Mycobacterium Tuberculosis in the adjuvant modulates the balance of Th immune response to self-antigen of the CNS without influencing a ?core? repertoire of specific T cells.

Gabriele Di Sante, Walter Ricciardi, Francesco Ria, Chiara Nicolo', Simona Rolla, Sandra Columba-Cabezas, Bosco Man Chu Chan

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

In the present study we use modified CDR3 beta-chain spectratyping (immunoscope) to dissect the effect of Mycobacterium Tuberculosis -derived proteins on individual PLP139-151 specific cells in the SJL mouse strain. In this model, the immunoscope technique allows the characterization of a public TCR that involves rearrangement of Vbeta10 and Jbeta1.1 and a semiprivate TCR characterized by rearrangement of Vbeta4 and Jbeta 1.6. Both rearrangements are specific for PLP139-151and sequences of the CDR3 region of the two beta-chains show a conserved motif for the public rearrangement and related but more variable sequences for the semiprivate rearrangement. Mycobacterium Tuberculosis -derived proteins promote increase of IFN-gamma secreting cells. However, we observe that presence and amount of Mycobacterium Tuberculosis used during immunization have no effect on the frequency of usage, polarization and in vivo expansion of cells carrying the studied rearrangements. Rather, the strong Th1 promoting effect of adjuvant is possibly due to recruitment towards Th1 of a wider spectrum of TCR repertoires. Therefore, instead of having a comprehensive effect on the entire repertoire, Mycobacterium Tuberculosis modulates the immune response by affecting a subset of antigen-specific T cells whose polarization can be adapted to the environment. This step establishes the final balance between Th1 and Th2 and may be essential for the enhancement or protection of disease.
Original languageEnglish
Pages (from-to)363-374
Number of pages12
JournalInternational Immunology
DOIs
Publication statusPublished - 2006

Keywords

  • Mycobacterium Tubercolosis
  • TCR
  • Th1
  • Th2

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