I am trying to look at what apoptotic genes are activated after treating the B-cell leukemic cell lines with Dexamethasone. I have gone over some literature on the genes that are activated in T- cell leukemia post treatment with dexamethasone. Wanted to know if there is any difference between the biology of B-cell leukemia and T-Cell leukemia. Thanks :)
In one cell type we can find differences in the apoptotic signaling pathways , according to the nature of the stimulus. For example, the Fas receptor is activated in reactive T cells to establish T cell homeostasis. In contrast, Bcl-2 protects T cells against apoptosis in the absence of stimulation. In the case of cancer, Bcl-2 protection is not provided (like in physiological conditions), especially when the tumor evades immunological control.
Dexamethasone treatment induces in T and B cells up-regulation of the Glucocorticoid Receptor (GR), at the transcriptional and proteic levels.
While the same threshold levels of GRs are required in the two cell types, to trigger apoptosis, there are differences in the expression levels of target genes.
In fact, the sensitivity to apoptosis of these two cell leanages can vary, so down-regulation of Bcl-2 would tend to promote steroid-mediated cell death and Bim (BH3-only) is also mediated in apoptosis for the two cell types.
Nevertheless, the Granzyme A is implicated in B cells apoptosis, and Protein Kinase A Regulatory Subunit II, in T cells apoptosis.
Kalthoum Abid
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