Objective. We sought new susceptibility markers for rheumatoid arthritis (RA) among the T cell receptor y (TCRy) genes.Methods. We analyzed restriction fragment length polymorphisms (RFLP) of the first variable subgroup of TCRy genes in a group of French control subjects and a group of French RA patients.Results. No significant difference in Eco RI HFLP was found between the 2 study populations: Allele frequencies were virtually identical. There was no polymorphism using Hind 111.Conclusion. These results exclude TCRVyI polymorphism as a disease susceptibility marker in RA.Rheumatoid arthritis (RA), a common anti potentially disabling disease, develops in genetically susceptible hosts, as demonstrated by the association with certain HLA class I1 DRP alleles (1). RA results in T lymphocyte infiltration of the synovium, with paradoxical proliferative characteristics (2). IiLA class I1 molecules participate in the immune process by presenting peptides to T lymphocytes, which spe- The variable domains of the chains constituting the TCR a/@ or y/a heterodimers are encoded by V genes, D segments (for P and a), and J segments, which undergo somatic rearrangements, thus generating the combinatorial diversity of the TCR repertoire. Sequential rearrangements seem to begin with the TCRy locus (3), leading either to limited TCRy/S expression on 5% of human circulating T lymphocytes, or to P and then a gene rearrangements, producing a functional d p receptor in most peripheral T cells (4). As a consequence of this chronology, the y genes are rearranged in all dp+ and y/6+ T lymphocytes.Restriction fragment length polymorphisms (RFLP) of the TCRy genes have been previously documented for the constant region genes in various normal populations, showing either a duplication or a triplication of exon 2 of TRGC2, and for the variable region genes belonging to the VyI and to the VyIV subgroups (for review, see ref. 5). Seven haplotypes resulting from a variation of the Vyl subgroup gene number due to deletion, insertion events, or polymorphic restriction sites have been described (5,6).Numerous attempts have been made, with conflicting results (for review, see ref . 7), to analyze the T cell repertoire associated with the development of RA, either by dissecting the TCR-expressing subset distribution or by seeking an oligoclonal T cell response to a hypothetical dominant antigen. However, little is known about the possible influence of ontogenic rearrangements on the TCR repertoire during the pathogenesis of RA. A number of investigators, including
