Deviated Overexpression of TCR-β, TCR-γ, CD4, and CD8 on Thymic Lymphomas Induced by 1-Propyl-1-Nitrosourea: Destruction of the Allelic Exclusion of TCR-β and Expression of Functional TCR-βγ Heterodimer on a Lymphoma, cFTL53

Thymic lymphomas (FTLs) induced by the chemical carcinogen 1-propyl-1-nitrosourea (PNU) in F344 rats showed deviated overexpression of TCR-β, TCR-γ, CD4, and CD8. Even though most FTLs were in the CD4⁺CD8⁺ stage, all FTLs expressed TCR-β mRNA with TCR-γ mRNA, but without TCR-α mRNA or TCR-δ mRNA. One of the FTLs, cFTL53, expressed two kinds of TCR-β mRNA and two kinds of TCR-γ mRNA, but did not express any mRNA of TCR-α or TCR-δ. Both alleles of TCR-β loci were rearranged on cFTL53. cDNA cloning and sequencing analysis showed that one TCR-γ mRNA, Vγ4-Jγ1-Cγ1, and both TCR-β mRNA, Vβ2-Dβ2-Jß2.1 and Vβ19-Dβ2-Jβ2.1-Cβ2, on cFTL53 were in the productive form, while the other TCR-γ mRNA, Vγ1-Jγ4-Cγ4L, was not. Both TCR β-chains and a TCR γ-chain were expressed on cFTL53, making a novel set of TCR-βγ heterodimer. Cross-linking of TCR-βγ heterodimer on cFTL53 resulted in a calcium flux, indicating that TCR-βγ works as a signal transduction receptor. Thus, there are four strange phenomena on FTLs; CD4 and CD8 are expressed without TCR-αβ or TCR-γδ, TCR-β mRNA and TCR-γ mRNA were expressed simultaneously without TCR-α and TCR-δ mRNA on FTLs, the allelic exclusion of TCR-β was destroyed in cFTL53, and a novel set of functional TCR-βγ heterodimer was expressed on cFTL53.