Abnormalities in autologous mixed lymphocyte reaction-activated immunologic processes in systemic lupus erythematosus and their possible correction by interleukin 2.
The autologous mixed lymphocyte reaction (AMLR) represents the activation, proliferation and differentiation of T cells in response to signals from autologous non-T cells. Upon stimulation by autologous non-T cells, OKT4+ cells produce interleukin 2 (IL2); cells contained within both OKT4+ and OKT8+ cell populations can also be activated by autologous non-T cells to become sensitive to IL2. Once these activated OKT4+ and OKT8+ cells are exposed to IL2 produced by OKT4+ cells, they will proliferate and go on to differentiate into effector cells. Patients with systemic lupus erythematosus (SLE) have a defect in the AMLR. The ability of OKT4+ cells to produce IL2 in the AMLR is impaired. Upon triggering with autologous non-T cells, their OKT8+ cells become sensitive to proliferative signals of IL2; however, their OKT4+ cells fail to express IL2 receptors. These defects are a consistent feature in patients with SLE. AMLR-induced immunologic processes which require cell interactions between OKT4+ cell subpopulations are not correctable even by the addition of normal IL2. However, the immunologic processes mediated through OKT4+-OKT8+ cell interactions can be corrected with normal IL2. The latter finding suggests that the partial correction of the AMLR-induced immunologic processes with IL2 might lead to suppressed B cell hyperactivity of patients with SLE.
Takada
S
S
Ueda
Y
Y
Suzuki
N
N
Murakawa
Y
Y
Hoshino
T
T
Green
I
I
Steinberg
A D
AD
Horwitz
D A
DA
Sakane
T
T
D000328:Adult; D006801:Humans; D007376:Interleukin-2 / Q000096:biosynthesis / Q000627:therapeutic use*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D007959:Lymphocyte Culture Test, Mixed; D013601:T-Lymphocytes / Q000145:classification / Q000378:metabolism
D007376:Interleukin-2