Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LE CELLS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

[Finding of Tart cells in asthmatic patients. Relation to IgE and other parameters].

Fifty randomly selected asthmatic patients were studied. In each the sex, age, time of onset of symptomatology, symptomatologic score (from 0 to 3), blood eosinophilia, IgE by the PRIST method and Tart cells in blood (investigated by the same method as is used in the search of LE cells in collagen diseases) were considered. Tart cells were recognized as in Miale Haemotology (9) as monocytes and occasionally polymophonuclar leucocytes with one or two round inclusions in their protoplasm owing to the phagocytosis of leukocyte nuclei. In contrast with LE cells, these inclusions are not homogeneous contain chromatin and nuclear membrane material and often have a dark ring of hyperchromic material. We have found that these cells can not be evoked passively by application of patient serum to normal leukocytes. In no case of positive Tart cells was antinuclear serum factor found by immunofluorescence as seen in lupus erythematous disease. 33 per cent of the 50 asthmatic patients tested had Tart cells in their blood. They were very scarce, only one or two in four Wright stained smears. This fact is probably why these cells were not recognized before. The positive Tart cell group was on the average the same age as the negative group. On the other hand, in the positive Tart cell group the proportion of men with respect to women, the time span from the onset of asthmatic symptoms (p less than 0,05), the symptomatology score (p less than 0,005) and blood eosinophilia (p less than 0,005) were increased. In contrast IgE was decreased on the average (p less than 0,05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Autoantibodies to protein transport and messenger RNA processing pathways: endosomes, lysosomes, Golgi complex, proteasomes, assemblyosomes, exosomes, and GW bodies.

Over 50 years ago the lupus erythematosus (LE) cell phenomenon was described and this was quickly followed by the introduction of the LE cell test and indirect immunofluorescence (IIF) to detect antinuclear antibodies (ANA) in clinical laboratories. Recently, attention has turned to the identification of the autoantigens that bind to cytoplasmic organelles such as the Golgi complex, endosomes and other "cytoplasmic somes". Three endosome autoantigens include early endosome antigen 1 (EEA1, 160 kDa), cytoplasmic linker protein-170 (CLIP-170, 170 kDa), and lysobisphosphatidic acid (LBPA). Antibodies to EEA1 were seen in a variety of conditions but approximately 40% of the patients had a neurological disease. Despite the prominence of lysosomes in cells and tissues, reports of autoantibodies are limited to the lysosomal antigen h-LAMP-2 and the cytoplasmic antineutrophil antibodies (cANCA). Autoantigens in the Golgi complex include giantin/macrogolgin, golgin-245, golgin 160, golgin-97, golgin 95/gm130, and golgin-67. More recently, there has been an interest in autoantibodies that bind components of the "SMN complex" or the "assemblyosome". Arginine/glycine (RG)-rich domains in components of the SMN complex interact with Sm, like-Sm (LSm), fibrillarin, RNA helicase A (Gu), and coilin proteins, all of which are antigen targets in a variety of diseases. More recently, components of a novel cytoplasmic structure named GW bodies (GWBs) have been identified as targets of human autoantibodies. Components of GWBs include GW182, a unique mRNA-binding protein, like Sm proteins (LSms), and decapping (hDcp1) and exonuclease (Xrn) enzymes. Current evidence suggests that GWBs are involved in the cytoplasmic processing of mRNAs. Autoantibodies to the "cytoplasmic somes" are relatively uncommon and serological tests to detect most of them are not widely available.

Animals↗

Anti-chromatin (anti-nucleosome) autoantibodies.

