Dysregulation of interleukin-10 production in relatives of patients with systemic lupus erythematosus
Article first published online: 12 DEC 2005
Copyright © 1997 American College of Rheumatology
Arthritis & Rheumatism
Volume 40, Issue 8, pages 1429–1435, August 1997
How to Cite
Llorente, L., Richaud-Patin, Y., Couderc, J., Alarcon-Segovia, D., Ruiz-Soto, R., Alcocer-Castillejos, N., Alcocer-Varela, J., Granados, J., Bahena, S., Galanaud, P. and Emilie, D. (1997), Dysregulation of interleukin-10 production in relatives of patients with systemic lupus erythematosus. Arthritis & Rheumatism, 40: 1429–1435. doi: 10.1002/art.1780400810
- Issue published online: 12 DEC 2005
- Article first published online: 12 DEC 2005
- Manuscript Accepted: 17 MAR 1997
- Manuscript Received: 16 JAN 1997
- CONACYT. Grant Number: 0005PM
Objective. To evaluate interleukin-10 (IL-10) production in relatives of patients with systemic lupus erythematosus (SLE).
Methods. Production of IL-10 was evaluated in 13 families in which several members had SLE. The constitutive IL-10 production in SLE patients (n = 16) was compared with that in healthy members of these multiplex families (n = 70), in 30 SLE patients who had no relatives with SLE, and in 46 healthy unrelated controls.
Results. The level of IL-10 production did not differ between SLE patients who were members and those who were not members of multiplex families (mean ± SEM 4,384 ± 908 pg/ml and 4,709 ± 560 pg/ml, respectively), but was higher in both groups than in healthy unrelated controls (515 ± 88 pg/ml). The healthy members of the multiplex families constitutively produced large amounts of IL-10 (3,080 ± 311 pg/ml; P < 0.001 compared with healthy unrelated controls). This high IL-10 production was independent of age and sex, and was similar in first- and second-degree relatives of SLE patients. The IL-10 was produced both by monocytes and by a subpopulation of B lymphocytes in SLE patients and in their relatives.
Conclusion. The dysregulation of IL-10 production previously identified in SLE patients is also present in healthy members of families with several cases of SLE, and it may contribute to the immunologic abnormalities affecting relatives of SLE patients.