Monoclonal TCR-V beta 13.1(+)/CD4(+)/NKa(+)/CD8(-/+dim) T-LGL lymphocytosis: evidence for an antigen-driven chronic T-cell stimulation origin

• Tipo: Artigo em Revista Científica Internacional
• Data: 2007

Autores

Garrido, P (Autor) Outra; Ruiz Cabello, F (Autor) Outra; Barcena, P (Autor) Outra; Sandberg, Y (Autor) Outra; Canton, J (Autor) Outra; Lima, M (Autor) ICBAS; Balanzategui, A (Autor) Outra; Gonzalez, M (Autor) Outra; Lopez Nevot, MA (Autor) Outra; Langerak, AW (Autor) Outra; Garcia Montero, AC (Autor) Outra; Almeida, J (Autor) Outra; Orfao, A (Autor) Outra

Revista

Título: Blood

Vol. 109

Páginas: 4890-4898

ISSN: 0006-4971

Editora: Elsevier

Indexação

ISI Web of Knowledge - 32 Citações

Scopus - 27 Citações

Outras Informações

ID Authenticus: P-004-9J4

DOI: 10.1182/blood-200605-022277

Abstract (EN): Monoclonal TCR alpha beta(+)/CD4(+) T-large granular lymphocyte (T-LGL) lymphocytosis is a T-cell disorder with a restricted TCR-V beta repertoire. In the present study we explored the potential association between the expanded TCR-Vp families, the CDR3 sequences of the TCR-V beta gene, and the HLA genotype of patients with monoclonal TCR alpha beta(+)/CD4(+) T-LGL lymphocytosis. For that purpose, 36 patients with monoclonal TCR alpha beta(+)/CD4(+) T-LGL lymphocytosis (15 TCR-V beta 13.1 versus 21 non-TCR-V beta 13.1) were selected. For each patient, both the HLA (class I and 11) genotype and the DNA sequences of the VDJ-rearranged TCR-V beta were analyzed. Our results show a clear association between the TCR-V beta repertoire and the HLA genotype, all TCR-V beta 13.1(+) cases being HLA-DRB1 -0701 (P =.004). Interestingly, the HLA-DR7/TCR-V beta 13.1-restricted T-cell expansions displayed a highly homogeneous and strikingly similar TCR arising from the use of common TCR-Vp gene segments, which shared (1) unique CDR3 structural features with a constantly short length, (2) similar combinatorial gene rearrangements with frequent usage of the J beta 1.1 gene, and (3) a homolog consensus protein sequence at recombination junctions. Overall, these findings strongly support the existence of a common antigen-driven origin for monoclonal CD4(+) T-LGL lymphocytosis, with the identification of the exact peptides presented to the expanded T cells deserving further investigations.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 9