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PubMed1996

[A case showing recurrence of myelopathy and optic nerve disturbance accompanied by pusturosis palmaris et plantaris and positive anticardiolipin antibody].

The patient is a 62-year-old woman who was admitted to our hospital with chief complaints of paresthesia in the four extremities and the trunk and gait disturbance in February 1993. Habitual abortions and left retrobulbar optic neuritis were present in the past history. She had been suffering from pusturosis palmaris et plantaris for 10 years. On admission, weakness of the distal muscles in the right upper extremity and severe disturbance of the deep sensations in the bilateral lower extremities and the right upper extremity were present. With the progress of the neurological symptoms, pusturosis palmaris et plantaris progressed. After the admission, the neurological symptoms became better by the administration of corticosteroid hormone medicine. After that, myelopathy and left optic nerve disturbance relapsed and IgG anti-cardiolipin antibody in the serum was present. The neurological symptom, pusturosis palmaris et plantaris and positive IgG anti-cardiolipin antibody in the serum may be caused by immunological mechanism. Anti-phospholipid antibodies such as IgG anti-cardiolipin antibody in the serum should be examined in patients with clinical multiple sclerosis like our case.

Abortion, Habitual↗
PubMed1995

[Anticardiolipin antibodies and Horton disease].

A prospective study, including 86 patients with giant cell arteritis proven by temporal artery biopsies, was performed to determine the prevalence of anticardiolipin antibodies, the antibody isotype, the relationship of antibodies to ischemic involvement and their evolution during corticosteroid treatment. Controls were obtained from 50 subjects without vasculitis or autoimmune disorders. Before treatment, 50% of patients' sera contained anti-cardiolipin antibodies (vs 8% in controls, p < 0.0001). These antibodies were IgG-ACL in 36% of patients and IgM-ACL in 17% of patients (vs respectively, 4% and 2% in controls). No significant association was observed between the incidence of ischemic ocular complications and the levels of anti-cardiolipin antibodies. During corticosteroid treatment, the level of anti-cardiolipin antibodies, mostly IgG class, decreased to become negative in 2 months. An increase of these antibodies was observed with the occurrence of relapses in four patients, after the end of corticosteroid therapy. The significance of IgG and IgM antibodies is different in giant cell arteritis. IgG antibodies may be markers of the course of this vasculitis.

Adrenal Cortex Hormones↗
PubMed1995

Clinical manifestations of the antiphospholipid syndrome in patients with systemic lupus erythematosus associate more strongly with anti-beta 2-glycoprotein-I than with antiphospholipid antibodies.

OBJECTIVE: To investigate antibodies to phospholipid-free beta 2-glycoprotein-I (a beta 2 GP-I) in the serum of patients with systemic lupus erythematosus (SLE). METHODS: We studied alpha beta 2 GP-I by Western blot, dot blot, and ELISA in 94 patients with SLE. Twenty-one had antiphospholipid syndrome (APS) by clinical and serological criteria, 33 had neither of these features, 18 had the clinical criteria for APS but no serum antiphospholipid antibodies (aPL). and 22 had positive aPL but no related clinical manifestations. As controls, we also studied 76 normal sera. Sera were also inhibited with cardiolipin micelles and tested for anticardiolipin antibodies (aCL) or a beta GP-I activities. RESULTS: Thirty-five of 39 patients with SLE with clinical manifestations of APS has serum a beta 2 GP-I, while only 2 of 55 patients with SLE without such clinical manifestations had them (p = 0.000000001). Sixteen patients with SLE with clinical APS but aPL negative were a beta GP-I positive. All 35 patients with SLE who were a beta 2 GP-I positive had vascular manifestations, but these antibodies were present in only 4 of 55 patients with SLE without vascular manifestations (p = 0.00000001). No patient having either aPL or a beta 2 GP-I had clinical manifestations of APS, whereas all 19 patients positive for both antibodies had clinical APS. The a beta 2 GP-I positive, aPL negative patients with SLE had clinical APS more frequently (16/18) than did a beta GP-I negative, aPL positive patients with SLE (2/24) (p = 0.000000001). The association of clinical manifestations of APS with a beta 2 GP-I was stronger than with aPL. Inhibition studies also indicate that aPL and a beta 2 GP-I are 2 different antigen/antibody systems. CONCLUSIONS: Our findings indicate that the so called APS associates strongly with antibodies recognizing phospholipid-free beta 2 GP-I. There are patients' sera that also recognize cardiolipin and/or its cofactor beta 2 GP-I, the latter perhaps by reacting with a neoepitope on this protein that appears after its interaction with cardiolipin. These would be the previously considered (beta 2 GP-I dependent) aCL.

