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D Isenberg

Publications and source records attributed to D Isenberg.

At least 109 records · Page 6Linked to original sources
PubMed1989

Autoantibodies against a nuclear 56 kDa protein: a marker for inflammatory muscle disease.

Antibodies to a 56 kDa nuclear protein have been found in the sera of 85% of patients with myositis using an immunoblotting technique. This auto-antibody appears to be relatively disease-specific though more frequently detectable in both adult and childhood onset dermatomyositis. In adult patients with myositis the anti-56 kDa antibody level reflects disease activity. This antibody is thus much more frequently found than previously described disease-specific autoantibodies in patients with myositis such as the Jo-1 antibody, and may represent a useful diagnostic aid in patients with muscle weakness.

Animals↗
PubMed1989

Elevation of the levels of SmB, B' and D proteins but not that of the La (SS-B) antigen during HSV infections.

Three Sm proteins, B, B' and D, which are highly immunoreactive in systemic lupus erythematosus (SLE), increase in abundance in Vero cells infected with laboratory strains and clinical isolates of herpes simplex virus (HSV) types 1 and 2. The autoimmune antigen La (SS-B) does not accumulate in identical infections. The significance of the Sm antigen accumulation is discussed in terms of its possible role in HSV infection and in connection with the origin of autoantibodies in SLE.

Animals↗
PubMed1988

Age-related galactosylation of the N-linked oligosaccharides of human serum IgG.

In a study of 151 normal, healthy individuals of both sexes varying in age from 1-70 yr, it was found that the relative incidence of agalactosyl (with both outer arms terminating in N-acetylglucosamine) N-linked oligosaccharides on total serum IgG decreased from birth to a minimum (at 25 yr of age) and then increased with age. The relative incidence of digalactosyl structures varied inversely to this, and the relative incidence of monogalactosyl structures was constant. Galactosylation of the N-linked oligosaccharides of the human serum IgG of normal individuals is therefore an age-related molecular parameter. Several reports have suggested that rheumatoid arthritis is associated with a decreased galactosylation of serum IgG (3-5). The normal variation in galactosylation with age as described here allows a true assessment of disease-associated changes in this parameter, and raises the possibility that one of the lesions in rheumatoid arthritis is an accelerated aging of the immune system. In addition, heterogeneity within age groups may be due to intrinsic differences in genetic endowment, or may reflect the impact of extrinsic factors (8).

Adolescent↗
PubMed1988

Sjögren's syndrome: a study of its neurological complications.

A detailed retrospective study of 105 patients with Sjögren's syndrome (50 primary and 55 secondary cases), showed that 31 had vasculitis and 18 had neurological abnormalities which after full investigation were not attributable to other causes. Most of the neurological symptoms were mild and when found in patients with secondary Sjögren's syndrome were more characteristic of the underlying autoimmune rheumatic disease. We found no significant association between the frequency of either vasculitis or any autoantibodies and the presence of neurological disease, but did confirm a significant association between vasculitis and the presence of antibodies to extractable nuclear antigens. We therefore question whether severe and relapsing neurological disease is common in patients with Sjögren's syndrome.

Antibodies, Antinuclear↗
PubMed1988

Acute pancreatitis in systemic lupus erythematosus: report of a case unrelated to drug therapy.

Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease that can affect most organs or systems. It most frequently involves the joints, skin, and the kidneys. It less commonly involves the central nervous system, heart, and lungs. Acute pancreatitis in SLE is rare. It is usually mild, occurring in association with more severe organ involvement elsewhere. A patient with newly diagnosed SLE is reported who developed acute fulminant pancreatitis unrelated to concomitant drug therapy and who eventually died of complications including a systemic fungal infection related to this.

Acute Disease↗
PubMed1988

Human monoclonal antibodies to phenolic glycolipid-1 from leprosy patients cross react with poly(ADP-ribose), polynucleotides and tissue bound antigens.

