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)

Patients with active systemic lupus erythematosus (SLE) had a decrease in a subpopulation of cells (fraction D) when peripheral blood lymphocytes were separated on a discontinuous Ficoll gradient. Preincubation of SLE cells at 37 degrees C for 30 min led to a marked decrease in this fraction, composed primarily of thymus-derived (T) cells. Supernates of such preincubations were found to cause a reduction in fraction D cells from normal humans. The active factor in the supernate was found to be an IgG antibody. Similarly, serum from patients with active SLE produced a reduction in fraction D cells from normal donors. This activity was also found in the IgG fraction, and could be absorbed with a pure T-cell population. Depletion of macrophages and complement did not reduce the SLE anti-T-cell antibody-mediated loss of cells from fraction D; however, heat-aggregated human gamma globulin led to impairment of the reaction. These findings suggest that antibody-dependent direct lymphocyte-mediated cytotoxicity may play a role in T-cell lymphopenia of SLE. It was further noted that the SLE anti-T-cell antibodies, in contrast to rabbit antihuman thymocyte serum, recognized fraction D cells but not fraction E cells from normals. Since both fractions are largely T cells, it appeared that the SLE serum was directed against cell-membrane antigenic determinants present on fraction D T cells, which were absent or reduced in quantity on fraction E T cells. Thus, evidence was presented indicating the presence of at least two subpopulations of cells in man. This was supported by differential absorption of the anti-T-cell sera with fractions D and E.
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PMID:Fractionation of cells on a discontinuous Ficoll gradient. Study of subpopulations of human T cells using anti-T-cell antibodies from patients with systemic lupus erythematosus. 5 18

Immunological investigations concerning pathological autoantibodies and defects of humoral immunity were performed in 7 patients with thymomas, 5 of which showed invasive growth. The number of B and T lymphocytes in blood was determined at the same time using membrane markers as well as blood lymphocyte stimulation with phytohaemagglutinine. Two of the 3 patients with auto-antibodies against striated muscles or nuclei showed the clinical signs of accompanying disease (myasthenia gravis, lupus erythematodes). A humoral immunodisturbance with IgM deficiency was demonstrable in one patient and was accompanied by clinical symptoms. Lymphopenia with decreased numbers and functional disturbance of T and B lymphocytes could be shown in the majority of patients. Immunological investigations simplify proof of accompanying diseases in thymomas. These represent an important prognostic criterium in the same way as does invasive growth.
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PMID:[Thymomas (author's transl)]. 30 88

An active subpopulation of T lymphocytes characterized by their ability to form early rosettes with sheep erythrocytes (active E-RBL) was studied in the blood of 50 patients with untreated systemic lupus erythematosus (SLE) and in 50 normal controls. The findings were related to the absolute number of circulating lymphocytes and total E-receptor-bearing lymphocytes (total E-RBL). Lupus patients with active disease had markedly decreased absolute lymphocyte counts, but the decrease of both the total and the active E-RBL surpassed what would be expected from the lymphopenia. Patients with inactive disease had moderately decreased absolute lymphocyte counts with a marked and disproportionate decrease in total E-RBL and a moderate decrease in active E-RBL, which seemed to reflect only the absolute lymphopenia. Patients with active disease had significantly lower active E-RBL than those with inactive disease. The changes of these and other lymphocyte subpopulations in relation to disease activity in SLE may reflect the influence of factors leading to T-cell depletion and immaturity. Circulating thymic products may be one of those factors.
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PMID:T-lymphocyte subpopulation in untreated SLE. Variations with disease activity. 33 83

This review of recent and new directions in clinical immunologic studies of systemic lupus erythematosus (SLE) is restricted to the areas of lymphocyte surface markers, antigen binding lymphocytes, immune complexes, and lymphocyte hyporesponsiveness in lupus patients. First, it is not clear whether the T-lymphopenia observed in SLE is related to viral destruction of T cells, anti-lymphocyte antibodies, or tissue sequestration. Second, the increase in DNA-binding B lymphocytes observed in active lupus patients may be related to minor alterations in the balance of immunoregulatory T cells or to a bypass of DNA-specific helper T cells. Third, it is speculated that the removal of immune complexes which play a role in lupus glomerulitis by various extracorporeal immune absorbents may be important in the future therapy of SLE. Fourth, the mechanisms of T-lymphocyte hypofunction are unexplained. It is postulated from studies done in other diseases that this hypoactivity may be mediated by the secretion of prostaglandin or other humoral agents from one leukocyte subpopulation suppressing another potentially responsive lymphocyte subpopulation. Also an investigation into the lymphocyte subpopulation reactive with virus-infected fibroblasts may be useful in delineating immunoregulatory lymphocytes important in the pathogenesis of SLE.
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PMID:Clinical immunologic studies in systemic lupus erythematosus. 35 65

