The Jurkat cell line (originally called JM) was established in the mid-1970s from the
peripheral blood of a 14-year-old boy with T cell leukemia.[2][3] Different derivatives of the Jurkat cell line that have been mutated to lack certain genes can now be obtained from cell culture banks.[4]
Examples of derivatives
The JCaM1.6 cell line is deficient in
Lck activity due to the deletion of part of the
LCK gene (
exon 7) from the LCKtranscript.
J.RT3-T3.5 cells have a mutation in the
T cell receptor beta chain locus precluding expression of this chain. This affects the cells in several ways; they do not express surface
CD3 or produce the T cell receptor alpha/beta
heterodimer. Since they are deficient in the TCR complex, these cells are a useful tool for transfection studies using T cell receptor alpha and beta chain genes and are widely used in labs in which
T cell receptor gene transfer technologies are studied.
The I 9.2 and I 2.1 cell lines. The I 2.1 cell line is functionally defective for
FADD and the I 9.2 cell line is functionally defective for
caspase-8, both defective molecules being essential to
apoptosis or
necroptosis of cells.
The D1.1 cell line does not express the
CD4 molecule, an important
co-receptor in the activation pathway of
helper T cells.
The J.gamma1 subline contains no detectable
phospholipase C-gamma1 (PLC-γ1) protein and therefore has profound defects in T cell receptor (TCR)
calcium mobilization and activation of nuclear factor of activated T cells (
NFAT, an important
transcription factor in T cells).
J-Lat contains integrated but transcriptionally latent HIV proviruses, in which
GFP replaces nef coding sequence, and a frameshift mutation in env.
Cell line contamination
Jurkat J6 cells have been found to produce a
xenotropic murine leukemia virus (X-MLV) (referred to as
XMRV) that could potentially affect experimental outcomes. There is no evidence that this virus can infect humans. This infection may also change the virulence and tropism of the virus by way of phenotypic mixing and/or recombination.[5]
References
^Abraham, Robert; Weiss, Arthur (2004). "Jurkat T cells and development of the T-cell receptor signalling paradigm". Nature. 4 (4): 301–308.
doi:
10.1038/nri1330.
PMID15057788.
S2CID13253575.
^Schneider U, Schwenk H, Bornkamm G (1977). "Characterization of EBV-genome negative "null" and "T" cell lines derived from children with acute lymphoblastic leukemia and leukemic transformed non-Hodgkin lymphoma". Int J Cancer. 19 (5): 621–6.
doi:
10.1002/ijc.2910190505.
PMID68013.
S2CID23684046.