Quantification and phenotypic characterization of peripheral blood Vδ1 + T cells in chronic lymphocytic leukemia and monoclonal B cell lymphocytosis.
Cytometry B Clin Cytom
; 96(2): 164-168, 2019 03.
Article
em En
| MEDLINE
| ID: mdl-30334339
ABSTRACT
BACKGROUND:
Vδ1+ T cells, a subset of γδ T cells, are responsible for innate-like immune responses. Recently, an anti-tumor function mediated by MHC-unrestricted recognition of lipid and stress molecules, has also been described in these cells. This study aimed to quantify and phenotypically characterize circulating Vδ1+ T cells in B cell Chronic Lymphocytic Leukemia (CLL) and Monoclonal B cell lymphocytosis (MBL).METHODS:
This study enrolled 58 individuals distributed in five groups Binet B and C CLL (n = 9), Binet A CLL (n = 26), High count-MBL (n = 10), Low count-MBL (n = 5), and a control group (n = 8). The phenotypic characterization of Vδ1+ T cells, as well as the other T cell subpopulations (CD4+ , CD8+ , CD4+ /CD8+ , and Vδ1- γδT cells), were assessed by flow cytometry, evaluating the frequency of each subset expressing CD27, CD69, and cytoplasmic granzyme B.RESULTS:
We observed an increasing percentage of Vδ1+ T cells belonging to CD27- compartment from controls to advanced stages of the disease, which was accompanied by an increasing percentage of these cells expressing granzyme B, a phenotypic pattern that was also observed in the other T cell subpopulations under study since earlier stages of the disease. Moreover, a striking expansion of Vδ1+ T cells in Binet B and C CLL was observed.CONCLUSIONS:
These experiment findings point to an expansion of CD27- Vδ1+ T cells with a cytotoxic profile, from controls to advanced stages of the disease, which points to a role of Vδ1+ T cells in the host's anti-tumor responses against clonal B-cells in MBL and CLL. © 2018 Clinical Cytometry Society.Palavras-chave
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Base de dados:
MEDLINE
Assunto principal:
Linfócitos B
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Leucemia Linfocítica Crônica de Células B
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Subpopulações de Linfócitos T
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Linfocitose
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article