title: Interleukin-2, soluble interleukin-2 receptor and tumor necrosis factor in sera from patients with rheumatoid arthritis.
abstract: Interleukin-2 (IL-2), soluble interleukin-2 receptor (IL-2R) and tumor necrosis factor (TNF) have been measured in sera from 47 patients affected by classic rheumatoid arthritis (RA) using an enzyme-linked immunosorbent assay. The patients were divided into 4 groups as follows: group A, 18 patients with inactive disease; group B, 19 patients with active disease under treatment with non-steroidal antiinflammatory drugs (NSAID) and second-line drugs; group C, 5 patients with active disease under treatment with NSAID and cyclosporine A (CSA) for at least 4 months; group D, 5 patients in the same condition as patients of group C, but treated with azathioprine (AZA) instead of CSA. IL-2 was undetectable in all patients except two, both characterized by active disease. Soluble IL-2R levels were above the upper limit of the normal range in most of the patients studied, but the mean value ( +/- 1 SD) was significantly higher in patients of group B (1,288 +/- 421 U/ml) than in patients of group A (686 +/- 205 U/ml) and group C (842 +/- 414 U/ml). In two patients affected by active RA treated with pulse methylprednisolone therapy (1 g/day for 3 alternate days) the values of soluble IL-2R dropped from 948 to 662 U/ml and from 660 to 518 U/ml, respectively. No statistically significant correlation was observed between the serum level of IL-2R and the RF titre or percentage of C1q-binding activity, respectively. TNF was found within the normal range in all patients except one, who was characterized by active arthritis, high number of rheumatoid skin nodules and extremely high RF titre.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Istituto di Clinica Medica Generale e Terapia Medica, Università degli Studi di Ancona.
authors.forename: A
authors.initials: A
authors.lastname: Corvetta
authors.forename: M M
authors.initials: MM
authors.lastname: Luchetti
authors.forename: G
authors.initials: G
authors.lastname: Pomponio
authors.forename: R
authors.initials: R
authors.lastname: Della Bitta
authors.forename: A
authors.initials: A
authors.lastname: Recchioni
authors.forename: P
authors.initials: P
authors.lastname: Strusi
authors.forename: G
authors.initials: G
authors.lastname: De Sio
authors.forename: G
authors.initials: G
authors.lastname: Danieli
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy; D001379:Azathioprine / Q000627:therapeutic use; D015922:Complement C1q / Q000032:analysis; D003524:Cyclosporins / Q000627:therapeutic use; D005260:Female; D006801:Humans; D007376:Interleukin-2 / Q000097:blood*; D008297:Male; D015375:Receptors, Interleukin-2 / Q000097:blood*; D012217:Rheumatoid Factor / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D003524:Cyclosporins; D007376:Interleukin-2; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D015922:Complement C1q; D012217:Rheumatoid Factor; D001379:Azathioprine