PROGRESSION MECHANISMS IN COLON-CANCER - SOLUBLE INTERLEUKIN-2 (IL-2)RECEPTOR, IL-2 PLUS ANTI-CD3 PROLIFERATIVE RESPONSE AND TUMOR STAGE CORRELATIONS

Citation
Am. Berghella et al., PROGRESSION MECHANISMS IN COLON-CANCER - SOLUBLE INTERLEUKIN-2 (IL-2)RECEPTOR, IL-2 PLUS ANTI-CD3 PROLIFERATIVE RESPONSE AND TUMOR STAGE CORRELATIONS, Cancer immunology and immunotherapy, 38(3), 1994, pp. 160-166
Citations number
59
Categorie Soggetti
Immunology,Oncology
ISSN journal
03407004
Volume
38
Issue
3
Year of publication
1994
Pages
160 - 166
Database
ISI
SICI code
0340-7004(1994)38:3<160:PMIC-S>2.0.ZU;2-7
Abstract
Soluble interleukin-2 receptor (sIL-2R) levels have been found to be e levated in several clinical conditions, including disseminated solid n eoplasms, whereas they are generally within the normal range in patien ts with locally limited neoplastic disease. The aim of the present stu dy was to examine this in our colon cancer patients, and to assess if this situation can affect the in vitro activation of peripheral blood mononuclear cells (PBMC), examining the proliferative response to IL-2 and anti-CD3 monoclonal antibody, the IL-2 serum levels and the PBMC phenotype. The results show that sIL-2R levels were significantly corr elated with the stage of the disease, showing an in crease from stage I to stage IV; moreover, it is worth noting that the proliferative res ponse to IL-2 plus anti-CD3 is significantly higher than to IL-2 alone in stage IV, without significant alteration in the numerical presence of T and natural killer cells. So it seems that in the peripheral blo od of patients, connected with the disease progression, are present ce llular populations showing a different response to activation, and tha t T cells acquire a better response condition than NK. Thus, since the T cellular population includes the tumour-specific cytotoxic precurso r cells, this should be helpful for its tumour regressive activity, bu t it is conceivable that this population cannot perform its functions, owing to a deficiency in responsiveness of the specific ThCD4(+) subp opulation.