Antibodies which bind to poly(ADP-ribose) have been described in Systemic Lupus Erythematosus (SLE) and a variety of infectious diseases. Two IgM kappa human monoclonal antibodies (MAbs), TH3 and PR4, produced from the fusion of peripheral blood lymphocytes of leprosy patients with the GM4672 lymphoblastoid cell line, were found to bind to poly(ADP-ribose) in direct binding and inhibition ELISAs. Significant inhibition of binding of these MAbs to poly(ADP-ribose) occurred with phenolic glycolipid-1, the M. leprae specific glycolipid, ssDNA, dsDNA, poly(dT), as well as poly(ADP-ribose) itself. Up to 80% of binding of TH3, and 90% of binding of PR4, to poly(ADP-ribose) was inhibited by 10 mcg of ssDNA suggesting that there may be sharing of some conformational determinants. Although the serological binding profiles of TH3 and PR4 are similar, only PR4 was found to bind to basal keratinocytes of normal human interfollicular epidermis and astrocyte cytoplasm in normal brain tissue. These results support the concept that an antibody binding site may accommodate more than one epitope. Furthermore, small differences in antigen binding potential may distinguish relatively innocuous antibodies from those which may be more pathogenic.

Antibodies, Monoclonal↗
PubMed1988

Anti-DNA antibody synthesis after bone marrow transplantation: implications for IgG subclass restrictivity and pathogenicity of autoantibodies.

Two patients developed antinuclear antibodies (ANA) including antibodies directed against double-stranded DNA (dsDNA) after bone marrow transplantation. In one of the patients very high levels of IgM, IgG as well as IgA anti-dsDNA were found during 6 months in the absence of symptoms of systemic lupus erythematosus (SLE). The other patient made IgM anti-dsDNA antibodies for a period of more than 3 years, also in the absence of SLE symptoms. The ANA were restricted to the IgG1 and IgG3 isotypes as is the case in SLE but did not express idiotypes commonly found in this autoimmune disease. The occurrence of these antibodies may reflect a non-antigen induced expansion of the existing donor B-lymphocyte repertoire.

Antibodies, Antinuclear↗
PubMed1988

Expression of an interspecies idiotype in sera of SLE patients and their first-degree relatives.

Sera from 29 SLE patients and 81 first-degree healthy family members were tested for quantitative expression of a cross-reactive idiotype present on a murine monoclonal anti-Sm autoantibody (Y2). Forty-one percent of SLE patients and 27% of all relatives showed increased serum levels of the Y2 idiotype compared to 6% in a normal, unrelated control group. In addition, female relatives of SLE patients showed slightly increased levels of anti-Sm antibodies compared to male relatives (15% vs 3%). In one of the 28 families and three unrelated SLE patients studied, there was a significant correlation between the Y2 idiotype expression and expression of another idiotype present on anti-DNA antibodies (1341d). Affinity column absorption studies showed that these two idiotypes were present on different antibody molecules. This study demonstrates: (1) a genetic predisposition for an anti-Sm antibody idiotype expression in humans; and (2) that two different idiotypes may be under parallel or coordinate regulation.

Antibodies, Antinuclear↗
PubMed1987

DNA antibody idiotypes: a review of their genetic, clinical, and immunopathologic features.

The initial studies of anti-DNA antibody idiotypes we performed, along with those of our colleagues and other groups, focused on the narrow question of their relevance to lupus autoantibodies. The subsequent studies in this report have forced us to examine a much broader range of issues. It is evident that despite the great advances in understanding the structure and function of antibodies, lymphocytes, and receptors, our knowledge of many fundamental elements in autoimmune disease is woefully incomplete. We are still unsure whether the germ line gene sequences controlling antibody production have evolved solely in response to exposure to new foreign antigens. Alternatively, these antibodies (and the idiotypes they bear) may have developed largely in response to changes in the internal environment. Superficially, it can be argued that "self reactivity" associated with the clinical expression of a disease results from a combination of immunologic, genetic, hormonal, and environmental elements. For example, the expression of the 16/6 Id in an appropriate setting may have pathogenetic consequences for some individuals. However, our knowledge of the precise sequence of events that result in devastating disease for some but minimal disease for others is just one of the remaining mysteries.

