Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The PHA and MLC reactivity of lymphocytes from patients with cancer, SLE or renal allografts was comparatively tested in the presence of autologous and of normal homologous serum. Sera from patients with advanced cancer, active SLE or chronic allograft rejection strongly inhibited the MLC reactivity of autologous lymphocytes. It is suggested that serum inhibitory factors might be antibodies which are directed against modified antigenic determinants of the major histocompatibility complex, and are capable of blocking T lymphocyte receptors.
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PMID:Comparison of lymphocyte reactivity in patients with cancer, systemic lupus erythematosus and renal allografts. 12 68

A naturally occurring T-lymphocytotoxic autoantibody (Hu-NTA) in serum from a patient with systemic lupus erythematosus (SLE) showed a differential cytotoxic effect on functionally different T cell subsets as did natural thymocytotoxic autoantibody (NTA) of NZB mice. When the normal peripheral blood lymphocytes were treated, in the presence of complement, with Hu-NTA at a dilution that eliminated 25 to 30% of Hu-NTA-sensitive T cells, there was a marked reduction or a total depletion in the ability of resultant cells to show Con A-activated suppression on the proliferative response of responder cells in mixed lymphocyte reaction. The treatment of PBL in the same manner also resulted in a marked reduction in its responsiveness to Con A and PHA. However, the responder cells to allogeneic stimulator cells in MLR were found to be much more resistant to the cytotoxicity of Hu-NTA than other functional T cell subsets tested. These results suggest that Hu-NTA is responsible for the selective loss of certain functional T cell subsets including suppressor T cells in patients with SLE.
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PMID:Differential sensitivity of functional subsets of T cells to the cytotoxicity of natural T-lymphocytotoxic autoantibody of systemic lupus erythematosus. 15 30

Administration of thymosin fraction V to NZB/NZW F1 mice, an animal model for human SLE, accelerated the appearance of proteinuria and anti-nDNA antibodies, increased deposition of immunoglobulins in kidneys, and significantly shortened survivals. Although the addition of thymosin to in vitro cultures of spleen and lymph node cells from thymosin-treated mice increased DNA synthesis in response to stimulation with Con A, in vivo treatment with thymosin did not affect the Con A response. There was no effect on in vitro responses to PHA or LPS, or on IgM antibody formation to SRBC (T cell dependent) or SSS III (T cell independent) immunizations. Antibodies to thymosin or contamination of our thymosin preparations with nucleic acids could not be demonstrated. The acceleration of autoimmune disease produced by thymosin treatment could not be explained by alteration of the T and B cell functions studied.
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PMID:Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice. III. Acceleration of disease by thymosin. 30 81

Two patients with systemic lupus erythematosus complicated with lupus nephritis were treated with levamisole, an immunomodulator. Clinical features, including urinary protein excretion and creatine clearance, were restored in one patient, also immunoparameters such as ANA, Ig-bearing cell number and PHA-skin test. The other patient did not respond to levamisole but did respond to cyclophosphamide.
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PMID:Levamisole in systemic lupus erythematosus. 31 48

Levamisole, a drug initially used for its antihelminthic properties has been recently emphasized when Renoux proved its immunostimulating effects in mice en 1971. Since this date, numerous publications concerned the immunological activity of this drug in animals and men. These come to the conclusion that levamisole is capable of restoring cellular immunity as demonstrated by clinical and biological tests (restoration of delayed skin hypersensitivity, increase of the percentage of rosette forming cells and PHA transformed cells). In men, its seems possible to confirm the therapeutic activity of this molecule in a wide range of disease with suspected or proven immunological deficiency. In different forms of cancer, when most of the tumor volume is first reduced, levamisole therapy significantly increases both remission and survival. In auto immune diseases (rheumatoid arthritis, systemic lupus erythematosus), levamisole seems to be strikingly effective. In viral infections (zoster, recurrent herpes, aphthous stomatitis) levamisole is able to reduce the duration of outbreaks and prolong the disease free interval. Finally, encouraging results have been obtained in patients with lepromatous leprosis. Other conditions, where an immunological deficiency is suspected are under study with levamisole therapy. This low molecular weight synthetic drug is perhaps the first pharmacological agent which acts on the host defense mechanisms.
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PMID:[Levamisole, stimulant of the immune system in animal and man (author's transl)]. 32 37

The mechanism of poor lymphocyte transformation to mitogens was studied in selected patients with rheumatoid arthritis and systemic lupus erythematosus. Low lymphocyte response to PHA and Con-A in media containing autologous and homologous sera was usually associated with poor response to the calcium ionophore A23187, which induces blastogenesis by a different mechanism. The low lymphocyte response to mitogens in patients with rheumatoid arthritis could be restored by in vivo treatment with the anthelmintic drug, levamisole. The present findings suggest that intrinsic defects are responsible for the decreased cellular response in patients with rheumatoid arthritis and systemic lupus erythematosus.
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PMID:Decreased lymphocyte response to PHA, Con-A, and calcium ionophore (A23187) in patients with RA and SLE, and reversal with levamisole in rheumatoid arthritis. 34 4

