Acquired Resistance to Experimental Autoimmune Encephalomyelitis Is Independent of Vβ Usage

In Lewis rats, activated encephalitogenic T-helper cells elicit a single bout of experimental autoimmune encephalomyelitis (EAE). Recovery from EAE is marked by reduced susceptibility to disease reinduction. The purpose of this study was to determine whether a dominant expression of Vβ gene segments by encephalitogenic T cells was required for development of recovery-associated resistance. Several polyclonal and monoclonal T cell lines were derived from Lewis rats sensitized with R72-86, a synthetic peptide representing the 72- to 86-amino-acid sequence of rat myelin basic protein (RMBP). The results revealed broad heterogeneity among encephalitogenic T cells specific for R72-86 in regard to Vβ expression and CDR3 sequence. Encephalitogenic clones exclusively bearing either Vβ4 or Vβ10 TCR or polyclonal T cells bearing heterogeneous TCR transferred EAE to recipient rats and elicited resistance to EAE as revealed by subsequent challenge with guinea pig (GP)MBP in complete Freundʹs adjuvant (CFA). Nonpathogenic Vβ3+and Vβ8.6+clones specific for the 68–86 and 55–66 regions of MBP, respectively, did not elicit effective protection from EAE. These data indicate that induction of postrecovery resistance to EAE does not depend upon a particular Vβ usage.