Adolescent↗
PubMedDate not supplied

Experimental studies on the bacterial product CANTASTIM derived from Pseudomonas aeruginosa. III. Suppression of lipopolysaccharide-induced tumor necrosis factor alpha: are the lipid components involved?

We previously reported that the bacterial immunomodulator CANTASTIM inhibited the LPS-induced TNF-alpha production in murine macrophages both in vivo and in vitro. In this report, we compared the activity of CANTASTIM with that of two phospholipids (cardiolipin and phosphatidylethanolamine) which are among the components of its lipid fraction. We noticed a significant reduction in the production of TNF-alpha upon stimulation with LPS in murine peritoneal macrophages pretreated for at least 3 h with CANTASTIM or cardiolipin. CANTASTIM was active at much lower concentrations than cardiolipin. Preliminary experiments with partially deacylated CANTASTIM indicated some decrease of TNF-alpha secretion. However, further studies are necessary to clarify this matter. Also, while CANTASTIM and its partially deacylated derivative could trigger the TNF-alpha secretion in murine macrophages, individual phospholipids did not. Based on these results, we concluded that CANTASTIM could induce the TNF-alpha suppression by multiple mechanisms, including the induction of regulatory cytokines such as IL-10 and CD14 receptor blockade/downregulation.

Adjuvants, Immunologic↗
PubMed1998

Heterogeneity and immunochemical properties of anti-beta2-glycoprotein I autoantibodies.

Most anticardiolipin antibodies (ACA) associated with antiphospholipid syndrome (APS) are directed against epitopes expressed on beta2-glycoprotein I (beta2GPI). Despite a good correlation between standard ACA assays and those using purified human beta2GPI as the sole antigen, some sera from APS patients only react in the latter. This is indicative of heterogeneity in anti-beta2GPI antibodies. To characterize their reactivity profiles, human and bovine beta2GPI were immobilized on gamma-irradiated plates (beta2GPI-ELISA), plain polystyrene precoated with increasing cardiolipin concentrations (CL/beta2GPI-ELISA), and affinity columns. Fluid-phase inhibition experiments were also carried out with both proteins. Of 56 selected sera, restricted recognition of bovine or human beta2GPI occurred respectively in 10/29 IgA-positive and 9/22 IgM-positive samples, and most of the latter (8/9) were missed by the standard ACA assay, as expected from a previous study. Based on species specificity and ACA results, IgG-positive samples (53/56) were categorized into three groups: antibodies reactive to bovine beta2GPI only (group I) or to bovine and human beta2GPI, group II being ACA-negative, and group III being ACA-positive. The most important group, group III (n = 33) was characterized by (i) binding when beta2GPI was immobilized on gamma-irradiated polystyrene or cardiolipin at sufficient concentration (regardless of beta2GPI density, as assessed using 125I-beta2GPI); (ii) and low avidity binding to fluid-phase beta2GPI (Kd in the range 10(-5) M). In contrast, all six group II samples showed (i) ability to bind human and bovine beta2GPI immobilized on non-irradiated plates; (ii) concentration-dependent blockade of binding by cardiolipin, suggesting epitope location in the vicinity of the phospholipid binding site on native beta2GPI; (iii) and relative avidities approximately 100-fold higher than in group III. Group I patients were heterogeneous with respect to CL/beta2GPI-ELISA and ACA results (6/14 scored negative), possibly reflecting antibody differences in terms of avidity and epitope specificity. Affinity fractionation of 23 sera showed the existence, in individual patients, of various combinations of antibody subsets solely reactive to human or bovine beta2GPI, together with cross-species reactive subsets present in all samples with dual reactivity namely groups III and II, although the latter antibodies were poorly purified on either column. Therefore, the mode of presentation of beta2GPI greatly influences its recognition by anti-beta2GPI antibodies with marked inter-individual heterogeneity, in relation to ACA quantitation and, possibly, disease presentation and pathogenesis.

Adolescent↗
PubMedDate not supplied

Correlation between peritoneal fluid and serum antiphospholipid antibodies in women with primary infertility.

