Natural cytotoxicity in rheumatoid arthritis and systemic lupus erythematosus

Karsh, Jacob; Dorval, G.; Osterland, C. K.

doi:10.1016/0090-1229(81)90086-6

Cited by 59 publications

(30 citation statements)

References 27 publications

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“…Our findings differ from those of Morgenstern and Machtey ( I ) as well as from those of Sirnkin ( 2 ) ; however, our results are similar to those of Menkcs et a1 (6) and Ambanelli (7).…”

Section: Zinc and Rheumatic Diseasecontrasting

confidence: 50%

Natural killer cells and the pathogenesis of systemic lupus erythematosus

Schattner

Duggan

1984

Arthritis & Rheumatism

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LETTERSprednisone, new skin lesions and tense bilateral knee effusions were noted; bilateral knee corticosteroid injections were given and Dapsone was restarted (100 mglday). On November 18, 1983 she developed severe epigastric pain which prompted another admission. She had new bullous lesions around the elbows, was in diabetic ketoacidosis, and her abdomen was tender. When abdominal radiographs demonstrated free air under the diaphragm, surgical exploration revealed a perforated duodenal ulcer. She recovered uneventfully, receiving parenteral corticosteroids to an equivalent of 120 mg of prednisone initially, and was discharged 10 days later receiving 60 mg/day of prednisone as well as insulin to control her diabetes. She received no Dapsone during this hospitalization.On December 4, 1983 she was readmitted because of a worsening skin condition and development of new joint pain 2 days before, for which Dapsone (100 mg/day) and Plaquenil (200 mg twice a day) had been started. Soon thereafter, she developed new skin lesions. She also presented some behavioral changes which could not be related to hypoglycemia. The diagnosis of central nervous system lupus was considered, but her neurologic evaluation results were normal as were an electroencephalogram and a lumbar puncture. Prednisone was continued at the same dose, but Plaquenil and Dapsone were discontinued since it was impossible to determine if the behavioral changes were in any way related to either of these medications. Two days later Dapsone was restarted. She rcceived 1 dose that evening; by midnight she had severe itching, erythema, and bullae around her elbows, forearms, and knees. She received her next dose of Dapsone the following morning and by midday had more skin lesions. Dapsone was discontinued and prednisone was maintained at the same dosage. Over the next few days the skin lesions rapidly cleared. She was discharged 3 days later with marked improvement of her skin. As of now, her prednisone dosage has been tapered to 45 mg/day, and she has remained free of new skin lesions.Although during the first 2 instances it was not completely clear that the worsening of the skin lesions was related to the use of Dapsone, during the third attemptwhile she was in the hospital-the relationship between its use and the worsening of her skin lesions was unquestionable. A very severe dermatitis which can be bullous in nature has been described as a possible side effect of this sulfa derivative product (Dapsone, Physician's Desk Reference. Thirty-seventh edition. Oradell, NJ, Medical Economics Co., 1983, pp 1021-1022). Therefore, we want to call the attention of the practicing rheumatologist to this side effect which can be mistaken as a failure to respond to the initial dose.

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“…Our findings differ from those of Morgenstern and Machtey ( I ) as well as from those of Sirnkin ( 2 ) ; however, our results are similar to those of Menkcs et a1 (6) and Ambanelli (7).…”

Section: Zinc and Rheumatic Diseasecontrasting

confidence: 50%

Natural killer cells and the pathogenesis of systemic lupus erythematosus

Schattner

Duggan

1984

Arthritis & Rheumatism

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“…Similar results were obtained when Tac+ cells were enumerated by monoclonal antibody rosetting (data not shown). In related experiments, the addition of exogenous IL-2 on day 0 or day 1 dramatically enhanced maximum day 5 [3H]TdR incorporation in control cultures but only partially restored the response in SLE serumcontaining cultures (Fig. 7).…”

Section: Methodsmentioning

confidence: 82%

“…In brief, plastic adherent macrophages (>85% esterase+) were harvested with a rubber policeman, resuspended at a density of 1 X 105 cells/ml in medium containing 6.0 Ag/ml tetanus toxoid and either normal AB serum or SLE serum, and incubated for 18 h in 95% air, 5% CO2 at 370C. The antigen-pulsed macrophages were then washed three times with RPMI 1640, recombined with 2 X I0W T cells (<1% esterase+), purified by passage over nylon wool columns, and cultured in the usual fashion for 5 Preparation ofserum Igfractions. IgG (7S) and IgM (19S) frastions were obtained from serum by sucrose density gradient ultracentrifuigation using acid buffers (glycine-Ha, pH 3.0) as described previously (37).…”

