Ole Petter Rekvig

UiT The Arctic University of Norway

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Ugo Moens

UiT The Arctic University of Norway

Natalya Seredkina

UiT The Arctic University of Norway

Elin Mortensen

University Hospital of North Norway

Kristin Andreassen Fenton

UiT The Arctic University of Norway

Signy Bendiksen

University Hospital of North Norway

Kristian Hannestad

University of Oslo

Johannes C. Nossent

University of Western Australia

Dhivya Thiyagarajan

UiT The Arctic University of Norway

Silje Fismen

University Hospital of North Norway

Knut Fredriksen

University Hospital of North Norway

Cooperative Institutions

UiT The Arctic University of Norway

University Hospital of North Norway

Oslo University Hospital

University of Oslo

Center for Rheumatology

Heidelberg University

Harvard University

National Institutes of Health

National Institute for Occupational Safety and Health

Centers for Disease Control and Prevention

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A longitudinal study of human cytomegalovirus serology and viruria fails to detect active viral infection in 20 systemic lupus erythematosus patients

Lupus (2000)

Signy Bendiksen Marijke Van Ghelue Ole Petter Rekvig Tore Jarl Gutteberg Hans‐Jacob Haga

In this study, we investigated whether active human cytomegalovirus infection could be detected in 20 systemic lupus erythematosus (SLE) patients over a one-year observation period by polymerase chain reaction on serial urine specimens and by monitoring of IgG and IgM HCMV-specific antibody profiles in serial serum samples. Of 788 urine samples analysed for the presence of human cytomegalovirus DNA, only 2 specimens (0.25%) collected from two different patients contained genuine human cytomegalovirus sequences as determined by polymerase chain reaction and subsequent sequencing of the PCR products. These two patients had one positive sample out of 36 samples or 40 samples, respectively. Nineteen of the patients (95%) possessed IgG antibodies against human cytomegalovirus, while 9 (45%) produced IgM antibodies. However, none of the patients showed signs of an active virus infection as judged by the stable anti-HCMV IgG or IgM antibody levels during the observation period, nor was any correlation between disease activity and HCMV serology/viruria observed. Of single serum samples of 26 age- and sex-matched blood donors, 21 (81%) were HCMV IgG positive and 1 (3.8%) was IgM seropositive. In conclusion, our data fail to establish an active human cytomegalovirus infection in SLE patients.

Cytomegalovirus

Immunoglobulin M

Betaherpesvirinae

10.1191/096120300678828118

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Citations (33)

T cell lines specific for polyomavirus T-antigen recognize T-antigen complexed with nucleosomes: a molecular basis for anti-DNA antibody production

European Journal of Immunology (1999)

Karin Andreassen Geir Bredholt Ugo Moens Signy Bendiksen Goran Kaurić

We have previously demonstrated that in vivo expression of the polyomavirus DNA-binding T-antigen initiated production of IgG antibodies to T-antigen and to DNA, but not to a panel of autoantigens not related to nucleosomes, indicating an antigen-selective T cell-dependent B cell response. In this study, we demonstrate that CD4-positive T cells from both normal and systemic lupus erythematosus (SLE) patients readily proliferate in response to pure T-antigen, and also to T-antigen in complex with nucleosomes. T-antigen-specific T cell lines from both normal individuals and SLE patients proliferate in response to nucleosome-T-antigen complexes, but not to nucleosomes or histones. B cells co-cultured with T-antigen-specific T cells and stimulated with nucleosome-T-antigen complexes produce anti-T-antigen and anti-DNA antibodies, indicating that such CD4-positive T cells have the potential to interact with B cells specific for individual components of nucleosome-T-antigen complexes. Thus, a non-self DNA-binding protein like polyomavirus T-antigen may initiate and maintain an antibody response to DNA when T-antigen is actively expressed.

Pan-T antigens

10.1002/(sici)1521-4141(199909)29:09<2715::aid-immu2715>3.0.co;2-

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Citations (42)

Systemic Lupus Erythematosus: Definitions, Contexts, Conflicts, Enigmas

Frontiers in Immunology (2018)