OBJECTIVE: To compare the peritoneal and serum levels of antiphospholipid antibodies (aPLs) against the following phospholipids: cardiolipin, L-alpha-phosphatidic acid, L-alpha-phosphatidylethanolamine, 1-alpha-phosphatidyl-DL-glycerol, L-alpha-phosphatidyl-inositol, L-alpha-phosphatidyl-L-serine in immunoglobulin isotypes of G, M, and secretory A. PATIENTS AND METHODS: A group of 107 women with primary infertility were immunologically examined. An ELISA method was used for detection of aPLs. RESULTS: aPL-L-serine and aPL-cardiolipin predominate over peritoneal fluid in all studied Ig isotypes (G, M, secretory A). Levels of aPL-ethanolamine are much higher in peritoneal sIgA and IgM than in sera. There is a predominance of IgG-aPLs-inositol, DL-glycerol, and aPL-acid in serum, and of sIgA in peritoneal fluid. CONCLUSION: Our patients had higher levels of aPLs (IgG, IgM, sIgA) against cardiolipin, serine, and ethanolamine in peritoneal fluid than in sera. The prevalence of aPLs in IgG was against DL-glycerol, phosphatidyl-inositol, and phosphatidic acid. It is quite difficult to estimate whether the aPLs have an influence directly through phospholipid epitopes on uterine mucous membrane, on the surface of oocytes, or on the surface of the early embryo during the fertilization and/or implantation process.

Adult↗
PubMed1996

Discrimination of respiratory dysfunction in yeast mutants by confocal microscopy, image, and flow cytometry.

Living yeast cells can be selectively stained with the lipophilic cationic cyanine dye DiOC6(3) in a mitochondrial membrane potential-dependent manner. Our study extends the use of flow cytometric analysis and sorting to DiOC6(3)-stained yeast cells. Experimental conditions were developed that prevented the toxic side effect of the probe and gave a quantitative correlation between fluorescence and mitochondrial membrane potential, without any staining of other membranes. The localization of the fluorochrome was checked by confocal microscopy and image cytometry. The mitochondrial membrane alterations were also tested through cardiolipin staining with nonyl acridine orange. Differences in light scattering and in fluorescence were detected in mutants (rho-, rho degrees, mit-, or pet-) and wild-type (rho+mit+) populations of yeast. The dye uptake of respiratory-deficient yeast strains was significantly reduced as compared to that of the wild-type. Application of an uncoupler (mCICCP), which collapsed the mitochondrial membrane potential (alphapsi(m)), led to a drastic reduction of the dye uptake. It was observed that a decrease in deltapsi(m), was usually correlated with a decrease in cardiolipin stainability by nonyl acridine orange (NAO). Quantitative flow cytometry is a fast and reproducible technique for rapid screening of yeast strains that might be suspected of respiratory dysfunction and/or mitochondrial structural changes. We give evidence that it is an adequate method to characterize and isolate respiratory mutants through sorting procedure, with selective enrichment of the population studied in respiring or non-respiring yeast cells. Confocal microscopy and image cytometry corroborate the flow cytometry results.

Acridine Orange↗
PubMed2004

X-linked cardioskeletal myopathy and neutropenia (Barth syndrome): an update.

X-linked cardioskeletal myopathy and neutropenia (Barth syndrome, MIM302060, BTHS) is a disorder with mitochondrial functional impairments and 3-methylglutaconic aciduria that maps to Xq28. The associated G4.5 or TAZ gene has been identified but the encoded proteins have not yet been characterized. Following the prediction that the gene encodes one or more acyltransferases, lipid studies have shown a deficiency of cardiolipin, especially its tetralinoleoyl form (L(4)-CL). Deficiency of L(4)-CL was subsequently demonstrated in a variety of tissues, and determination in thrombocytes or cultured skin fibroblasts is now the most specific biochemical test available. BTHS is the first identified inborn error of metabolism that directly affects cardiolipin, a component of the inner mitochondrial membrane, necessary for proper functioning of the electron transport chain. We report here the finding of deficient docosahexaenoic acid and arachidonic acid in a proportion of patients with BTHS. The initial impression of a uniformly lethal infantile disease has to be modified. Age distribution in 54 living patients ranges between 0 and 49 years and peaks around puberty. Mortality is the highest in the first 4 years. The apex of the survival curve around puberty and the emergence of adults may reflect a dynamic shift towards increased survival. This trend is exemplified in a large pedigree previously published.

Abnormalities, Multiple↗
PubMed2004

Safety and efficacy of tumor necrosis factor alpha blockade in systemic lupus erythematosus: an open-label study.