The clinical details of a five-year-old boy with systemic lupus erythematosus and an inherited deficiency of the fourth component of complement (C4) have been reported elsewhere. In this study of his immune responses, immunization with bacteriophage phi X 174 demonstrated diminished antibody formation, abnormal immunologic memory and failure to switch from IgM to IgG during secondary response. We also noted persistent lymphopenia and reductions in peripheral-blood T lymphocytes, lymphocyte responses to mitogens and allogeneic cells and granulocyte chemotaxis. Kinetic studies revealed that delayed activation of the alternative pathway was corrected by purified C4 only if the classical pathway was not blocked. This finding is consistent with the concept that minute amounts of C3b provided through the classical pathway are necessary to prime the properdin system. Inability to activate the classical complement pathway, abnormal kinetics of alternative-pathway activation and depressed antibody responses to a T-cell-dependent antigen may predispose C4-deficient patients to viral infection or immune-complex formation.
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PMID:Immune response of a patient with deficiency of the fourth component of complement and systemic lupus erythematosus. 43 36

One hundred fifty-eight patients with active, untreated systemic lupus erythematosus (SLE) were studied from the time of diagnosis. Lymphopenia was present in 75%, and another 18% of those patients developed lymphopenia subsequent to disease reactivation. Lymphopenia of less than 1500 cells/microliter occurred more frequently than any of the preliminary criteria for the classification of SLE, and it was the most prevalent initial laboratory abnormality. Lymphocyte counts were significantly lower in lupus than in the other connective tissue diseases except mixed connective tissue disease and polymyositis.
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PMID:Lymphopenia in systemic lupus erythematosus. Clinical, diagnostic, and prognostic significance. 64 28

Four women with fever, arthromyalgias, pericarditis, pleural effusion, high erythrocyte sedimentation rates, and lymphopenia had mitochondrial antibodies in the serum in the absence of antinuclear antibody. Their illness lasted 5-12 weeks and the antibody test results became negative on remission. Absence of specific bacteriological findings, normal antistreptolysin O titres, resistance to antibiotics, and good response to steroids suggested that these cases represented a milder and less persistent form of the syndrome resembling systemic lupus erythematosus described by German authors.
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PMID:Pericarditis, pleural effusion, and pneumonitis with transient mitochondrial antibodies. 107 82

In a prospective study 26 of 29 patients with systemic lupus erythematosus had cold-reactive antilymphocyte antibodies cytotoxic for autologous lymphocytes and lymphocytes from normal subjects. The level of antilymphocyte antibodies was highly correlated, by linear regression analysis, with lymphopenia in these patients. The data suggested that both the avidity and the concentration of these antibodies were important determinants in this relationship. A clear association between increased antilymphocyte antibody activity and exacerbation of SLE was demonstrated. Apart from lymphopenia, however, neither type of clinical manifestation nor any particular serologic abnormality appeared to be related to the presence of antilymphocyte antibodies.
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PMID:Association of cold-reactive antilymphocyte antibodies with lymphopenia in systemic lupus erythematosus. 108 76

Peripheral blood lymphocyte subpopulations determined in 40 patients with systemic lupus erythematosus, revealed significant lymphopenia in comparison to normal controls. The lymphopenia was caused by decreases in the absolute numbers of both T cells and surface immunoglobulin bearing (SIg) cells. There were significant percentage decreases in T cells and normal percentages of SIg cells, resulting in an increased percentage of "null" cells. The lymphopenia was significantly greater in patients considered to have active disease on the basis of clinical parameters, and was strongly correlated with lymphocytotoxic antibodies, DNA antibodies, and hypocomplementemia. The lymphocytotoxic antibodies were reactive with both T and B lymphocytes from normal and ill donors, human organs, and various lymphoblastoid cell lines. In 30 patients who were followed for up to 22 months, the lymphopenia was clearly seen to develop during, but not before, periods of clinical disease activity, independent of changes in therapy.
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PMID:Relationship of lymphocytotoxic antibodies to lymphopenia and parameters of disease activity in systemic lupus erythematosus. 108 29

Phytohaemagglutinin-induced lymphocyte transformation was studied in 19 patients with systemic lupus erythematosus (SLE) in relation to disease activity, peripheral blood lymphocyte count, serum iron and folate levels, and corticosteroid treatment. Similar studies were performed on a group of 28 age- and sex-matched controls and on 10 patients with facial palsy who were examined before and after 7 days of high-dose corticosteroid treatment. The patients with SLE were found to have an impairment of lymphocyte transformation which was most marked in active stages of the disease and associated with a lymphopenia. This depressed transformation, which improved with the development of a remission, could not be attributed to the effects of corticosteroid treatment, inhibitory serum factors, iron deficiency, or any numerical reduction in blood lymphocytes, thus indicating along with evidence from other sources that SLE patients have a defect of cell-mediated immunity. The aetiological implications of these findings are discussed.
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PMID:Relationship of phytohaemagglutinin-induced lymphocyte transformation to disease activity in systemic lupus erythematosus. 108 34


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