Peripheral blood lymphocytes from patients with cancer lack interleukin-2 (IL-2) receptor expression: isolation of mRNA encoding IL-2R
Hakim, A.A.
Cancer Detection and Prevention 12(1-6): 59-71
1988
ISSN/ISBN: 0361-090X PMID: 2460238 Document Number: 308783
In healthy adults, tumor cells stimulate the cellular immune defense mechanisms: natural killer (NK), antigen-specific cytotoxic lymphocytes (CTL), and synthesis of antigen-specific cytotoxic antibodies, all aimed at the destruction of the intruding tumor cells. The experiments described in this study examined responsiveness of peripheral blood lymphocyte mononuclear (MNC) cells, natural killer (NK) cells, T-helper (THC) cells, and NILL (cells obtained from patients with advanced breast cancer) cells from 10 of each age-matched subjects from 10 healthy adults and patients, 10 with benign breast diseases (BBD), and 10 from patients from each of the breast carcinoma pathological stage BCa PS I, BCa PS II, BCa PS III, and BCa PS IV. Cellular responsiveness to graded levels of phytohemagglutinin (PHA), concanavalin A (Con A), and recombinant interleukin-2(r IL-2) was monitored by 3H-thymidine (3H-TdRO) uptake, production, and release of interleukin-2 (IL-2) and interleukin-2 receptor (IL-2R) and cytotoxic activities against K-562 and breast carcinoma (BCa) short-term cell lines. Suppressed cellular responsiveness is caused by the lack of functional IL-2R in peripheral blood lymphocytes with metastatic breast carcinoma (MBCa). This is confirmed by suppression of the anti-Tac antibodies binding and lack of cellular mRNA encoding IL-2R.