Ole Petter Rekvig

SLE is an inadequately defined syndrome. Etiology and pathogenesis remain largely unknown. SLE is on the other hand a seminal syndrome that has challenged immunologists, biologists, genetics and clinicians to solve its nature. The syndrome is characterized by multiple, etiologically unlinked manifestations. Unexpectedly they seem to occur in different stochastically linked clusters, although single gene defects may promote a smaller spectrum of symptoms/criteria typical for SLE. There is no known inner coherence of parameters (criteria) making up the disease. These parameters are, nevertheless, implemented in The American College of Rheumatology (ACR) and The Systemic Lupus Collaborating Clinics (SLICC) criteria to classify SLE. Still, SLE is an abstraction since the ACR or SLICC criteria allow us to define hundreds of different clinical SLE phenotypes. This is a major point of the present discussion and uses "The anti-dsDNA antibody" as an example related to the problematic search for biomarkers for SLE. The following discussion will show how problematic this is: The disease is defined through non-coherent classification criteria, its complexity is recognized and accepted, its pathogenesis is plural and poorly understood. Therapy is focused on dominant symptoms or organ manifestations, and not on the syndrome itself. From basic scientific evidences, we can add substantial amount of data that are not sufficiently considered in clinical medicine, which may change the paradigms linked to what "The Anti-DNA antibody" is - and is not - in context of the imperfectly defined syndrome SLE.

Etiology

Causation

10.3389/fimmu.2018.00387

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Citations (42)

Lupus Nephritis

American Journal Of Pathology (2008)

Elin Mortensen Kristin Andreassen Fenton Ole Petter Rekvig

Nephritis

10.2353/ajpath.2008.070563

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Citations (95)

Fibronectin, complement and immunoglobulins in serum after surgery

British journal of surgery (1985)

T Gauperaa Giercksky Ke Arthur Revhaug Ole Petter Rekvig

Abstract In recent years it has been suggested that fibronectin is a non-specific opsonic protein of significance in host resistance against septic complications following trauma and surgery. The aim of the present study was to investigate the fluctuations in serum levels of fibronectin, immunoglobulins IgG and IgM, and complement factors C3 and C4 postoperatively. Serum samples were obtained pre-operatively and at different intervals postoperatively in 72 patients admitted for elective surgical procedures on the alimentary tract, the heart and the hip joint. The mean pre-operative fibronectin values were 257±79 μg/ml. The lowest values (166±65 μg/ml) were found immediately after the operation, followed by an increase which did not reach pre-operative levels within 120 h. Five patients who developed postoperative complications and 14 patients with malignant disease did not differ significantly either in their pre- or postoperative fibronectin levels, compared with the whole group. The lowest fibronectin levels seen were also significantly above the concentrations necessary to promote binding of gelatinized test particles to macrophages and monocytes in vitro. There was a significant decrease in C3, C4 and IgG levels postoperatively whereas IgM levels were unaltered. The observed reduction did not extend below the lower normal levels for these proteins. The probable mechanism behind the reduction in serum levels seems to be a sequestration at the site of tissue injury. The postoperative reduction in circulating fibronectin levels has probably no implications for host resistance against septic complications. When sequestered into the site of injury, it may, however, be of significance for normal wound healing, due to its cell-matrix interactions.

10.1002/bjs.1800720123

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Citations (21)

Deposition of chromatin‐IgG complexes in skin of nephritic MRL‐lpr/lpr mice is associated with increased local matrix metalloprotease activities

Experimental Dermatology (2010)

Annica Hedberg Silje Fismen Kristin Andreassen Fenton Elin Mortensen Ole Petter Rekvig

Chromatin-IgG complexes appear as electron dense structures (EDS) in glomerular basement membranes in lupus nephritis. Here, we present results of comparative analyses of the composition of EDS in murine lupus dermatitis and nephritis. One focus was to perform an analytical approach to understand why such complex structures bind skin basement membrane components. Transcription of skin membrane-encoding genes was analysed to see if expression of such genes was increased, eventually indicating that binding capacity of immune complexes increased when dermatitis developed. Variations in matrix metalloprotease 2 (MMP2), MMP9 and Dnase1 mRNA levels and enzymatic activities were correlated with circulatory chromatin-IgG complexes and deposition in skin. We also examined if glomerular deposits of EDS predicted similar deposits in skin of (NZB x NZW)F1 or MRL-lpr/lpr mice, as we observed chromatin-IgG complexes in capillary lumina in skin and glomeruli in both strains. EDS consisting of chromatin fragments and IgG were found sub-epidermally in skin with LE-like lesions of end-stage nephritic MRL-lpr/lpr mice. Dermal MMP-encoding genes were up-regulated during disease progression, and gelatinolytic activity was increased in affected skin. Dnase1 mRNA level and total nuclease activity remained stable in skin during the disease, in contrast to progressive loss of renal Dnase1 mRNA and total renal nuclease activity during development of nephritis. Loss of renal Dnase1 may explain release of chromatin fragments, while increased MMP activity may disrupt membranes making them accessible for chromatin fragment-IgG complexes. Circulatory chromatin-IgG complexes, and up-regulated intradermal MMP activity may be crucial for deposition of immune complexes in skin of lupus-prone mice.

