Induction of Suppressor T Cells in Systemic Lupus Erythematosus by Thymosin and Cultured Thymic Epithelium

Horowitz, Stuart; Borcherding, Wayne; Moorthy, A. Vishnu; Chesney, Russell W.; Schulte-Wisserman, H; Hong, Richard

doi:10.1126/science.302032

Cited by 175 publications

(61 citation statements)

References 16 publications

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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%

“…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). These findings are consistent with the present studies of the autologous MLR patients with active SLE are defective with regard to all T cell subpopulations studied, whereas those with inactive SLE are abnormal only with respect to Ty cells.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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“…Earlier studies demonstrated that patients with active SLE had a loss of suppressor T lymphocyte function (22)(23)(24)(25)(26)(27)(28). Several studies have emphasized the importance of anti-T cell antibodies in altering T cell number and function in patients with active SLE (7,8,(28)(29)(30)(31)(32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Autoantibody to an Immunoregulatory Inducer Population in Patients with Juvenile Rheumatoid Arthritis

Morimoto¹,

Reinherz²,

Borel³

et al. 1981

J. Clin. Invest.

109

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A B S T R A C T The human inducer (T4+) and reciprocal cytotoxic/suppressor (T5+/T8+) subsets have been defined by monoclonal antibodies. In the present study, we examined the relationship of naturally occurringanti-T cell autoantibodies found in patients with active juvenile rheumatoid arthritis (JRA) to these subsets. In one approach, normal T cells were treated with anti-T4 or anti-T8 to eliminate the corresponding subset of cells and then analyzed for reactivity with JRA sera. It was found that JRA sera were reactive with only 15% of an enriched cytotoxic/suppressor population, whereas they reacted with 37% of an enriched inducer population. In reciprocal studies, JRA+ T cells were eliminated with JRA sera and complement and the residual T cells (JRA-) reacted with monoclonal antibodies and indirect immunofluorescence on a fluorescence-activated cell sorter. As expected, the JRA sera and complement treatment of unfractionated T cells markedly diminished the T4+ subset, whereas there was a concomitant increase in T cells reactive with anti-T5 and anti-T8. A similar diminution in T4+ T cells was found in the circulating peripheral T cell compartment of patients with active JRA who possessed the JRA antibody.Functional studies demonstrated that removal of the JRA+ population of T cells diminished phytohemagglutinin and soluble antigen proliferative responses,

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“…The suppression was no different from that (23,24) as well as T-cell subsets determined by a number of other methodologies (25)(26)(27)(28)(29). This is of particular relevance in light of the fact that in several in vitro systems, SLE has been demonstrated to manifest a deficiency of suppressor cell function (23,(30)(31)(32)(33)(34)(35). Although the actual suppressor cell in most of these systems has not been conclusively identified, at least in some systems of in vitro B-cell function, the TG cell has been demonstrated to be the suppressor cell (16).…”

Section: Resultsmentioning

confidence: 82%