1991 Fiscal Year Final Research Report Summary

Induction of specific cytotoxicity for autologous leukemic cells by the use of keller T cells and bispecific antibodies

Research Project

Project/Area Number	02454522
Research Category	Grant-in-Aid for General Scientific Research (B)
Allocation Type	Single-year Grants
Research Field	Hematology
Research Institution	Tokyo Women's Medical College
Principal Investigator	OSHIMI Kazuo Tokyo Women's Med. Coll. Fac. Med. Associate Prof., 医学部, 助教授 (40089991)
Co-Investigator(Kenkyū-buntansha)	AKAHOSHI Masako Tokyo Women's Med. Coll. Fac. Med. Assistant, 医学部, 助手 (40150974) TAKAHASHI Masatomo Tokyo Women's Med. Coll. Fac. Med. Assistant, 医学部, 助手 (90119991) MOTOJI Toshiko Tokyo Women's Med. Coll. Fac. Med. Lecturer, 医学部, 講師 (00101808)
Project Period (FY)	1990 – 1991
Keywords	bispecific antibody / LAK cells / acute leukemia / blast colony assay / apoptosis
Research Abstract	Anti-CD3 Fab' x anti-CDIO Fab' bispecific antibody(BsAb)and anti-CD3 Fab' x anti-CD13 Fab' BsAb were generated. These BsAb were shovin to enhance lymphokine-activated killer(LAK)mediated cytotoxicity for CD10+ acute lymphoblastic leukemia(ALL)cells and CD13+ acute myeloid leukemia(At-IL)cells, respectively. Colony formation by blast progenitors of CD13+ A[iL cells was inhibited by addition of LAK cells, and the inhibition was further enhanced by addition of anti-CD3 Fab' x anti-CD13 Fab' BsAb. Ultrastructurally, these AFIL cells were killed in an apoptotic manner rather thati a necrotic process. Taken together, these findings indicate that BsAb may be used for inmunotherapy of acute leukemia.

(5 results)