Anti-chromatin autoantibodies were one of the first autoantibodies ever detected since they make up the majority of antibodies causing LE Cell formation. Anti-chromatin autoantibodies have had many names over the last few decades: LE cell factor; anti-nucleosome; anti-deoxyribonucleoprotein (DNP); and anti-(H2A-H2B-DNA). These autoantibodies are found in approximately 75% of people with systemic lupus erythematosus and up to 100% of people with drug-induced lupus. They are also found in 20-50% of patients with autoimmune hepatitis type I (lupoid hepatitis). Anti-chromatin are not generally found in any other disease, thus showing very good sensitivity and specificity for patients with lupus, drug-induced lupus and lupoid hepatitis. A number of studies have shown that in patients with lupus, anti-chromatin often correlates better with kidney disease than anti-DNA. Recent genetic analyses of murine models of lupus have identified at least three loci that work together to cause anti-chromatin antibodies and glomerulonephritis in mice. It will be an important breakthrough when the functions of the genes at these loci are identified.

Animals↗

Microhemagglutination test for the detection of nucleoprotein antibody in systemic lupus erythematosus.

A simple and practical microhemagglutination test that detects two antibodies, one showing reactivity to the DNA moiety of soluble nucleoprotein (sNP) and the other to the DNA-histone complex of sNP, is described. The method incorporates human erythrocytes formalinized at 30 C., tanned, and coated with sNP at 37 C. Antibody specificity was determined by inhibition experiments performed on sera with added DNA or sNP antigen. With the indirect LE cell technic, evidence that the anti-sNP antibody detected in this work is related to the serum LE factor commonly associated with the LE cell phenomenon was obtained. The hemagglutination test is helpful in establishing the specific diagnosis of systemic lupus erythematosus (SLE) and may be used to follow the course of the disease and response to therapy in SLE patients, as this is a semiquantitative technic and rise or fall in titer or antibody can be determined.

Antibodies↗

Clinicopathologic study of lupus nephritis.

Needle biopsies of kidney were done in 35 cases of systemic lupus erythematosus (SLE) with renal lesions. The lupus nephritis were classified according to WHO classification and were correlated with response to therapy and prognosis. Detailed clinical features, routine haematological, biochemical tests (e.g., serum urea, creatinine, total protein and albumin, cholesterol, etc), examination of urine (degree of proteinuria and cells) and occurrence of various auto-antibodies e.g., antinuclear antibody (ANA), anti double stranded DNA (anti DsDNA) by enzyme immunoassay (EIA) method, LE cells and rheumatoid factor (RF) were studied in all cases. Clinically hypertension was present in 19 (54.3%) cases and nephrotic range of proteinuria was detected in 20 (57.2%) cases. ANA was found in 31 (88.5%) cases, anti DsDNA 24 (68.5%) and LE cells were detected in 25 (71.5%) cases. RF was detected in 2 (5.7%) cases. Histologically the most frequent lesions were class IV occurring in 15 cases (42.8%) with initial complete remission achieved only 4 cases by immunosuppressive therapy. Active lesions were also most frequent in this class. Class III lesions were found in 8 (22.8%) cases with 6 cases had complete remission. The best prognosis was noted in class II cases with 4 out of 5 (14.3%) cases had complete remission. Class V lesions were found in 6 (17.2%) cases with complete remission achieved in 3 cases. Only one patient presented with class VI lesion. RF positive cases had milder renal lesions.

Adolescent↗

Diagnosis of systemic lupus erythematosus in an elderly male by pericardial fluid cytology: a case report.

Although pleural and pericardial effusions are common and may rarely be the initial manifestation of disease, there are few reports of SLE diagnosed in a cytopathology laboratory. We describe an unusual case of SLE in a 75-year-old man who presented with cardiac tamponade. Cytologic examination of the pericardial fluid revealed numerous LE cells and led to the diagnosis of SLE. This case illustrates the importance of careful evaluation of a serous effusion for LE cells in patients of either gender and of any age.

Aged↗

Antilupus activity of copper (II).

Collagen-like syndrome was induced in rats by oral hydralazine administration during 5 months. After 4 months, a subgroup of rats was shifted from the standard diet to the diet supplemented with copper (II) (60 micrograms of copper per g of pellet) as copper sulphate. A decreased serum copper concentration was noted, LE cells were observed in the blood of 75% of rats fed with standard diet. In the subgroup of copper supplemented rats, the LE cells were observed in 40% of rats only. The activity of superoxide dismutase, the antioxidative copper-dependent enzyme, was significantly lower in erythrocytes of rats fed with standard diet, than the activity in rats fed with copper supplemented diet. These results are briefly discussed.

