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songtree songtree
wrote...
12 years ago
I want to do a comparative study between the CD4+ Jurkat T cell line and primary CD4+ T cells to study cancer. I cannot seem to find any papers using this in vitro model for cancer. Is there a reason why?
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ppk
wrote...
Valued Member
On Hiatus
12 years ago
In my microbiology class, we looked into the difference between the two. To my understanding, Jurkat cells are a proliferating line of T lymphocyte cells that are used to study acute T cell leukemia, T cell signaling, and the expression of various chemokine receptors susceptible to viral entry, particularly HIV. And, unlike other cells lines, they have the ability to produce Il-2. I think the main reason why they don't typically use them in cancer studies is because they are hard to maintain. Depending on what you're studying, sometimes these cell lines can be hard to keep alive for a prolonged period of time (>month), and this makes isolating stuff like RNA a pain. Jurkat cells are also hard to transfect, and can grow very fast; in fact, if the cell density is too high, they’ll start to die off. This could be a problem when looking at things like cancer. But don't get me wrong, they are easy cells to grow as they don't require any special culturing conditions - to my knowledge. However, aside from all this, I have read that they are used extensively in the study of T-cell signaling and cancer drug development.

Check out this paper:

Natural Killer (NK) Cell–mediated Cytotoxicity: Differential Use of TRAIL and Fas Ligand by Immature and Mature Primary Human NK Cells



This article states: Because Jurkat cells are similar to peripheral blood T cells in  their  activation-dependent  integrin regulation  through PMA, CD2, CD3, and CD28 stimulation, we  used this  T- cell line to ascertain whether the various integrin regulatory molecules  are  interdependent,  or  whether activation through one receptor is independent of the presence of other integrin regulatory molecules. Thus, we produced a series of...

Differential  Activation-Dependent  Regulation of Integrin  Function  in Cultured  Human  T-Leukemic  Cell  Lines



This article states: Thus, it is possible that anti-apoptotic effects observed in Jurkat cells may not appear in activated T lymphocytes treated with IL-2, because Jurkat cells are well-known to be sensitive to various apoptotic signals. Taken together, our results suggest that galectin-3 is involved in proliferation of activated T lymphocytes mainly, although it is still possible that galectin-3 has anti-apoptotic effects.

Expression and function of galectin-3, a ß-galactoside-binding protein in activated T lymphocytes



Characterization of EBV-genome negative “null” and “T” cell lines derived from children with acute lymphoblastic leukemia and leukemic transformed non-Hodgkin lymphoma

Methotrexate Suppresses NF-kB Activation Through Inhibition of IkBalpha Phosphorylation and Degradation

Jurkat T cells and development of the T-cell receptor signalling paradigm

CD3 receptor modulation in Jurkat leukemic cell line

Catharanthus roseus aqueous extract is cytotoxic to Jurkat leukaemic T-cells but induces the proliferation of normal peripheral blood mononuclear cells

FasL is more frequently expressed in liver metastases of colorectal cancer than in matched primary carcinoma

5-Fluorouracil-induced Death of Jurkat T-Cells – A Role for Caspases and MCL-1

Cell lines:

Rightwards Arrow The JCaM1.6 cell line is deficient in Lck kinase activity due to the deletion of part of the lck gene (exon 7) from the Lck transcript.
Rightwards Arrow 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.
Rightwards Arrow 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 programmed cell death of cells.
Rightwards Arrow The D1.1 cell line does not express CD4 molecule, an important co-receptor in the activation pathway of helper T cells.
Rightwards Arrow The J.gamma1 subline contains no detectable phospholipase C-gamma1 (PLC-?1) protein and therefore has profound defects in T cell receptor (TCR) calcium mobilization, and nuclear factor of activated T-cells (NFAT) activation (an important transcription factor in T cells).

I can probably download a lot of these papers for you, for free, if you cannot.

Hope these resources help.
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