Section: Methodsmentioning

confidence: 99%

“…Many immune system functional abnormalities are recognized in systemic lupus erythematosus (SLE),' including defective T cell proliferative response to various specific and nonspecific stimuli (1)(2)(3)(4); impaired natural killer (5,6), antibody-dependent (7,8) and T cell-mediated (9, 10) cytotoxicity; failure of suppression in multiple systems (11)(12)(13)(14)(15); increased numbers of spontaneously activated B (13,(16)(17)(18) and T (19,20) cells; and decreased pokeweed mitogen-driven Ig production (13,18 (21), which carry over to in vitro experiments.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of soluble antigen-induced T cell proliferation by warm-reactive antibodies to activated T cells in systemic lupus erythematosus.

Yamada¹,

Winfield²

1984

J. Clin. Invest.

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bstract. One of the fundamental immunologic characteristics of systemic lupus erythematosus (SLE) is a depressed T cell proliferative response to various specific and nonspecific stimuli. Both intrinsic cellular defect(s) and inhibitory influences of humoral factors, e.g., antilymphocyte autoantibodies or immune complexes, have been postulated to underly this functional abnormality. Because patient serum can induce SLE-like T cell dysfunction in normal cells, an extrinsic mechanism is probably responsible, but the nature and site of action of this humoral activity has not been defined. This laboratory recently described a novel antibody specific for activated T cells in SLE, which raised the possibility that suppression of T cell proliferation by SLE serum involved antibodies directed to surface determinants expressed during the process of activation. In experiments to examine this concept further, relatively warm-reactive antibodies to T cell blasts were found to inhibit strongly the well-characterized T cell response to tetanus toxoid. These antibodies were distinct from conventional cold-reactive IgM antibodies to resting T cells, which exhibited little inhibitory activity. Inhibition involved noncytotoxic effects on early activation events at the level of the responding T cell, which markedly reduced the expression of receptors for interleukin 2. Inhibitory effects on antigen-pulsed macrophages or on T cells already committed to proliferate were not demonstrable. Anti-T blast antibodies were characteristic of active SLE and were detected only occasionally in Address reprint requests to Dr. Winfield.

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“…Antilymphocyte antibodies (4) and immune complexes (8) have been implicated in depressed NK function in some SLE patients. However, recent studies have demonstrated that the percentage of target binding cells is not decreased in SLE (9,lO).…”

Section: Impaired Release Of a Soluble Natural Killer Cytotoxic Factomentioning

confidence: 99%

Impaired release of a soluble natural killer cytotoxic factor in systemic lupus erythematosus

Sibbitt

Mathews

Bankhurst

1984

Arthritis & Rheumatism

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Disease states characterized by abnormalities in immune regulation often demonstrate concomitant abnormalities in cytotoxicity mediated by natural killer (NK) cells. For example, some patients with systemic lupus erythematosus (SLE) have depressed NK activity despite the presence of normal numbers of effector cell:target cell conjugates. This study was designed to determine if defects in NK cell function were directly related to impaired release of a soluble cytotoxic factor. NK activity of peripheral blood mononuclear cells and large granular lymphocytes was measured using "Crlabeled K562 target cells in 4 l o u r release assays. The SLE patients had significantly decreased NK activity relative to normal controls. However, the number of effector eelktarget cell conjugates was not different in SLE patients versus control subjects. The release of a soluble natural killer cytotoxic factor (NKCF) by peripheral blood mononuclear cells was measured by cytotoxicity induced in K562 cells. NKCF was released preferentially by suspensions enriched in NK cells (large granular lymphocytes). At a 1:l dilution, NKCF release was significantly lower in SLE patients than in controls. The release of NKCF correlated well with NK activity. Thus, this study shows that the defect in NK cell activity in SLE patients may be related to an impairment in release of a soluble cytotoxic factor with specificity for NK celknsitive targets.

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Natural cytotoxicity in rheumatoid arthritis and systemic lupus erythematosus

Cited by 59 publications

References 27 publications

Natural killer cells and the pathogenesis of systemic lupus erythematosus

Natural killer cells and the pathogenesis of systemic lupus erythematosus

Inhibition of soluble antigen-induced T cell proliferation by warm-reactive antibodies to activated T cells in systemic lupus erythematosus.

Impaired release of a soluble natural killer cytotoxic factor in systemic lupus erythematosus

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