ISSN:
1432-0851
Keywords:
Key words: Soluble TNF receptors – TNFα– Immunotherapy – IL-2 – IFNα
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract. Eleven metastatic cancer patients were studied during three different regimens of immunotherapy with interleukin-2 (IL-2) and/or interferon α (IFNα): group A received 4 days of IL-2 i. a. infusion (n = 3), group B IFNα s.c. during 5 days (n = 4), followed on day 3 by 5 days of a continuous IL-2 i. v. infusion, and group C had 4 days of IL-2 i. v. infusion together with s. c. IFNα on days 1 and 4 (n = 4). Soluble tumor necrosis factor receptors (sTNFR) p55 and p75 and TNFα concentrations in serum were analyzed before therapy and daily during 8 days of the first therapy cycle. sTNFR was measured by radioimmunoassay. sTNFR p55 increased in all patient groups from a baseline value of 5.2±0.9 ng/ml to a maximum of 13.6±1.2 ng/ml by days 3 – 4 (P = 0.003). sTNFR p75 increased from 7.6±1.1 ng/ml to peak values of 30.1±2.6 ng/ml in groups A and B (P = 0.02). In group C the sTNFR p75 response was weak (NS). In group B, the increase of both p55 and p75 occurred only after addition of IL-2 to IFNα. TNFα increased weakly during treatment with IFNα alone (group B); it rose strongly during IL-2 and the combined treatment (groups A – C) from 8±2 pg/ml to 115±13 pg/ml (P = 0.003). In group B, it reached the maximum 24 h after addition of IL-2 to IFNα and decreased thereafter. There was a significant relationship between TNFα and sTNFR p55 or sTNFR p75 in groups A and C, (P = 0.001), but not in group B. Group C was also investigated during the third therapy cycle. The increase of sTNFR p75 was stronger (P = 0.01) and that of TNFα weaker than in the first cycle; the sTNFR p55 response was similar in both cycles. In conclusion sTNFR p55 and p75 are rapidly induced during IL-2 and IL-2+ IFNα treatment, the increase of sTNF receptors parallels or exceeds that of TNFα and may influence the immunomodulatory effects of TNFα during cytokine therapy.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01526206