OBJECTIVE: To investigate the safety of therapeutic tumor necrosis factor alpha (TNFalpha) blockade in patients with systemic lupus erythematosus (SLE), in whom this proinflammatory cytokine is significantly increased and may be involved in the disease pathogenesis. METHODS: In an open-label study, 6 patients with moderately active SLE (4 with nephritis and 3 with arthritis refractory to other therapies) were given 4 300-mg doses of infliximab, a chimeric anti-TNFalpha antibody, in addition to immunosuppression with azathioprine or methotrexate. RESULTS: The only significant adverse events observed were urinary tract infection in 3 patients, 1 of which was accompanied by Escherichia coli bacteremia, and a prolonged febrile episode of putatively viral origin in 1 of them. These patients had similar infectious conditions in the past. In none of the patients was it necessary to terminate the treatment prematurely. Levels of antibodies to double-stranded DNA and cardiolipin increased in 4 patients each, but this was not associated with a decrease in serum complement levels, with vascular events, or with flares. In contrast, disease activity declined during therapy. All 3 patients with joint involvement experienced remission of arthritis, which relapsed 8-11 weeks after the last infliximab infusion. In the 4 patients with lupus nephritis, proteinuria decreased significantly within 1 week after initiation of therapy and was diminished by > or = 60% within 8 weeks, remaining at low levels until the end of the observation period (at least several months). CONCLUSION: Infliximab did not lead to adverse events related to an increase in SLE activity, although autoantibodies to double-stranded DNA and cardiolipin increased, as expected. This finding, coupled with the clinical improvement in the inflammatory manifestations of the disease, indicates that further study in larger controlled trials is warranted.

Adult↗
PubMedDate not supplied

Surface enhanced Raman scattering of a lipid Langmuir monolayer at the air-water interface.

Surface enhanced Raman spectra were recorded from a phospholipid monolayer directly at the air-water interface. We used an organized monolayer of negatively charged tetramyristoyl cardiolipins as a template for the electrochemical generation of silver deposits. This two-dimensional electrodeposition of silver under potentiostatic control was the substrate for enhancement of Raman spectra. We report the optimized conditions for the Raman enhancement, the microscopic observations of the deposits, and their characterization by atomic force microscopy. Laser excitation at 514.5 nm leads to intense and reproducible surface enhanced Raman scattering spectra recorded in situ from one monolayer of cardiolipin, using 0.5 mol % of 10N nonyl acridine orange or 5 mol % of acridine in the film, and demonstrates the possibility of estimating the pH at the metal/phospholipidic film interface.

Acridine Orange↗
PubMed1994

Phospholipid antibodies in alcoholic liver disease.

Alcoholic liver injury has been reported to be directed preferentially against the proteins of the cell membrane, sparing the phospholipids. However, antiphospholipid antibodies against certain cell membrane phospholipids are known to be associated with a variety of diseases. We undertook this investigation to determine whether antiphospholipid antibodies were present in the serum of patients with alcoholic liver disease. We investigated seventy long-term alcoholic patients (> 80 gm ethanol/day for > 1 yr) and 8 normal nonalcoholic controls by means of enzyme-linked immunosorbent assay to determine whether serum antibodies were generated against the following membrane phospholipids: phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol (cardiolipin) and phosphatidic acid. Group 1 comprised alcoholic patients with normal liver function (n = 13), group 2 comprised alcoholic patients with abnormal liver function (n = 16), group 3 comprised patients with alcoholic hepatitis or cirrhosis (n = 41) and group 4 comprised nonalcoholic controls (n = 8). The antibody prevalence was 15% in group 1, 31% in group 2, 81% in group 3 and 0% in group 4. In group 3, 20 of 41 patients had antibodies against several cell membrane phospholipids (i.e., phosphatidylethanolamine, phosphatidylserine, phosphatidylglycerol, phosphatidic acid, cardiolipin and phosphatidylinositol). The antiphosphatidylethanolamine isotype was IgA or IgM in 25 of 41 of these patients. Both IgA (p < 0.01) and IgM (p < 0.008) antiphosphatidylethanolamine correlated significantly with disease severity. Antiphospholipid antibodies in alcoholic patients seem to reflect disease progression and correlate significantly with disease severity.

Adult↗
PubMed1983

Growth of the mitochondrial inner membrane in synchronous cultures of Tetrahymena pyriformis: an examination of phospholipid accumulation.