Animals↗

An uncommon presentation of systemic lupus erythematosus.

A patient who had discoid facial lesion for 10 years developed a right sided pleural effusion in which LE cells were demonstrated. The case is reported due to progression of DLE into SLE after a long interval and rare occurrence of LE cells in pleural fluid.

Adult↗

Canine systemic lupus erythematosus. Transmission of serologic abnormalities by cell-free filtrates.

The presence of viruses was sought in a colony of dogs bred from parents with systemic lupus crythematosus (SLE). Cell-free filtrates prepared from the spleens of these animals were injected into newborn dogs, mice, and rats. The canine recipients developed antinuclear antibody (ANA) and positive lupus erythematosus (LE) cell tests: ANA and, in some cases, antinative DNA antibodies were produced by the murine recipients: no abnormalities were detected in the rats. Serial passage of spleen cells or cell-free filtrates of spleen tissue in syngeneic mice reduced the time required for appearance of ANA from 9 to 4 mo. Some murine recipients of the canine filtrate developed malignant lymphomas. Murine leukemia viruses were identified in these tumors by electron microscopic, virologic, and serologic technics. These neoplasms, but not other tumors known to contain murine leukemia viruses, were associated with the production of ANA. Puppies inoculated with the canine filtrate-induced mouse lymphoma developed ANA and positive LE cell tests within 4 mo. THE RESULTS WERE INTERPRETED TO INDICATE THE PRESENCE IN CANINE SLE OF A VIRUS CAPABLE OF: (a) inducing the serologic abnormalities of SLE in normal dogs and mice: (b) activating latent murine leukemia viruses: and (c) spreading by both horizonal and vertical routes.

Animals↗

Evaluation of 125I-DNA for detecting anti-DNA antibodies in the diagnosis of systemic lupus erythematosus.

A 125I-DNA preparation for the detection of human anti-DNA antibodies (ADA) was evaluated as a diagnostic test for systemic lupus erythematosus (SLE). A normal range of 0-25 U/ml was established. Serum ADA level greater than 110 U/ml were diagnostic in clinically active SLE and levels greater than 45 U/ml were found in 75% of patients with inactive disease. This value was significantly greater than that found in rheumatoid arthritis, renal disease caused by non-immune mechanisms, post-streptococcal glomerulonephritis and a miscellaneous group of disorders comprising connective tissue diseases, auto-immune disorders and chronic active hepatitis. Anti-nuclear factor (ANF) titres greater than 1/160 and LE cells were found in 85% of these patients. In inactive disease the ADA levels ranged between 25 and 98 U/ml, ANF titres varied from 1/40 to 1/640, and LE cells were detected in only 20% of the cases. In 3 patients investigated during the course of the disease, the ADA levels correlated best with clinical improvement. Two patients with apparent active lupus nephritis showed intermediate ADA levels, which were probably caused by antigen-antibody formation and immune complex deposition in the kidneys.

Adolescent↗

Antibodies to new cytoplasmic autoantigens: anti-JA, a potential marker for disease activity in systemic lupus erythematosus.

1. We describe new autoantibodies which recognize two cytoplasmic proteins of 30 and 26 kDa. They were detected by Western blot analysis in the sera of 6 of 79 randomly selected systemic lupus erythematosus (SLE) patients and are denoted anti-JA antibodies. This antibody specificity is different from the previously described lupus autoantibodies, anti-P and anti-S10. 2. The targeted autoantigens are trypsin sensitive, and resistant to RNase and DNase treatment. The binding to the antigens was not modified when reticulocyte ribosomes were prepared with protease inhibitors indicating that these are primary antigens and not degradation products. Several lines of evidence suggest that these proteins are almost certainly part of the ribosome. 3. Anti-JA reactivity was not observed in the sera from 60 patients with other autoimmune diseases or from normal individuals. In contrast, 55% of lupus sera selected for a high titer of anti-dsDNA (double stranded DNA) and LE cells were also anti-JA positive. 4. Anti-JA antibodies may be useful as a specific serological marker for disease activity in SLE. The strong association with anti-dsDNA antibodies and LE cell in the sera of SLE patients requires further study.

