Studies of immune functions of patients with systemic lupus erythematosus. T-cell subsets and antibodies to T-cell subsets.

The contribution of immune regulation to the etiology of systemic lupus erythematosus (SLE) is poorly understood. Using the monoclonal antibodies OKT4 and OKTS, we quantitated, by flow cytometry, T inducer/ helper and T cytotoxicfsuppressor cells in patients with SLE. Serologically active patients, who had clinical manifestations such as arthritis or rash and were not receiving prednisone, were characteristically lymphopenic due to a marked reduction in OKT4+ cells. Prednisone therapy produced the same phenomenon. Untreated patients, who were serologically inactive, demonstrated no abnormalities. These studies have thus revealed two presumably independent factors that can produce similar immunoregulatory aberrations.Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by excessive immunoglobulin and autoantibody production. Although B cell function is increased, T cell functions which include delayed hypersensitivity (1-3, mitogenic reactivity (6,7), generation of antigen-specific reactivities (8), and development of nonspecific suppressor (14).We studied 28 patients with SLE who were divided into groups based on corticosteroid therapy and serologic evidence of disease activity. We will describe clinically significant abnormalities in the absolute number and relative proportions of immunoregulatory T cell subsets based upon this classification. PATIENTS AND METHODSPatients. This study included 28 patients (24 females, 4 males) with SLE according to the American Rheumatism Association ( M A ) preliminary criteria (15). Two to 3 patients were randomly selected in the lupus clinic visits each month from April 1981 to April 1982. These patients were then separated into 2 groups based on existing therapy, one receiving more than 10 mg prednisone per day, the other receiving 10 mg or less of prednisone per day. A special attempt was made to isolate newly diagnosed lupus patients being treated with 10 mg or less prednisone per day. During this 1-year period, 11 newly diagnosed patients were seen, but only 6 had 4 or more ARA preliminary criteria; of these 6, only 5 were treated with less than 10 mg prednisone per day.Control groups consisted of 16 women and 5 men with scleroderma and 16 patients with lepromatous leprosy. They will be described in detail elsewhere. Normal individ-

Section: Discussionmentioning

confidence: 99%

“…activity (9)(10)(11)(12) are depressed. The development of monoclonal antibodies reactive against specific T cell antigens has made it possible to quantitate subsets of T cells with specific immunoregulatory functions such as T inducedhelper cells and cytotoxic/suppressor cells.…”

mentioning

confidence: 99%

T Lymphocyte Subsets in Systemic Lupus Erythematosus

Bakke

Kirkland

Kitridou

et al. 1983

“…The inverse correlation of Con-A-induced suppressor function with disease activity indicates that this defect may be related to the basic underlying dysfunction of SLE and may be somewhat obscured by various other factors resulting from disease activity. These may include lymphocytotoxic (28,29) and antinuclear antibodies (1 3) that damage specific lymphocyte subpopulations causing further disturbance of immunoregulation. The finding of normal Con-A-induced suppressor function in some SLE patients could be explained by the interaction of various factors, the algebraic sum of which yielded a positive net regula tion.…”

Section: Discussionmentioning

confidence: 99%

Heterogeneity of the spontaneously expanded and mitogen‐induced generation of suppressor cell function of t cells on b cells in systemic lupus erythematosus

Ruı́z-Argüelles¹,

Alarcón‐Segovia²,

Llórente³

et al. 1980

Several studies have shown that there is decreased suppressor cell function in systemic lupus erythematosus (SLE) (1-9). These studies have used different methods both for the induction of the suppressor cell activity in vitro as well as for the detection and quantitation of suppressor function. Indeed, not all of these reports have dealt with the suppression of T cells on B cells (1,(4)(5)(6)(7)9) or studied its effect on immuno-

“…An additional defect in Tnony cells, perhaps induced by anti-T cell antibodies (25)(26)(27)(28)(29)(30), may further impair T cell control mechanisms, thereby allowing uncontrolled B cell hyperactivity. The failure of B cells from such active SLE patients to stimulate in the autologous MLR may be a related inability of activated B cells to stimulate autologous T cells.…”

Section: Discussionmentioning

confidence: 99%

Studies of immune functions of patients with systemic lupus erythematosus

Sakane

Steinberg

Arnett

et al. 1979

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