Nephritis

10.1111/j.1600-0625.2010.01064.x

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Citations (20)

Diagnostic Accuracy of Anti-dsDNA Antibodies in Unselected Patients with Recent Onset of Rheumatic Symptoms.

Michele Compagno Søren Jacobsen Ole Petter Rekvig Lennart Truedsson Niels H. H. Heegaard

Anti-dsDNA antibodies

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Stimulation of Clones Specific for dsDNA or Idiotypes of Anti-dsDNA as a Consequence of BK Virus Inoculation

Immunological Investigations (1989)

Ole Petter Rekvig Trond Flægstad Knut Fredriksen Terje Traavik

The human polyoma virus BK (BKV) has a 5 Kbp double-stranded (ds) DNA genome packed with host cell histones into a minichromosome. Two out of 5 rabbits inoculated with infectious BKV produced detectable anti-dsDNA antibodies. In two additional rabbits antibodies against idiotypes of anti-dsDNA antibodies were elicited. These findings strongly indicate the existence of immunocompetent anti-dsDNA clones which are regulated, at least in part, through a network mechanism by anti-idiotype antibodies.

Anti-dsDNA antibodies

10.3109/08820138909057753

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Citations (5)

Differences in the Reactivity of CD4⁺ T‐Cell Lines Generated against Free Versus Nucleosome‐Bound SV40 Large T Antigen

Scandinavian Journal of Immunology (2001)

Geir Bredholt Ole Petter Rekvig Kristin Andreassen Ugo Moens Tony N. Marion

Previous results have revealed a strong correlation between polyomavirus BK reactivation and disease activity and antinuclear auto-antibody production in the human autoimmune disease systemic lupus erythematosus. BK virus establishes a latent infection in most humans, and reactivation requires the production of the DNA-binding large T antigen. Experimentally induced expression of the polyomavirus SV40 large T antigen in mice induces both an immune response to large T antigen and autoimmune response to nuclear antigens and antinuclear antibody production. Previous results have indicated that human T-antigen-specific CD4+ T-cell lines are stimulated equally by free, soluble and nucleosome-bound T antigen. This study was designed to determine how antigen processing of nucleosomes containing bound SV40 large T antigen may affect the specificity and response characteristics of experimentally induced T-antigen-specific CD4+ T cells. The results indicated that CD4+ T-cell lines generated from mice immunized with soluble, free T antigen responded very poorly in response to stimulation with T antigen bound to nucleosomes. CD4+ T-cell lines generated from mice immunized with nucleosomes that had bound T antigen in situ responded to both free and nucleosome-bound T antigen. The T-antigen-specific, CD4+ memory T cells induced by latent polyomavirus infections in humans may be uniquely suited to initiate autoimmunity to nuclear antigens upon virus reactivation.

10.1046/j.1365-3083.2001.00873.x

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Lupus nephritis progression in FcγRIIB-/-yaa mice is associated with early development of glomerular electron dense deposits and loss of renal DNase I in severe disease

PLoS ONE (2017)

Kjersti Daae Horvei Hege Lynum Pedersen Silje Fismen Dhivya Thiyagarajan Andreá Schneider

FcγRIIB-/-yaa mice develop severe lupus glomerulonephritis due to lack of an inhibitory immune cell receptor combined with a Y-chromosome linked autoimmune accelerator mutation. In the present study, we have investigated nephritis development and progression in FcγRIIB-/-yaa mice to find shared features with NZB/NZW F1 lupus prone mice and human disease. We sacrificed 25 male FcγRIIB-/-yaa mice at various disease stages, and grouped them according to activity and chronicity indices for lupus nephritis. Glomerular morphology and localization of electron dense deposits containing IgG were further determined by immune electron microscopy. Renal DNase I and pro-inflammatory cytokine mRNA levels were measured by real-time quantitative PCR. DNase I protein levels was assessed by immunohistochemistry and zymography. Our results demonstrate early development of electron dense deposits containing IgG in FcγRIIB-/-yaa mice, before detectable levels of serum anti-dsDNA antibodies. Similar to NZB/NZW F1, electron dense deposits in FcγRIIB-/-yaa progressed from being confined to the mesangium in the early stage of lupus nephritis to be present also in capillary glomerular basement membranes. In the advanced stage of lupus nephritis, renal DNase I was lost on both transcriptional and protein levels, which has previously been shown in NZB/NZW F1 mice and in human disease. Although lupus nephritis appears on different genetic backgrounds, our findings suggest similar processes when comparing different murine models and human lupus nephritis.

Nephritis

Immune complex

Mesangium

10.1371/journal.pone.0188863

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Citations (6)