Abstract
We studied a well-selected population of patients with active rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) without immunosuppressive therapy. Control and patient peripheral blood mononuclear cells (PBMC) were incubated with IL-1β, IL-10, TGF-β or LPS for 20 h and the in vitro basal and stimulated secretions of IL-6, TNF-α, IL-1β and IL-1ra were measured by ELISA. We found that in the SLE patients the basal secretion of IL-6 was significantly lower and that of IL-1ra significantly higher than in control subjects, while in the RA group the basal IL-1ra secretion was higher than in healthy subjects. SLE and RA PBMC responded to LPS and IL-1β reaching higher cytokine secretion values man controls. The in vitro response of SLE and RA PBMC to TGFβ was normal, while that to IL-10 was defective: IL-10 was able to stimulate the production of IL-6 and IL-1ra in PBMC from normal subjects, but it was unable to enhance IL-6 secretion in RA cells and it was also completely ineffective in inducing IL-1ra secretion in both SLE and RA PBMC. Our work add new data useful for the evaluation of IL-10 and IL-1ra as therapeutic agents in rheumatic diseases.
| Lingua originale | Inglese |
|---|---|
| pagine (da-a) | 71-77 |
| Numero di pagine | 7 |
| Rivista | Autoimmunity |
| Volume | 36 |
| Numero di pubblicazione | 2 |
| DOI | |
| Stato di pubblicazione | Pubblicato - 2003 |
All Science Journal Classification (ASJC) codes
- Immunologia e Allergia
- Immunologia
Keywords
- Adolescent
- Adult
- Anti-Inflammatory Agents
- Arthritis
- Case-Control Studies
- Cytokines
- Female
- Humans
- IL-1
- IL-10
- In Vitro Techniques
- Inflammation Mediators
- Interleukin 1 Receptor Antagonist Protein
- Interleukin-1
- Interleukin-10
- Interleukin-6
- Leukocytes
- Lipopolysaccharides
- Lupus Erythematosus
- Middle Aged
- Mononuclear
- Mononuclear cells
- Non-Steroidal
- Recombinant Proteins
- Rheumatoid
- Rheumatoid arthritis
- SLE
- Sialoglycoproteins
- Systemic
- Transforming Growth Factor beta
- Transforming growth factors
- Tumor Necrosis Factor-alpha