DNA synthesis by peripheral lymphocytes from active non-treated SLE patients and matched normal donors was assessed at various times after stimulation with high and low doses of PHA, PWM and ConA and in non-stimulated control cultures. The time response curve of SLE lymphocytes stimulated with a suboptimal dose of PHA, and with both optimal and suboptimal doses of PWM and ConA was markedly depressed, while their spontaneous DNA synthesis was significantly increased. Preincubation of the cells to remove putative coating antibodies did not revert the response of patients' lymphocytes to normal values. The antibody-induced cell-mediated lysis of 51Cr-labelled chicken results demonstrate that cellular factors contribute to the depressed in vitro responses in active SLE, suggesting a wide defect of lymphocyte populations in this disease.
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PMID:Autoallergic states. Tumor immunology. Impaired function of peripheral lymphocytes in systemic lupus erythematosus. 59 Nov 6

Methodological problems which affect the assessment of humoral effects on mitogenic reactivity include: (1) the source and concentration of serum used to support cell cultures; (2) the day to-day variability of inhibitory effects and (3) the specific activity of [3H]thymidine added to the culture. These problems were alleviated by addition of half concentration (7-5%) of pooled normal human serum to all cultures, the intoruction of anti-lymphocyte serum as a suitable internal control for monitoring the suppressability of lymphocytes and a reduction of specific activity of the [3H]thymidine to 1-3 C2/mM. Inhibitory factors were loosely bound to the lymphocyte surface and eluted off after incubation at 37 degrees C for 1 hr. Cells from twenty-five subjects and paired controls were cultured simultaneously in medium containing either 15% normal human serum (NHS) or 7-5% patient and 7-5% NHS. The cells were stimulated with various dilutions of phytohaemagglutinin, Con A or pokeweed mitogen. Lupus serums suppressed the reactivity of autologous lymphocytes to PHA and pokeweed mitogen. Serums from subjects with RA and scleroderma did not significantly inhibit blastogenesis of autologous lymphocytes. One-half of the lupus serums significantly inhibited the reactivity of homologous lymphocytes to two of three mitogens. Only one of eight scleroderma serums and none of twelve RA serums and none of twelve RA serums had this effect. All patients serums were examined for antilymphocyte antibodies by microcytotoxicity and immunofluorescent techniques. These antibodies were usually found in SLE, and were often observed in subjects with rheumatoid arthritis but not scleroderma. A firm relationship between serum suppressors of lymphocyte blastogenesis and anti-lymphocyte antibodies was not found.
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PMID:Serum effects of mitogenic reactivity in subjects with systemic lupus erythematosus, rheumatoid arthritis and scleroderma. Technical considerations and lack of correlation with anti-lymphocyte antibodies. 84 43

Peripheral blood lymphocytes of thirty normal volunteers and fifty-two patients with systemic lupus erythematosus were fractionated using a discontinuous (5-30 percent) Ficoll gradient. Such fractionation permitted the isolation, identification of study of null cells, T cells and B cells. Patients with inactive SLE were found to have a cell distribution and responsiveness to PHA, Con A and Pokeweed mitogen (PWM) similar to controls. In contrast, patients with active SLE showed a significant decrease in T-cell fractions as well as a relative increase in null cells, a normal distribution of B cells, a marked reduction in responsiveness to Con A, a lesser reduction to PHA and only a minor reduction to PWM. With increasing disease activity, the number of null cells increased despite lymphopenia. Spontaneous lymphocyte transformation was observed in patients with SLE. This occurred predominantly in the fractions enriched in B cells and was observed both early (0-16 hr) and late (68-72 hr) in the lymphocyte cultures. The method of discontinuous Ficoll gradients is both versatile and reproducible with good correlations between isolated lymphoid subpopulations and disease activity.
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PMID:Study of lymphocyte subpopulations in normal humans and patients with systemic lupus erythematosus by fractionation of peripheral blood lymphocytes on a discontinuous Ficoll gradient. 108 53

Cellular-mediated immunity was examined in 6 consecutive patients with active SLE, 6 patients with low active SLE 6 patients with DLE, 8 patients with other collagen diseases, and 9 healthy controls. The following parameters were measured: delayed hypersensitivity, in vitro lymphocyte blast transformation, and MIF production after stimulation with five common antigens, DNA, and two nonspecific mitogens (PHA, PWM). The 6 active SLE patients were anergic and had a markedly depressed response in vitro to the specific antigens and PWM (P less than 0.001). When CMI was retested in 5 patients as early as 5 days after the start of prednisone (60 mc/day), the results were significantly improved in 4 who also improved clinically, and they remained unchanged in a fifth patieht who failed to improve. There was a less marked impairment of CMI among the low active SLE group, whereas the DLE and OCD patients did not differ significantly from the control subjects. DNA did not cause significant stimulation of blast transformation in any of the study groups.
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PMID:Depression of cellular-mediated immunity in systemic lupus erythematosus. relation to disease activity. 109 20


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