DNA↗
PubMed1987

The endocrinologic associations of the autoimmune rheumatic diseases.

Having seen five patients with both SLE and thyroid disease (case reports available on request) in a short period of time, we have undertaken a survey of the association between the ARD and endocrine disorders. On the basis of a literature review and our own reported study, it is apparent that an association between these major groups of disorders is well established with some individual diseases, though much more dubious in others (Table 3). The possibility of coexistent endocrine disease in a patient with a multisystem ARD should be carefully considered throughout the course of the patient's follow-up.

Autoimmune Diseases↗
PubMed1987

A cross-reactive idiotype on anti-DNA and lymphocytotoxic antibodies.

The possibility that shared idiotypes may be present on antibodies of different specificities was explored using sera from 13 patients with systemic lupus erythematosus. Eleven sera had anti-DNA and seven carried the 16/6 idiotype (ID). Two of the sera with 16/6 ID also had lymphocytotoxic antibodies, the activity of which was blocked by antibody to the 16/6 ID. Our studies reveal that 16/6 ID is present on two antibodies with different binding specificities.

Antibodies, Antinuclear↗
PubMed1987

Low serum antimycobacterial glycolipid antibody titers in the sera of patients with systemic lupus erythematosus associated with central nervous system involvement.

Antibodies which bind to glycolipids derived from Mycobacterium tuberculosis were sought in the sera of patients with systemic lupus erythematosus (SLE), with and without neurological disease, patients with active tuberculosis and normal controls. A significantly lower activity against the mycobacterial glycolipids was detected in the sera of patients with SLE with neurological involvement compared to other patients with SLE or controls. We suggest that low antibody levels against mycobacterial glycolipids may be useful in the diagnosis of patients with SLE in whom involvement of the central nervous system is suspected.

Antibodies, Bacterial↗
PubMed1987

A common anti-DNA idiotype and other autoantibodies in sera of offspring of mothers with systemic lupus erythematosus.

Since the immune response in fetuses of mothers with systemic lupus erythematosus (SLE) is unknown, we investigated sera from six mothers and their paired offspring by enzyme-linked immunosorbent assay (ELISA) for the presence of a common anti-DNA idiotype (16/6 Id) and, as control, for the presence of an unrelated public idiotype of antibody to hepatitis B surface antigen (HBsAg). In addition, maternal as well as fetal sera were evaluated for the presence of antibodies to ssDNA, dsDNA, poly(I), poly (dT), RNA, cardiolipin, total histones and the presence of lupus anticoagulant. Clinically active SLE mothers showed in general increased IgG and, to a lesser extent, IgM autoantibody activity. Circulating lupus anticoagulant was detectable in clinically active mothers only. All offspring of clinically active SLE mothers showed increased IgG autoantibodies to a variety of antigens, while IgM antibodies were detected in only one fetus. In contrast, fetuses of clinically inactive mothers showed only minor IgG activity. Common anti-DNA-idiotype (16/6 Id) activity also correlated with disease activity in both maternal and fetal compartments. One clinically active mother was 16/6-negative; her offspring was, however, positive, indicating de novo production of the idiotype by the fetus. In contrast, a control anti-HBsAg idiotype was not detected in either maternal or fetal sera. It therefore appears that offspring of clinically active SLE mothers serologically reflect maternal disease activity. Furthermore, autoantibodies and common idiotype of autoantibodies can be found within the fetal compartment even in the absence of such antibodies in the maternal serum. Discrepancies between mothers and offspring in IgM-autoantibody levels and the presence of new idiotypes in fetuses are indicative of fetal de novo autoantibody production.

Adult↗