| Abstract: | It has been demonstrated that induction of immune responses, infectious diseases and autoimmune manifestations can be associated with at least four gene loci: the major histocompatibility complex (MHC) locus; the immunoglobulin (Ig) heavy chain (Hc) locus; and the T–cell receptor (TCR) TCR–β or TCR–β chain loci. In the present study, we have analysed whether T–cell responses of IE–negative C57B1/6 (B6) mice to IE alloantigen (IEα transgenic B6 mice = B6. Eα 16) or to trinitrophenylated (TNP) syngeneic spleen cells were influenced by changes in the Ig–Hc locus or the TCRa locus. Whereas the fine specificity of T–cell responses to IE alloantigen was the same in B6 mice and in Ig–Hc congenic B6.26a or TCRa congenic B6.10TCa mice, the latter strain of mice demonstrated much higher IE–specific T–cell responses against B6. Eα16 spleen cells than B6 or B6.26a mice. This high responsiveness was a dominant feature and associated with the TCRa locus. In addition, the TCRVα or Vα repertoire of the congenic strains of mice was polyclonal and very similar. The TNP–specific T–cell responses of B6 and B6. 10TCa mice showed the same restricted TCRVα and Vα repertoire. It is concluded that in both an oligoclonal T–cell response (anti–TNP) and a polyclonal T–cell response (anti–IE), exchange of Ig–Hc or TCRa loci does not significantly influence the TCRVα or Vα repertoire in IE–negative C57B1/6 mice. |