Based on morphological evidence, mitochondrial inner membrane growth has been reported to be discontinuous in heat shock-synchronized Tetrahymena pyriformis. As a biochemical measure of membrane growth under these conditions, we have examined phospholipid accumulation in the cell. No marked modulation of the accumulation of any of the major phospholipids could be detected through the cell cycle. At least 89% of the cardiolipin in the cells is restricted to the mitochondria, and we have used it as a marker for the growth of the mitochondrial inner membrane. During the heat shock synchrony, cardiolipin accumulates uniformly in parallel with the exponential rate of increase of total cellular phospholipids. These results suggest that at least the phospholipid component of all membrane systems in the cell grow continuously and uniformly. Additionally, we have shown that the total phospholipid content of Tetrahymena increases by a factor of 2.4 per generation following a series of heat shocks. No such net overaccumulation is observed for protein content.

Animals↗
PubMed2001

Mitochondrial lipid alterations during Fas- and radiation-induced apoptosis.

In the present study, we investigated the dynamic alterations in mitochondrial lipids occurring during Fas- and radiation-induced cell death. Cross-linking of CD-95 on Fas-sensitive Jurkat cells produced rapid increases in two species of mitochondrial phosphatidylglycerol. By 2.5 h, phosphatidylglycerol decreases below basal levels, concomitant with an increase in mitochondrial ceramide. In addition, between 1.5 and 3.0 h after anti-Fas crosslinking, there is a continued loss of mitochondrial cardiolipin. When gamma irradiation was used to induce apoptosis, similar lipid changes occurred, although with somewhat slower kinetics. Fas-resistant Jurkat cells exhibited phosphatidylglycerol as the dominant lipid species in their mitochondria. Following Fas ligation, there is a transient decrease in phosphatidylglycerol, but cardiolipin and ceramide remained unchanged. The high basal levels of PG in Fas-resistant cells and the increase in PG levels in Fas-sensitive cells undergoing apoptosis was determined to be due to increased PGP synthase activity. Thus, critical mitochondrial lipids could potentially serve as novel targets in regulating the apoptotic process.

Apoptosis↗
PubMed2001

Inhibition of nitric-oxide-mediated apoptosis in Jurkat leukemia cells despite cytochrome c release.

We have recently shown that nitric-oxide (NO)-induced apoptosis in Jurkat human leukemia cells requires degradation of mitochondria phospholipid cardiolipin, cytochrome c release, and activation of caspase-9 and caspase-3. Moreover, an inhibitor of lipid peroxidation, Trolox, suppressed apoptosis in Jurkat cells induced by NO donor glycerol trinitrate. Here we demonstrate that this antiapoptotic effect of Trolox occurred despite massive release of the mitochondrial protein cytochrome c into the cytosol and mitochondrial damage. Incubation with Trolox caused a profound reduction of intracellular ATP concentration in Jurkat cells treated by NO. Trolox prevented cardiolipin degradation and caused its accumulation in Jurkat cells. Furthermore, Trolox markedly downregulated the NO-mediated activation of caspase-9 and caspase-3. Caspase-9 is known to be activated by released cytochrome c and together with caspase-3 is considered the most proximal to mitochondria. Our results suggest that the targets of the antiapoptotic effect of Trolox are located downstream of the mitochondria and that caspase activation and subsequent apoptosis could be blocked even in the presence of cytochrome c released from the mitochondria.

Adenosine Triphosphate↗
PubMed2000

Phospholipid-bound beta 2-glycoprotein I induces the production of anti-phospholipid antibodies.

Apoptotic-cell-bound beta2-glycoprotein I (beta2GPI), but not apoptotic cells or beta2GPI alone, can induce the production of anti-phospholipid (anti-PL) antibodies (Ab) in normal mice. Although it is presumed that beta2GPI binds to anionic phospholipid (PL) exposed on the apoptotic cell membrane, the precise nature of this complex and its immunogenicity is unclear. To address these issues, we investigated the structure and immunogenicity of human beta2GPI in the presence of different PL that may be expressed on the surface of apoptotic cells. BALB/c mice were immunized intravenously (iv) with beta2GPI in the presence of cardiolipin (CL), phosphatidylglycerol (PG), phosphatidylserine (PS), phosphatidylcholine (PC), or PS/PC (25%/75%) vesicles. Cardiolipin+beta2GPI induced the highest levels of anti-beta2GPI and anti-CL IgG Ab and lupus anticoagulant (LA) activity, while beta2GPI with PC or PS/PC vesicles produced no significant anti-PL Ab. PS+beta2GPI was somewhat immunogenic, but less so than PG+beta2GPI. beta2GPI was immunogenic in the presence of native (CL(N)), but not hydrogenated (CL(H)), CL. Circular dichroism analysis demonstrated that the structure of beta2GPI was altered specifically by interaction with CL(N), but not other anionic PL, including CL(H). Similarly, the structure of CL(N)was affected by interaction with beta2GPI, as detected by(31)P nuclear magnetic resonance. These findings demonstrate that beta2GPI complexed with CL(N)is structurally altered, highly immunogenic, and induces the production of IgG anti-PL Ab. Furthermore, the structural modification and the generation of immunogenic epitopes on beta2GPI upon interaction with CL(N)require the presence of unsaturated fatty acid chains, suggesting a role for oxidation in this process.

