Thyroid hormones (THs) are important regulators of cell physiology. They are essential for
the normal development and growth of mammals, especially for the neural differentiation and the
regulation of the metabolism and the immune system. THs also induce the proliferation of several cell
types. In human and murine T cell lymphomas (TCL) this effect involves the participation of genomic
and nongenomic mechanisms as it was described by the use of free THs and non-cell permeable THs coupled to agarose
(TH-ag). The classic actions of thyroid hormones involve the alteration of gene transcription via specific nuclear receptors.
The discovery of other effects, independent of this classic mechanism, characterizes a new and non-classic mechanism
that involves different signaling pathways. Both, free THs and TH-ag, activate protein kinase C, extracellular signalregulated
kinases and NF-kB and they increase the intracellular calcium levels. However, only the preincubation of T cells
with free THs leads to an increased intracellular content of signaling enzymes. T lymphomas display high expression levels
of both, the TH nuclear receptors (TRs) and the putative membrane receptor for THs, the integrin αvβ3, which has
been demonstrated to be responsible for THs non-genomic actions. Here, we reviewed the mechanisms involved in THs
modulation of the lymphocyte physiology, analyzing the interplay between genomic and nongenomic actions in T cells
and its contribution in the development of lymphomas.
Keywords: Genomic signaling, integrin αvβ3, nongenomic signaling, thyroid hormones, T cell lymphoma, tumor growth.
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