Annual Report 2011 - Center for Advanced Biotechnology and ...

Another important feature of HTLV-1-infected T cells expressing the Tax
transactivator is the production of multiple cytokines. The Rabson laboratory has
shown that Tax-expressing CD4+ T cells fail to properly “bias”, i.e. fail to
differentiate into specific T helper subtypes, such as Th1, Th2, Th17 and Treg cells.
Instead, the Tax-expressing cells express cytokines characteristic of all of these
different cells, suggesting a “confused” phenotype that may in turn lead to immune
dysregulation with the potential for both opportunistic infections and autoimmunelike
diseases.
The second major area of study in Dr. Rabson’s laboratory continues to be the
roles of transcriptional regulation in the pathogenesis of human cancer. In
collaboration with Drs. Ruth Steward (Waksman Institute), Dale Schaar (CINJ),
and Hatem Sabaawy (CINJ), the Rabson lab is investigating the functions of
PDCD2, a highly conserved nuclear and cytoplasmic protein, the mutation of
which disrupts hematopoiesis in Drosophila (Drs. Steward and Minakhina). The
Rabson lab has shown high levels of expression of this enigmatic protein in very
early developing embryos and is currently performing mouse genetic experiments
and transcriptional studies to determine its function. Dr. Rabson has also
continued collaborations with Dr. Roger Strair at CINJ on the potential utility of
NF-κB inhibition in leukemia therapy. A clinical trial, examining the effects of
NF-κB inhibition, as part of induction chemotherapy, on the molecular phenotype
of Acute Myeloid Leukemia is in the late stages of development and is a follow-up
to a published trial showing the feasibility of inhibiting NF-κB in patients.
Differentiated mouse embryonic stem cells
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