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Effect of Schlafen 2 on Natural Killer and T cell Development from Common T cell/ Natural Killer Progenitors
Author(s) -
ahmadi slahadin,
veinotte linnea L
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1034.7
Subject(s) - biology , lymphokine activated killer cell , progenitor cell , microbiology and biotechnology , population , natural killer cell , il 2 receptor , interleukin 21 , immunology , stem cell , t cell , cytotoxic t cell , immune system , medicine , genetics , environmental health , in vitro
Natural Killer (NK) cells are thought to develop from common lymphoid progenitors in the bone marrow. Even though thymus is not essential for NK cell development, Thymic T‐cell/natural killer–cell (T/NK) precursor, DN2 (CD44+CD25+) when cultured on an OP9 stroma, give rise to some NK1.1+ cells. The objective of this study was to see if the Schlafen 1 (Slfn1) and Schlafen 2 (Slfn2) genes differently affect the maturation of T cell and NK cells from DN2 progenitors. We transduced DN2 progenitors prepared from C57BL/6 (B6) mouse thymus with Slfn1 and Slfn2 genes using retroviral vector and cultured those Slfn1 and Slfn2 transduced progenitors on OP9 and OP9 stroma expressing the Notch ligand Delta‐like 1 (OP9‐DL1) with appropriate cytokines to see if it affects generating NK and T‐cells differently. We got a small number of Slfn1 and Slfn2 expressing mature T and NK cells upon culture of transduced DN progenitors on Op9‐DL1 and Op9 stroma cells. There was no difference between Slfn1 positive and Slfn1 negative population regarding CD3 expression but nearly all mature NK cells were belong to Slfn1 negative population. Slfn2 completely blocked maturation of T cells but not NK cells. The result of this study indicates that both Slfn1 and Slfn2 interfere with maturation of DN2 progenitors but T cell development is more sensitive to Slfn2 expression than NK cell development. This research was supported by Terry Fox Laboratory, British Columbia Cancer Research Center and Department of Pathology and Laboratory Medicine, University of British Columbia 675 West 10th Avenue, Vancouver, British Columbia, Canada.