Mechanism action of Calcitriol
The mechanism of action of calcitriol in the treatment of psoriasis is
accounted for by their antiproliferative activity for keratinocytes and
their stimulation of epidermal cell differentiation. The
anticarcinogenic activity of the active form of Calcitriol appears to be
correlated with cellular vitamin D receptor (VDR) levels. Vitamin D
receptors belong to the superfamily of steroid-hormone zinc-finger
receptors. VDRs selectively bind 1,25-(OH)2-D3 and retinoic
acid X receptor (RXR) to form a heterodimeric complex that interacts
with specific DNA sequences known as vitamin D-responsive elements. VDRs
are ligand-activated transcription factors. The receptors activate or
repress the transcription of target genes upon binding their respective
ligands. It is thought that the anticarcinogenic effect of Calcitriol is
mediated via VDRs in cancer cells. The immunomodulatory activity of
calcitriol is thought to be mediated by vitamin D receptors (VDRs) which
are expressed constitutively in monocytes but induced upon activation
of T and B lymphocytes. 1,25-(OH)2-D3 has also been found to
enhance the activity of some vitamin D-receptor positive immune cells
and to enhance the sensitivity of certain target cells to various
cytokines secreted by immune cells.
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