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...
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Veröffentlicht in: | European journal of immunology 1990-09, Vol.20 (9), p.2095-2103 |
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Sprache: | eng |
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Zusammenfassung: | 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 T cell 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 Vα1Jα112‐2 and Vβ10Dβ2.1Jβ2.7. Southern blot analysis of all the 127Ep+ CTL clones examined showed the same DNA rearrangement bands of both the TcR α and β 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. |
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ISSN: | 0014-2980 1521-4141 |
DOI: | 10.1002/eji.1830200931 |