Antibody Specificity↗

Antinuclear antibody testing.

The ANA test is an excellent screening test for patients with SLE and a few other connective tissue diseases. The LE cell preparation is an assay that is subjective and costly. Because of the presence of a superior screening test (the ANA) and superior specific auto-antibody tests, the author recommends that the use of LE cell preparations be discontinued. ANA screening tests may be performed either by indirect microscopic serology (usually IFA) or EIA. The latter technique is readily automated and many new products for this screening test have appeared in the past decade. The products differ, however, and laboratories are cautioned to test each in the context of the clinical needs of their clinicians. Proper use of the ANA test requires each laboratory to determine the cutoff used under their conditions of assay. Although either ANA screening test has a high negative predictive value in numerous studies, proper selection of patients to be tested is key to improving the predictive value of a positive result. The American College of Rheumatism criteria are reviewed and recommended as part of the patient selection process for this testing.

Antibodies, Antinuclear↗

Discordance between red cell and saliva Lewis phenotypes in patients with hydatid cysts.

Patients with hydatid cysts and controls of the same Tunisian area were typed for ABO, Lewis and secretor phenotypes. A high incidence of red cell Le(a-b-) phenotype (34-37%) was found among hydatid cyst patients as compared to normal controls (13-16%). However, a large proportion of the patients with Le(a-b-) red cell phenotype had discordant red cell and saliva Lewis phenotypes since they secreted Lea and/or Leb antigens in saliva. In addition, 1 patient with Le(a+b-) red cell phenotype secreted Leb antigen in saliva. The remaining patients and all the controls had concordant red cell and saliva Lewis phenotypes. The discordant results between the phenotypes obtained in serum and saliva of hydatid cyst patients are probably the consequence of a decrease in the concentration of the circulating Lewis glycosphingolipids, secondary to the disease.

ABO Blood-Group System↗

[Three cases presenting with systemic lupus erythematosus and minimal change nephrotic syndrome].

Three cases presenting with systemic lupus erythematosus (SLE) and minimal change nephrotic syndrome (MCNS) are reported in this paper. All cases were female; they abruptly developed nephrotic syndrome at the age of 30, 11 and 23 years, respectively. In Case 1, the diagnosis of SLE was based on fever, butterfly rash, Raynaud's phenomenon, leukopenia, lymphopenia, hypocomplementemia, a high titer of anti-DNA antibodies, positive DNA and LE test, and the presence of anti-nuclear antibodies (speckled pattern). In Case 2, the diagnosis was based on butterfly rash, central nervous system involvement, lymphopenia, hypocomplementemia, a positive LE cell phenomenon, a high titer of anti-DNA antibodies and a positive DNA test. In Case 3, the diagnosis was based on photosensitivity, alopecia, lymphopenia, hypocomplementemia, a high titer of anti-DNA antibodies, a positive DNA test and a positive LE cell phenomenon. In these three cases, initial symptoms were puffy face and pretibial edema which occurred suddenly. These symptoms disappeared completely after either corticosteroid therapy or a combination therapy using corticosteroids and immunosuppressive drugs. These patients took a favorable course and no aggravation was noted in the findings of urinalysis and renal functions. In two of these cases, the diagnostic criteria for SLE were satisfied, but the remaining patient fulfilled only three criteria except for renal disorder. In each of these cases, minor glomerular abnormalities were disclosed by renal histology. It seems likely that SLE was complicated by MCNS in these cases. From these cases, it is suggested that there is a possibility of immunological abnormalities associated with SLE and MCNS.