Adjuvants, Immunologic↗
PubMed1993

Membrane and phospholipid binding by murine coronaviral nucleocapsid N protein.

Evidence is presented which indicates that membrane binding of the murine coronavirus, mouse hepatitis virus (MHV) nucleocapsid (N) protein is mediated by certain lipids. Binding of N protein to membranes of mouse fibroblast L-2 cells is very specific and occurs under conditions in which no other viral or cellular proteins show detectable binding. Binding occurs with both free and nucleocapsid-associated N protein, arguing for membrane-binding sites on the N protein itself, rather than on RNA. Binding of N protein also occurs to membranes in the absence of MHV matrix (M) protein which is known to interact with the N protein. Both non-viral, single-stranded RNA and DNA inhibit membranes. Of various phospholipids tested, cardiolipin was the most effective in inhibiting membrane binding. The N protein was also shown to bind directly to phospholipid liposomes containing cardiolipin as well as to liposomes containing total lipids extracted from mouse L-2 cells. Because of certain structural similarities between phospholipids and nucleic acids, we speculate that membrane lipid association of the N protein may compete for RNA binding sites on the N protein. Such a mechanism may be important for processes such as nucleocapsid uncoating and nucleocapsid assembly. Most interestingly the properties of phospholipid and nucleic acid binding are markedly similar to those recently described for the bacterial DNA-binding proteins DnaA and recA.

Animals↗
PubMed1976

Action of polymyxin B on bacterial membranes. Binding capacities for polymyxin B of inner and outer membranes isolated from Salmonella typhimurium G30.

Radioactive mono-N-acetyl-14C-polymyxin B or natural polymyxin B are within 60 s absorbed by isolated inner (cytoplasmic) and outer membranes from Salmonella typhimuriumG30. The sigmoidal binding isotherms indicate saturation of inner and outer membranes with approximately 30 and 60 nmoles polymyxin B bound per mg membrane, respectively. Based on the known content of these membranes in lipopolysaccharide, phosphatidylglycerol, cardiolipin and phosphatidylethanolamine, a calculation of the theoretical binding capacities yields almost identical values if lipopolysaccharide, phosphatidylglycerol and cardiolipin are assumed to function as the actual binding sites for the antibiotic in the isolated membranes. The excellent agreement between theoretical evaluation and experimental determination of polymyxin B-binding capacities leaves little doubt that the named anionic compounds are the chemoreceptors for the cationic antibiotic. This is further substantiated by very similar binding and killing kinetics of polymyxin B.

Binding Sites↗
PubMed1986

Distribution of an anti-DNA idiotype among autoantibodies in patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA).

Autoantibodies from patients with systemic lupus erythematosus, rheumatoid arthritis, or other connective tissue disorders were probed for the presence of a cross-reactive idiotype (AM Id) originally defined on human anti-double-stranded DNA antibodies. The AM Id was distributed primarily among antibodies to double-stranded DNA, single-stranded DNA, or cardiolipin in patients with systemic lupus erythematosus and antibodies to single-stranded DNA or cardiolipin and rheumatoid factor in patients with rheumatoid arthritis, thus tending to codistribute with the predominant primary autoantibodies in both diseases. Strong associations were observed particularly between the AM Id and anti-single-stranded DNA antibodies in patients with systemic lupus erythematosus and the AM Id and anticardiolipin antibodies in patients with rheumatoid arthritis. Affinity absorption experiments with sera from individual lupus patients showed that up to 41% of the anti-single-stranded DNA antibodies were Id positive. The results indicate that the AM Id may be widely distributed among antibodies that have a potential for binding DNA.

Antibodies, Anti-Idiotypic↗