Effect Of Human-Serum Anti-Htlv Antibodies On Viral-Antigen Induction In Invitro Cultured Peripheral Lymphocytes From Adult T-Cell Leukemia Patients And Healthy Virus Carriers

Leukemic cells of adult T-cell leukemia (ATL) patients contain human T-cell leukemia virus type I (HTLV-I) genomes. However, viral antigens (HTLV-A) are not usually expressed in vivo. It has been shown that HTLV-I antigens are spontaneously induced after culture of peripheral blood lymphocytes (PBL) from patients with ATL and healthy carriers (HC), who are viral antibody-positive. In the present communication, we show the suppressive effect of human serum antibodies against HTLV-I on viral antigen expression in PBL derived from ATL patients and HC. Viral antigen synthesis in various PBL specimens is variable in terms of frequencies and kinetics. (1) Low concentrations (2%) of antibody-positive but not of antibody-negative sera efficiently suppressed HTLV antigen induction in lymphocytes from both ATL patients and HC. (2) An inhibitory effect was exerted by HTLV-I-specific antibodies which originated from either ATL, HC or even HTLV-I-positive monkeys. (3) Sera showed a fairly wide range of suppressive activity in view of their concentrations. (4) At the late stage of cultures even continuous presence of antibodies frequently failed to suppress antigen synthesis in lymphocytes. (5) Antibodies were less effective in suppressing the increase of antigens if they were added to cultures which had already HTLV-A-positive lymphocytes in antibody-free media. (6) Pretreatment with protein A completely abolished the activities of the suppressive plasmas. (7) Antibodies did not affect the inhibition of spontaneous or chemical induction of HTLV-A in 2 HTLV-I-positive cell lines. These results suggest that HTLV-I antigen expression in leukemic cells from patients with ATL in vivo and in vitro is partly regulated by antibodies to HTLV-I. Furthermore, at least 2 different pathways, one antibody-sensitive and the other -insensitive, might exist to express HTLV-A.