Abstract

Background: SLE is characterized by abnormalities in T helper and supressor cell function, possibly due to a dysfunction in the T cell receptor complex. A decreased in vitro production of IL-2 and defective proliferative responses by T lymphocytes have been shown in adult patients. Similar data are not available for children. The duration of disease is shorter in children with SLE, thus, we proposed the hypothesis that the defective proliferative responses seen in adults would not be found in children. Methods: We obtained data from 8 children with active SLE and control data from adults and age-matched children without SLE. Peripheral blood lymphocytes from patients and controls were stimulated with antibodies directed at the T cell receptor complex and costimulator molecules. Four sets of data were obtained using the following antibodies: 1) anti-CD3(OKT3), which directly stimulates the T cell receptor complex, 2) anti-CD3 with IL-2, used to correct an IL-2 defect that was found previously in adults, 3) OKT3+anti-CD28(9.3) to stabilize the mRNA for IL-2, 4) OKT3+anti-CD45(9.4), a factor which plays a role in signal transduction. We also performed reverse transcriptase/PCR to determine if mRNA for IL-2 was being made in all of the above groups. Results: No significant differences were found between the patients (PT) and the controls(Cont). (BL PT=3172±1997, Cont=3269±1702; OKT3 PT=188305±132548, Cont=125644±78520; OKT3+IL-2 PT=258636±51591, Cont=234000±59319; OKT3+9.3 PT=209484±129630, Cont=234485±106213; OKT3+9.4 PT=463577±192609, Cont=446091±278407). The mRNA for IL-2 was found in all the patient groups as well as the controls. Conclusions: We conclude that children with SLE do not have defective lymphocyte proliferation with stimulation using OKT3 and anti-CD28 or anti-CD45. The mechanisms for T cell activation through the T cell receptor complex appear to be intact in children with SLE.

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