Suppressor function of peripheral blood mononuclear cells in normal individuals and in patients with systemic lupus erythematosus.

Bresnihan, Barry; Jasin, Hugo E.

doi:10.1172/jci108607

Cited by 374 publications

(114 citation statements)

References 23 publications

(22 reference statements)

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“…These cells have been suggested as etiologic or contributory in the pathogenesis of several diseases, including common variable hypogammaglobulinemia (43), IgA deficiency (44), multiple myeloma (45), Hodgkin's disease (11,40,46), and systemic lupus erythematosus (47). Work in this area has been hindered, however, by lack of a suitable assay of suppressor cell activity.…”

Section: Discussionmentioning

confidence: 99%

“…Human suppressor cell activity was shown by adding circulating lymphocytes from patients with those diseases to normal lymphocytes and demonstrating an inhibition of various in vitro T-and B-cell functional assays. More recently, several groups have reported on assays for suppressor cell activity in peripheral blood leukocytes from normal humans (16,24,47). These assays are similar and involve stimulating normal lymphocytes with Con A for 24 h, then adding them to fresh mitogen-stimulated or mixed lymphocyte cultures from the same or different donors.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Suppression of human T-cell mitogenesis by prostaglandin. Existence of a prostaglandin-producing suppressor cell.

Goodwin¹,

Bankhurst²,

Messner³

1977

The Journal of Experimental Medicine

723

120

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Prostaglandins (PGs) I of the E series have been shown to inhibit many in vitro measurements of immune function in experimental animals. These include macrophage inhibitory factor production in guinea pigs (1, 2), direct cytolysis in murine lymphocytes (3), hemolytic plaque formation by murine leukocytes (4), and mitogen-induced stimulation of murine lymphocytes (5). In the human, Lomnitzer et al. (6) have shown that PGEI and PGE2 cause reduction in leukocyte inhibitory factor production by phytohemagglutinin(PHA)-stimulated human lymphocytes. Smith et al. (7) demonstrated significant inhibition of [3H]thymidine incorporation into PHA-stimulated human lymphocytes by PGEI, E2, At, and F~. As in the study by Lomnitzer, the final concentration of PGs was relatively high, I0-~-I0-4M. Ferraris and Derubertis have reported (8) that stimulation of 10 ~ human luekocytes with optimal concentrations of PHA produced -10-8M PGE.These data suggest that PGs of the E series might act as endogenous modulators in human immune reactions. PGEI is produced in the mitogen stimulation of human leukocytes, and may in turn inhibit this stimulation. Thus, data are accumulating to support the hypothesis of Bourne et al. (9) that PGs are important regulators of immune function. One troublesome aspect of the studies on human leukocytes is the great disparity between the amount of PGE produced during mitogen stimulation (~10-SM or 5 ng/ml) and the amount required to suppress mitogen stimulation when added to cultures (~10-5M or 5 pg/ml).In the present paper we describe the effects of lower, more physiologic concentrations of PGs on mitogen stimulation of human lymphocytes and lymphocyte subpopulations. We also describe the effect of PG synthetase inhibitors on mitogen-induced stimulation of these cells. We have identified a population of glass adherent mononuclear cells that suppress T-cell mitogenic activity through production of PGs of the E series.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Suppression of human T-cell mitogenesis by prostaglandin. Existence of a prostaglandin-producing suppressor cell.

Goodwin¹,

Bankhurst²,

Messner³

1977

The Journal of Experimental Medicine

723

120

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“…Thus, the finding of a non-T cell abnormality in the autologous MLR in active but not in inactive SLE patients is consistent with the previous functional studies. T cell defects observed in patients with SLE include impaired delayed hypersensitivity (17,18), reduced responsiveness to stimulation with allogeneic cells and T cell mitogens (19,20), and impaired generation of suppressor T cells (21)(22)(23)(24). SLE patients with active disease are especially predisposed to all of the abnormalities; however, defects in suppressor cell generation have been observed even in patients in remission (23).…”

Section: Discussionmentioning

confidence: 99%

Studies of immune functions of patients with systemic lupus erythematosus

Sakane

Steinberg

Arnett

et al. 1979

Arthritis & Rheumatism

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In normal individuals T cells are stimulated to proliferate by autologous non-T cells; this is called the autologous mixed lymphocyte reaction (MLR). Previous studies demonstrated that such an autologous MLR was markedly impaired in patients with active systemic lupus erythematosus (SLE). To determine whether the defect resided in the responding cell or the stimulating cell, mixing experiments were performed using cells from identical twins. We identified two sets of identical twins discordant for SLE activity and correspondingly discordant in their degree of responsiveness in the autologous MLR. Reciprocal mixing experiments were performed in which T cells from one twin of each pair were mixed with non-T cells from the other twin of that pair. These studies indicated that patients with active SLE

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“…In patients with SLE various autoantibodies due to a B cell hyperactivity (4)(5)(6) and an impairment of T and suppressor cell functions (7)(8)(9)(10) are observed. An association between SLE and HLA-B8 has been reported in several studies (1 1-13).…”

Section: Brief Reportsmentioning

confidence: 99%