Intestinal alphabeta T cells of symptomatic celiac disease patients show oligoclonal TCRBV repertoire but polyclonal rearrangement patterns.
Celiac disease is an immunological disease provoked by some cereal proteins in HLA-DQ-mediated susceptible individuals. The role of intestine infiltrating alphabeta T cells in the pathogenesis of the disease has been functionally established. In the present report, we have studied the repertoire of TCRBV genes, spectratype distribution, and CDR3 sequences of intestinal T cell populations isolated from three CD patients at diagnosis and two normal control biopsies. Oligoclonal TCRBV usage was observed both in CD and control samples. However, a much more restricted TCRBV usage was evident in normal mucosa. The use of BV gene families was linked to no dominant rearrangements in CD, while apparent oligoclonal patterns were found in normal biopsies. Only 3 out of 73 sequenced transcripts derived from preponderant TCRBV genes in the three celiac samples were obtained twice. In contrast, only 13 different rearrangements were found out of 32 analyzed in control samples. In spite of the polyclonal behavior of T cells in CD mucosa, some conserved motifs in the CDR3 region were noticed among rearrangements derived from different TCRBV genes and patients. The lack of expanded T cell clones in the damaged tissue could be explained in terms of antigen diversity or by non-specific immunological responses in the symptomatic phase of the disease.
Balas
A
A
Laboratory of Histocompatibility, Regional Transfusion Center, Madrid, Spain.
Garcia-Novo
M D
MD
Martinez
J
J
García-Sánchez
F
F
Santos
S
S
Vicario
J L
JL
D002446:Celiac Disease / Q000175:diagnosis / Q000276:immunology*; D002648:Child; D015333:Gene Rearrangement, beta-Chain T-Cell Antigen Receptor; D019674:Genes, T-Cell Receptor beta; D006801:Humans; D007413:Intestinal Mucosa / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics*; D013601:T-Lymphocytes / Q000276:immunology*
D016693:Receptors, Antigen, T-Cell, alpha-beta