## Abstract ## BACKGROUND. Rituximab in sequential combination with fludarabine (Flu) allowed patients with B‐cell chronic lymphocytic leukemia (B‐CLL) to achieve higher remission rates and longer response duration. Based on their recent experience in indolent non‐Hodgkin lymphomas, in this study,
FCRL6 distinguishes mature cytotoxic lymphocytes and is upregulated in patients with B-cell chronic lymphocytic leukemia
✍ Scribed by Daniel M. Schreeder; Jicun Pan; Fu Jun Li; Eric Vivier; Randall S. Davis
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 242 KB
- Volume
- 38
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Fc receptor‐like 6 (FCRL6), the most recently characterized member of the FCRL family, is a cell surface glycoprotein with tyrosine‐based regulatory potential. An extensive survey of human hematopoietic tissues disclosed that FCRL6 expression by NK‐ and T‐cell subpopulations increases as a function of differentiation and is remarkably restricted to mature lymphocytes with cytotoxic capability. In particular, FCRL6 distinguishes perforin‐expressing CD56^dim^ NK cells, Vδ1^+^ and Vδ2^+^ γδ T cells, effector and effector memory CD8^+^ T cells, and rare cytotoxic CD4^+^ T cells in adult tissues. Analysis of this receptor in B‐cell chronic lymphocytic leukemia (CLL) was also performed. FCRL6 was found to mark significantly expanded populations of cytotoxic CD8^+^ T, CD4^+^ T, and NK cells in patients with CLL. Despite sequence homology with the known Fc receptors for IgG and IgE, FCRL6 did not bind Ig. Although FCRL6 can be tyrosine‐phosphorylated, its antibody‐mediated ligation was unable to influence cellular activation. Collectively, these results demonstrate that FCRL6 is a distinct indicator of cytotoxic effector lymphocytes that is upregulated in diseases characterized by chronic immune stimulation.
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## Abstract B‐cell chronic lymphocytic leukemia (CLL) is characterized by a high rate of clonal genomic alterations and a low proliferative activity with cell cycle arrest in G~0~/G~1~ phase. Recently, centrosome aberrations have been described as a possible cause of chromosomal instability and ane