A syngeneic anti-idiotype monoclonal antibody (MAb) (CM-I I) directed against an anti-carcinoembryonic antigen (CEA) murine MAb (NP-4) was evaluated as a second antibody (SA) to promote the rapid clearance of radiolabeled NP-4 from the blood. Initial studies confirmed that CM-I I IgG removed l3Il-NP
Participation of a dominant cytotoxic T cell population defined by a monoclonal antibody in syngeneic anti-tumor responses
β Scribed by Yuji Matsubayashi; Toshiyasu Hirama; Atsuo Morioka; Michihiro Iwashiro; Tohru Masuda; Haruto Uchino; Sunao Takeshita; Hideo Yamagishi; Heiichiro Udono; Masahiro Mieno; Eiichi Nakayam; Hiroshi Shiku; Akiko Uenaka; Kagemasa Kuribayashi
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 806 KB
- Volume
- 20
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
β¦ Synopsis
Participation of a dominant cytotoxic T cell population defined by a monoclonal antibody in syngeneic anti-tumor responses*
Cytotoxic T lymphocyte (CTL) clones against a syngeneic Friend virus-induced erythroleukemia (FBL-3) were generated in C57BL/6 (B6) mice. A monoclonal antibody (mAb, N9-127) was then raised from spleen cells of a B6 mouse immunized syngenically against one of these CTL clones.This mAb detected the epitope (127Ep) of the T cell antigen receptor (TcR) on the immunizing CTL clone in tests of immunoprecipitation, specific blocking and proliferation, and induction of TcR-mediated nonspecific lysis of the clone. In addition, more than 10% of the FBL-3-specific CTL clones isolated independently from B6 mice were 127Ep+. Further investigations revealed that up to 30% of B6 anti-FBL-3 Tcell blasts from mixed lymphocyte tumor cell cultures were positive for this epitope, and that its expression was confined to CD8+ T cells. This epitope was not detected in naive lymphoid cells from the spleen, lymph nodes or thymus or in T cell clones specific for tumors other than FBL-3. The FBL-3-specific CTL clones were next grouped into 127Ep+ and 127Ep-clones. Sequence analyses of the CTL clone used for immunization showed the rearrangements of Va1Ja112-2 and VglODg2.1Jg2.7. Southern blot analysis of all the 127Epf CTL clones examined showed the same DNA rearrangement bands of both the TcR a and p genes. These findings suggested that mAb N9-127 recognized the shared determinant of the TcR molecule which was expressed by the dominant CTL population in the response to FBL-3. * This work was supported by Grants-in-Aid for Cancer Research from the Ministry of Education, Science and Culture Of Japan.
Recently, we showed that anti-idiotypic antibodies were generated against the TcR of UV-induced tumor-specific CTL clones, but these antibodies detected only a very low frequency of cells bearing the idiotype [12]. In the present determinant defined by a mAb designated as N9-127 which recognized a TcR expressed in appreciably high frequency by CD8+ T cells responding to the C57BLI6 (β¬36) FBL-3
π SIMILAR VOLUMES
## Abstract The properties of human lymphocyte fractions isolated either by sheep red cell (E) rosetting or by fluorescenceβactivated cell sorting after staining with UCHT1 monoclonal antiβT cell antibody have been compared. Two populations of E^+^ cells with very different phenotype and function h
## Abstract Two monoclonal antibodies (KHβ1 and KHβ2) against a transplanted fibrosarcoma (KMTβ17) in WKA rats were produced by fusing a mouse myeloma (P~3~βX63βAg8.653) with spleen cells from syngeneic rats hyperimmunized with KMTβ17. Both antibodies showed complementβdependent cytotoxicity agains
Minute amounts of the anti-L3T4 antibody designated GK1.5 were found to deeply suppress in vivo antibody responses to T-dependent antigens. Primary responses to sheep erythrocytes were completely inhibited even when GK1.5 was administered up to 6 days before or 4 days after the antigen. Secondary re
## Interleukin -2-activated, cultured NK cells (A-NK) cells were adoptively transferred into a syngeneic rat liver-tumor model. The kinetics of tumor infiltration by NK cells, originating either from adoptively transferred or from endogenous sources, the localization of these cells in the tumor, a
Activation of protein kinase C (PKC) causes a rapid and sustained increase in the F-actin of T lymphocytes. Because the phosphatidylinositol pathway and the cytoskeleton play a role in lymphocyte activation, we examined the relationship between signal transduction and the F-actin increase in human b