Adult↗

Seronegative systemic lupus erythematosus.

The diagnosis of systemic lupus erythematosus (SLE) often depens on positive tests for antinuclear antibody, LE cells, and antibody to DNA. In fact, the presence of such serological markers is virtually required for the diagnosis of active disease. This report describes 5 well-studied patients with SLE who initially presented with negative serology despite active multisystemic disease. When followed from 10 months to 7 yr, negative serologic markers, including the ANA, LE cell test, and anti-DNA were seen to change from negative to positive, analogous to the seronegative rheumatoid patient who may become seropositive. In a few cases of lupus, therefore, negative serologic tests do not always exclude SLE, and serial testing at periodic intervals may be indicated.

Adult↗

Glomerulonephritis in procainamide induced lupus erythematosus: report of a case and review of the literature.

A 61-year-old man developed clinical lupus syndrome with positive antinuclear antibody, positive lupus erythematosus (LE) cell preparation, and diffuse proliferative glomerulonephritis following 26 months of procainamide therapy. He was treated sequentially with prednisone and azathioprine (2 weeks), decreasing doses of prednisone alone (21 months), and no immunosuppressive drugs (10 months). Coincidental with this treatment, the immunopathology of the glomerulonephritis improved dramatically, dramatically, renal function returned almost to normal, and both antinuclear antibody and LE cell preparation became negative. The course of this patient's renal disease contrasts sharply with diffuse proliferative glomerulonephritis of idiopathic systemic lupus, and suggests that this rare complication of procainamide therapy may have a favorable course.

Azathioprine↗

Serology and immunoglobulin profile in rheumatoid arthritis.

One hundred and twenty cases of clinically diagnosed rheumatoid arthritis, 80 non-rheumatoid cases suffering from various other diseases and 40 healthy individuals were investigated for the presence of rheumatoid factor, quantitation of serum immunoglobulin, demonstration of ANA and LE cell phenomenon. Microlatex agglutination test of serum for rheumatoid factor showed 56.6% positivity in rheumatoid group and 3.7% positivity in non-rheumatoid group. All three serum immunoglobulins (IgG, IgM, IgA) were raised in serum in significant titre in cases of rheumatoid arthritis, whereas only IgA lever was elevated in the group of non-rheumatoid diseases. ANA and LE cell phenomenon were observed in 11.7% and 4.4% cases of rheumatoid arthritis who had severe underlying disease. In non-rheumatoid group, only one of 6 cases of systemic lupus erythematosus showed rheumatoid factor and that too in an insignificant titre (less than 1:20). Synovium and synovial fluid contained plenty of plasma cells and lymphocytes. It has been observed that RF appears first in synovial fluid and it may take several months to a year to attain detectable level in serum.

Adolescent↗

Serodiagnosis and immune profile in rheumatoid arthritis.

One hundred and seventy-five cases of clinically diagnosed rheumatoid arthritis, 82 non-rheumatoid cases suffering from various other diseases and 40 healthy normal controls were investigated for detection of rheumatoid factor, quantitation of serum immunoglobulin, demonstration of antinuclear antibody (ANA) and LE cell phenomenon. Microlatex agglutination test of serum for rheumatoid factor (RF) showed 64% positivity in rheumatoid group and 1.2% positivity in non-rheumatoid group. All three immunoglobulins (IgG, IgM, IgA) were found to be raised in serum of patients with rheumatoid arthritis, whereas only IgA level was elevated in serum of patients with non-rheumatoid diseases. ANA and LE cell phenomenon were observed in 3.4% and 2.8% cases respectively in cases of clinically diagnosed rheumatoid arthritis who had been suffering from severe active rheumatoid arthritis. In non-rheumatoid group RF was positive in significant titre in only one case of leprosy. Synovial fluid and synovium were found to be heavily infiltrated by plasma cells and lymphocytes. RF appears first in synovial fluid and then in serum. Hence RF titre in blood may not attain significant level for the first several months.

Antibodies, Antinuclear↗