Clearance of human antibody/DNA immune complexes and free DNA from the circulation of the nonhuman primate

Cosio, Fernando G.; Hebert, Lee A.; Birmingham, Daniel J.; Dorval, Brent L.; Bakaletz, Alan P.; Kujala, Gregory A.; Edberg, Jeffrey C.; Taylor, Ronald P.

doi:10.1016/0090-1229(87)90167-x

Cited by 34 publications

(30 citation statements)

References 14 publications

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“…Both inherited [3,7] and acquired [1,4,6] factors have been reported to contribute to the deficiency of E-CRl in SLE patients. This deficiency is related to disease activity [4,11] and one of its functional consequences may be impaired clearance of immune complexes (IC) from the circulation [12][13][14][15]. It has also been reported that expression of CRl on blood leucocytes and of CR2 on B cells are reduced in patients with SLE [16].…”

Section: Introductionmentioning

confidence: 99%

Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE)

Marquart

Svendsen

Rasmussen

et al. 1995

Clinical and Experimental Immunology

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SUMMARYIt has previously been reported that the expression of the complement receptors, CRl on erythrocytes and blood leucocytes and CR2 on B cells, is reduced in patients with SLE, and that the reduced expression of CRl on erythrocytes is related to disease activity. We have earlier demonstrated that normal B cells are capable of activating the alternative pathway (AP) of complement in a CR2-dependent fashion. In this study we have investigated whether disturbances in this activity may be related to the altered phenotype of SLE B cells. Flow cytometry was used to measure expression of complement receptors and regulatory proteins on B cells from SLE patients, as well as the deposition of C3 fragments occurring in vivo or after in vitro AP activation. We have confirmed, for a proportion of the patients studied, reduced expression of CRl and CR2 on B cells, and shown a consistency between low CR2 expression and reduced in vitro AP activation in the presence of homologous, normal serum. In addition, the B cells, like erythrocytes, bear raised levels of in v/vo-deposited C3dg, but not C3b fragments, compared with normal B cells. The erythrocytes from SLE patients were unable to inhibit in vitro AP activation by B cells in homologous serum. Finally, we demonstrated an inverse relationship between SLE disease activity index (SLEDAI) and the expression of complement receptor 2 (CR2) on SLE B cells. Thus, determination of CR2 on B cells may emerge as an additional laboratory tool in the assessment of SLE activity.

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Section: Introductionmentioning

confidence: 99%

Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE)

Marquart

Svendsen

Rasmussen

et al. 1995

Clinical and Experimental Immunology

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“…Circulating IC are removed by binding to receptors for the Fc portion of IgG and receptors for C3 fragments on the fixed tissue mononuclear phagocytes ofthis system (5,(8)(9)(10)(11)(12). Recent work by Hebert (13)(14)(15)(16) and others (17)(18)(19)(20), however, has emphasized the importance of complement (C) receptor type 1 (CRl)-mediated binding of circulating C-fixing IC to human and nonhuman primate erythrocytes (E). These observations suggest that E can act as a "buffer," which can bind C-fixing IC by way of CR1 and may decrease the probability of deposition of these IC in target tissues (21,22).…”

Section: Introductionmentioning

confidence: 99%

In vivo handling of soluble complement fixing Ab/dsDNA immune complexes in chimpanzees.

Kimberly

Edberg²,

Merriam³

et al. 1989

J. Clin. Invest.

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We used soluble, C-fixing antibody/dsDNA IC to investigate immune complex (IC) handling and erythrocyte (E)-to-phagocyte transfer in chimpanzees. IC bound efficiently to chimpanzee E in vitro and showed minimal release with further in vitro incubation in the presence of serum in EDTA (c 15% within 1 h). These IC also bound rapidly to E in vivo (70-80% binding within 1 min) and did not show detectable release from E in the peripheral circulation after infusion in vivo (< 2% within 1 h). Despite such slow C-mediated release of IC from E, IC were rapidly stripped from E by the mononuclear phagocyte system (T50 for E-IC1500 = 5 min) without sequestration of E.

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“…At the end of the experiment, cells were washed with acetate buffer (pH, 2.5) according to the method of Menozzi et al 11 Results are expressed as mean ± s.e.m., n = 3. highly extracted across the liver which has been shown previously to remove DNA from the circulation via the scavenger receptor system. 12 Incubation of complex with plasma in vitro for up to 60 min showed no evidence of degradation suggesting that plasma DNases were not a major cause of complex degradation in vivo (data not shown). However, when polyinosinic acid, an inhibitor of the hepatic scavenger receptor system, 13 was coadministered with the complex, clearance decreased to 1.2 ml/min and the half-life increased to 10 min.…”

Section: Resultsmentioning

confidence: 99%

Targeting of a cholecystokinin–DNA complex to pancreatic cells in vitro and in vivo

Carpenter

Minchin

1998

Gene Ther

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The carboxy terminal octapeptide of cholecystokinin by 100 nM CCK 8 . The complex appeared to be (CCK 8 ) is a hormone that binds high affinity receptors in a internalised since it could not be removed by acid wash. number of tissues including pancreas and pancreatic When administered intra-arterially, the complex was raptumours. As part of our studies to develop effective gene idly removed from the circulation with no evidence of tartherapy for the treatment of pancreatic cancers, we have geted delivery to the pancreas. However, following a sininvestigated various gene delivery systems that depend on gle intraperitoneal dose, the pancreas accumulated 5-CCK 8 receptor targeting. In this paper, we describe the 8% of the total administered complex by 24 h. These synthesis of a CCK 8 -DNA complex designed to deliver results suggest that peptide-dependent gene delivery to foreign DNA to cholecystokinin receptor-positive cells.CCK receptor positive cells in vivo is feasible but, when CCK 8 was ligated to avidin and then complexed to linadministered directly into the circulation, diffusional barearised biotinylated DNA (pSV-CAT). The uptake of 32 Priers across the endothelium may limit distribution to perlabelled CCK 8 -DNA complex by rat pancreatic acini was ipheral tissues. Intraperitoneal administration therefore linear with time over 4 h with 65-70% of uptake inhibited may be a useful alternative for targeting the pancreas.

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Clearance of human antibody/DNA immune complexes and free DNA from the circulation of the nonhuman primate

Cited by 34 publications

References 14 publications

Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE)

Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE)

In vivo handling of soluble complement fixing Ab/dsDNA immune complexes in chimpanzees.

Targeting of a cholecystokinin–DNA complex to pancreatic cells in vitro and in vivo

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