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 Blood, 1 June 2007, Vol. 109, No. 11, pp. 4890-4898.
Prepublished online as a Blood First Edition Paper on February 15, 2007; DOI 10.1182/blood-2006-05-022277.

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NEOPLASIA

Monoclonal TCR-Vβ13.1+/CD4+/NKa+/CD8–/+dim T-LGL lymphocytosis: evidence for an antigen-driven chronic T-cell stimulation origin

Pilar Garrido1, Francisco Ruiz-Cabello2, Paloma Bárcena3,4, Yorick Sandberg5, Julia Cantón1, Margarida Lima6, Ana Balanzategui4,7, Marcos González4,7, Miguel Angel López-Nevot1, Anton W. Langerak5, Andrés C. García-Montero3,4, Julia Almeida3,4, and Alberto Orfao3,4

1 Servicio de Hematología, Hospital Universitario Virgen de las Nieves, Granada, Spain; 2 Servicio de Análisis Clínicos, Hospital Universitario Virgen de las Nieves, Granada, Spain; 3 Servicio de Citometría & Departamento de Medicina, Universidad de Salamanca (USAL), Spain; 4 Instituto de Biología Molecular y Celular del Cáncer, Centro de Investigación del Cáncer/IBMCC (CSIC-USAL), Salamanca, Spain; 5 Department of Immunology, Erasmus Medical Center, Rotterdam, The Netherlands; 6 Servicio de Hematología, Hospital Geral de Santo António, Porto, Portugal; 7 Servicio de Hematología, Hospital Universitario de Salamanca, Spain

Monoclonal TCR{alpha}β+/CD4+ T-large granular lymphocyte (T-LGL) lymphocytosis is a T-cell disorder with a restricted TCR-Vβ repertoire. In the present study we explored the potential association between the expanded TCR-Vβ families, the CDR3 sequences of the TCR-Vβ gene, and the HLA genotype of patients with monoclonal TCR{alpha}β+/CD4+ T-LGL lymphocytosis. For that purpose, 36 patients with monoclonal TCR{alpha}β+/CD4+ T-LGL lymphocytosis (15 TCR-Vβ13.1 versus 21 non–TCR-Vβ13.1) were selected. For each patient, both the HLA (class I and II) genotype and the DNA sequences of the VDJ-rearranged TCR-Vβ were analyzed. Our results show a clear association between the TCR-Vβ repertoire and the HLA genotype, all TCR-Vβ13.1+ cases being HLA-DRB1*0701 (P = .004). Interestingly, the HLA-DR7/TCR-Vβ13.1–restricted T-cell expansions displayed a highly homogeneous and strikingly similar TCR arising from the use of common TCR-Vβ gene segments, which shared (1) unique CDR3 structural features with a constantly short length, (2) similar combinatorial gene rearrangements with frequent usage of the Jβ1.1 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.


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