virus, and ability to form LI. A trace protein of an estimated molecular mass of 36 kD (p36) and an isoelectric point of 5.6 was detected on two-dimensional gels only of a-IFN-treated Raji and Daudi cells. Gamma-IFN did not induce p36 or LI in any of these seven cell lines. In Daudi cells p36 and LI formed simultaneously in response to IFLrA, and persisted until the a-IFN-induced death of the culture. In Raji cells, p36 and LI appearance and disappearance coincided with the addition and removal of a-IFN. Fractionation of Raji cells with nonionic-detergent buffer placed p36 with the inclusions in the cytoplasmic supernatant. With detergentfree buffer p36 and LI were distributed evenly between the nuclear and cytoplasmic fractions. Pulse-chase experiments revealed that p36 was secreted. The de novo synthesis of p36 with a-IFN treatment was shown by labeling the cell proteins with [35S] methionine before and after the addition of a-IFN. These results along with previous results on the de novo synthesis of LI in the endoplasmic reticulum (which is involved in the processing and secretion of proteins) suggest a role for LI in the synthesis and secretion of p36. (J. Clin. Invest. 1995 95:219-226.)

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Systemic lupus erythematosus: RNA-protein autoantigens, models of disease heterogeneity, and theories of etiology

Harley

Scofield

1991

J Clin Immunol

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Human lupus‐type inclusions in umbilical cord blood mononuclear cells

Cited by 7 publications

References 28 publications

Purification, Microsequencing, and Immunolocalization of p36, a New Interferon-α-induced Protein That Is Associated with Human Lupus Inclusions

Purification, Microsequencing, and Immunolocalization of p36, a New Interferon-α-induced Protein That Is Associated with Human Lupus Inclusions

De novo synthesis and secretion of a 36-kD protein by cells that form lupus inclusions in response to alpha-interferon.

Systemic lupus erythematosus: RNA-protein autoantigens, models of disease heterogeneity, and theories of etiology

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